[Senate Hearing 110-1186]
[From the U.S. Government Publishing Office]





                                                       S. Hrg. 110-1186

                 PLASTIC ADDITIVES IN CONSUMER PRODUCTS

=======================================================================

                                HEARING

                               before the

   SUBCOMMITTEE ON CONSUMER AFFAIRS, INSURANCE, AND AUTOMOTIVE SAFETY

                                 OF THE

                         COMMITTEE ON COMMERCE,
                      SCIENCE, AND TRANSPORTATION
                          UNITED STATES SENATE

                       ONE HUNDRED TENTH CONGRESS

                             SECOND SESSION

                               __________

                              MAY 14, 2008

                               __________

    Printed for the use of the Committee on Commerce, Science, and 
                             Transportation






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       SENATE COMMITTEE ON COMMERCE, SCIENCE, AND TRANSPORTATION

                       ONE HUNDRED TENTH CONGRESS

                             SECOND SESSION

                   DANIEL K. INOUYE, Hawaii, Chairman
JOHN D. ROCKEFELLER IV, West         TED STEVENS, Alaska, Vice Chairman
    Virginia                         JOHN McCAIN, Arizona
JOHN F. KERRY, Massachusetts         KAY BAILEY HUTCHISON, Texas
BYRON L. DORGAN, North Dakota        OLYMPIA J. SNOWE, Maine
BARBARA BOXER, California            GORDON H. SMITH, Oregon
BILL NELSON, Florida                 JOHN ENSIGN, Nevada
MARIA CANTWELL, Washington           JOHN E. SUNUNU, New Hampshire
FRANK R. LAUTENBERG, New Jersey      JIM DeMINT, South Carolina
MARK PRYOR, Arkansas                 DAVID VITTER, Louisiana
THOMAS R. CARPER, Delaware           JOHN THUNE, South Dakota
CLAIRE McCASKILL, Missouri           ROGER F. WICKER, Mississippi
AMY KLOBUCHAR, Minnesota
   Margaret L. Cummisky, Democratic Staff Director and Chief Counsel
Lila Harper Helms, Democratic Deputy Staff Director and Policy Director
   Christine D. Kurth, Republican Staff Director and General Counsel
                  Paul Nagle, Republican Chief Counsel
                                 ------                                

   SUBCOMMITTEE ON CONSUMER AFFAIRS, INSURANCE, AND AUTOMOTIVE SAFETY

MARK PRYOR, Arkansas, Chairman       JOHN E. SUNUNU, New Hampshire, 
JOHN D. ROCKEFELLER IV, West             Ranking
    Virginia                         JOHN McCAIN, Arizona
BILL NELSON, Florida                 OLYMPIA J. SNOWE, Maine
MARIA CANTWELL, Washington           GORDON H. SMITH, Oregon
FRANK R. LAUTENBERG, New Jersey      DAVID VITTER, Louisiana
THOMAS R. CARPER, Delaware           JOHN THUNE, South Dakota
CLAIRE McCASKILL, Missouri           ROGER F. WICKER, Mississippi
AMY KLOBUCHAR, Minnesota












                            C O N T E N T S

                              ----------                              
                                                                   Page
Hearing held on May 14, 2008.....................................     1
Statement of Senator Kerry.......................................    31
Statement of Senator Klobuchar...................................    27
Statement of Senator Nelson......................................    24
Statement of Senator Pryor.......................................     1
Statement of Senator Sununu......................................     7
    Prepared statement...........................................     8

                               Witnesses

Alderson, Ph.D., Norris E., Associate Commissioner for Science, 
  Food and Drug Administration, Department of Health and Human 
  Services.......................................................     9
    Prepared statement...........................................    10
Hentges, Ph.D., Steven G., Executive Director, Polycarbonate/BPA 
  Global Group, American Chemistry Council.......................    50
    Prepared statement...........................................    52
Hitchcock, Elizabeth, Public Health Advocate, U.S. Public 
  Interest Research Group........................................    43
    Prepared statement...........................................    44
Myers, Ph.D., John Peterson, CEO and Chief Scientist, 
  Environmental Health Sciences..................................    35
    Prepared statement...........................................    37
Schumer, Hon. Charles E., U.S. Senator from New York.............     3
    Letter dated May 13, 2008 from the Consumers Union, Consumer 
      Federation of America, Kids in Danger, Public Citizen, 
      National Research Center for Women & Families and the U.S. 
      Public Interest Research Group to Hon. Mark Pryor..........     5
Wind, Dr. Marilyn L., Deputy Associate Executive Director for 
  Health Sciences, U.S. Consumer Product Safety Commission.......    13
    Prepared statement...........................................    15

                                Appendix

Response to written questions submitted by Hon. Daniel K. Inouye 
  to:
    Norris E. Alderson, Ph.D.....................................    79
    Elizabeth Hitchcock..........................................    99
    John Peterson Myers, Ph.D....................................    89
Response to written questions submitted by Hon. John F. Kerry by:
    Norris E. Alderson, Ph.D.....................................    84
    Steven G. Hentges, Ph.D......................................   116
    Elizabeth Hitchcock..........................................   104
    John Peterson Myers, Ph.D....................................    95
    Dr. Marilyn L. Wind..........................................    89
Response to written question submitted by Hon. Mark Pryor to:
    Norris E. Alderson, Ph.D.....................................    79
    Steven G. Hentges, Ph.D......................................   106
    Elizabeth Hitchcock..........................................    99
    John Peterson Myers, Ph.D....................................    90
    Dr. Marilyn L. Wind..........................................    86
White Paper (summary), entitled, EA/Free Plastics: The Only 
  Alternative for Safe Plastics, submitted by George D. Bittner, 
  Ph.D., Professor of Neurobiology, The University of Texas at 
  Austin and CEO, CertiChem, PlastiPure, Austin, Texas...........   119

 
                 PLASTIC ADDITIVES IN CONSUMER PRODUCTS

                              ----------                              


                        WEDNESDAY, MAY 14, 2008

                               U.S. Senate,
  Subcommittee on Consumer Affairs, Insurance, and 
                                 Automotive Safety,
        Committee on Commerce, Science, and Transportation,
                                                    Washington, DC.
    The Subcommittee met, pursuant to notice, at 10:05 a.m., in 
room SR-253, Russell Senate Office Building, Hon. Mark Pryor, 
Chairman of the Subcommittee, presiding.

             OPENING STATEMENT OF HON. MARK PRYOR, 
                   U.S. SENATOR FROM ARKANSAS

    Senator Pryor. I will call the meeting to order. I want to 
thank everyone for being here. Senator Schumer is going to be 
here in just a minute. So I will go ahead and do my opening 
statement.
    Just for everybody's knowledge, we have three panels today. 
We have, first, Senator Schumer and he has legislation. Second, 
we have a government panel, the FDA and the Consumer Product 
Safety Commission, and third, we have people who are--I am 
going to call them industry people or they are people that are 
familiar with this issue that are not inside the government. We 
look forward to hearing comments from everyone on this issue.
    The purpose of the hearing today is to gather information 
and try to help us in the Senate start the process of getting 
the facts together and understanding this issue, understanding 
the facts and the science here. Like many of you, I have seen 
some media reports. Some of this has been on the sensational 
side. Some has not been. I think it is very important for the 
Senate and the Commerce Committee specifically to understand 
the science that is involved here.
    So let me go ahead and open it up. Several Senators are 
going to be coming and going. There are other Committees 
meeting right now. So we expect to have several Senators here 
throughout the course of the hearing.
    But again, I would like to say welcome to everyone.
    I know that Senator Sununu will be here. I look forward to 
working with him on this issue, as well as other issues that we 
have been doing over the last couple years here.
    We are here today to talk about plastic additives in 
consumer products. The focus of the hearing will include common 
chemicals found in plastics and consumer products, most notably 
phthalates and BPA, and their relevant scientific and health 
assessments by leading governmental and nongovernmental bodies. 
I will also note that we are trying to gather relevant 
information from these experts and from people who understand 
these issues in an effort for Congress to, like I said before, 
get a better handle on this. So we are trying to, at today's 
hearing, get a wide range of input as our starting point, and 
then we will see where that leads us in subsequent weeks in 
subsequent hearings.
    Again, there have been several news accounts of phthalates 
and BPA that are used in plastic consumer products. Many of 
these press reports talk about specific or potential health 
effects of exposure to these chemicals. I know that whenever 
you talk about chemical exposure, there are a lot of questions 
that come up about how the testing is done and whether you use 
high doses, low doses, how that testing process works. I am 
sure we will talk at least some about that today.
    The panels here know what phthalates and BPA chemicals are, 
but let me go ahead and explain it to the general public 
because I think even Senators sometimes struggle with these 
scientific terms.
    Phthalates are a common class of chemicals used in many 
household products to improve flexibility in plastics. 
Phthalates are primarily used to make PVC, a plastic used in 
many consumer products such as raincoats, vinyl furniture, 
flooring, medical and personal care products, and even in 
recreational and also lots of children's toys.
    BPA is a chemical used to make polycarbonate plastics which 
are clear and nearly shatterproof. These plastics are used to 
make a variety of common products, including things like baby 
and water bottles, sports equipment, medical devices, CD's, 
household electronics. Any product that is made of hard, clear 
plastic likely includes BPA unless the manufacturer 
specifically states it is BPA-free.
    The industry regulatory actions on these chemicals varies 
widely. California, the European Union, as well as numerous 
countries have banned certain phthalates in children's toys. 
Though no government entities have yet banned BPA, many states 
and Canada have begun initiatives to either regulate or ban 
BPA. So this is an emerging area when it comes to regulation, 
and again, it is important for us to understand what is going 
on out there.
    Some of the larger companies like Wal-Mart, Toys ``R'' Us, 
IKEA, either have or will be phasing out the use of phthalates 
in some of their consumer products. I think Wal-Mart Canada and 
Nalgene, which makes these unbreakable kind of water bottles 
and these little containers, have begun phasing out the use of 
BPA.
    Though the scientific studies for these chemicals are 
varied and robust, I believe it is essential for Congress to 
develop a clearer picture of the landscape for the use of these 
and other chemicals in plastics in consumer products. It is my 
hope that this hearing will allow us to get some of the facts 
straight.
    It is also my hope that those here today can address not 
only the scientific studies of themselves and others with 
regard to phthalates and BPA, but also shed light upon 
alternative needs assessments and possible actions with regard 
to those other alternatives that exist in the marketplace.
    It is imperative that Congress act judiciously when 
considering such vast reform to the regulatory nature of these 
consumer products and take into consideration not only the here 
and now but the future path that we might forge.
    I very much look forward to hearing the testimony today. As 
I said, we will have other colleagues join us throughout the 
hearing. I look forward to their comments and questions and 
their input. I know that we will all have lots of questions and 
thoughts on this.
    I would say this, that one of the things we talked about as 
we were on the floor passing the consumer product safety 
legislation, which we passed several weeks ago, was phthalates. 
That issue was hitting the news media about that time, and it 
raised a lot of discussion on the floor about what are 
phthalates, why are they used, how are they used, should we 
regulate them, should we ban them. I mean, we got into these 
questions.
    One of the things that I learned is that there are many, 
many different kinds of phthalates, and some have been tested 
and tested and tested, and others we really do not know that 
much about. So we need to be careful in how we proceed, I 
think, because if we are not careful, if we ban one thing, some 
other phthalate may come on the market that may be more 
hazardous, more dangerous. So we just do not know. So we will 
talk about all those questions today.
    And we are honored now to have Senator Charles Schumer of 
New York here. He has legislation. He is our first panel, and I 
know that he has a very, very busy schedule today. He is 
running between about 20 different stops he has to make this 
morning. So, Senator Schumer, thank you and welcome to the 
Subcommittee.

             STATEMENT OF HON. CHARLES E. SCHUMER, 
                   U.S. SENATOR FROM NEW YORK

    Senator Schumer. Well, thank you, Mr. Chairman. Good 
morning. I want to thank you for holding this hearing. More 
importantly, I want to thank you for your really fine, 
exquisite leadership on these issues and CPSC reform. It has 
just been great. You have done all of this in a directed way 
where solving the problem is important, but a careful and 
measured way as well where you listen to all sides and try to 
balance the considerations. And I would just like to say, Mr. 
Chairman, I think the American people are lucky to have you in 
this position at this crucial time.
    I would also like to thank Chairman Inouye for his work and 
determination and leadership on these issues as well. And I 
appreciate the Committee making some time to hear me on this 
issue because I care a lot about it and I think we have some 
things to do.
    So I am here today to talk about bisphenol A, commonly 
known as BPA, and the legislation that I have introduced along 
with a whole bunch of my colleagues, the BPA-Free Kids Act of 
2008.
    The legislation is an important step in addressing the 
gathering storm of BPA safety. It will ban BPA in children's 
products, including baby bottles, sippy cups, and other toys. 
It is always a scary day when the health and safety of our 
children is called into question. Obviously, we want to protect 
them from harm and not expose them to possible danger.
    When the National Toxicology Program of the NIH released 
their study that BPA could very well cause certain types of 
cancer and hormonal and developmental disorders, the world took 
note. The NTP cited studies showing that BPA can cause 
developmental problems in infants, particularly boys, which 
could lead to serious reproductive problems in later life. It 
also cited studies that indicated a possible link between 
childhood exposure to BPA and impaired neurological 
development.
    When the report came out, the study, I heard from many 
concerned and confused parents around New York who read 
articles about the report, and they are now researching on 
websites and turning bottles over in stores and asking 
shopkeepers does this contain BPA. And now they are asking 
themselves was the bottle they used to feed their child safe. 
What about the teething ring? What about the sippy cup?
    And the question I heard the loudest was why was the 
Government not doing anything about this. That was the biggest 
question we had, Mr. Chairman, and it was a good one because at 
the same time the report came out, we also read that Canada was 
taking action and banning this chemical in baby bottles. We 
heard that Nalgene--this is the water bottle maker from my home 
state. They are in Rochester, New York. They are a fine 
company, and they announced on their own they were 
discontinuing BPA produced bottles. We heard that Wal-Mart in 
your state, Mr. Chairman, was pulling its children's products 
containing BPA immediately from its Canadian stores and, by the 
beginning of the next year, from stores here in the states. 
Toys ``R'' Us took similar action. And in California, a ban on 
BPA in children's products is making its way through the State 
legislature.
    Yet, here in Washington, we seem to have an FDA that was 
looking the other way, that was not taking the studies and 
concerns into account. I am now pleased that the FDA has 
initiated a task force to look into its prior approval of BPA 
and to determine if further action needs to be taken.
    But I answer that right here and right now we cannot wait 
any longer. Congress must act. As I have said over the last 
month, when dealing with our vulnerable population, our 
children, it is better to be safe than sorry. We buy things for 
our kids to keep them safe: shatter-resistant sippy cups, chip-
proof baby bottles. And then we find out later that the very 
products we thought would be safe could actually be much more 
dangerous for our children than the harm that they were 
intended to prevent.
    So along with my colleagues, Senators Feinstein, Kerry, 
Clinton, Durbin, Menendez, and Boxer, I have introduced the S. 
2928, BPA-Free Kids Act of 2008. The Act would ban BPA from 
children's products and mandate the CDC conduct a study into 
the negative effects of BPA on all age groups, including 
expectant mothers.
    I would like to thank and commend my colleagues who have 
worked with me in creating this legislation, pushed this 
important issue. Particularly Senator Feinstein had some very 
important suggestions and we heeded most of them.
    Mr. Chairman, parents always err on the side of caution 
when it comes to their kids' health. We think the law should do 
the same. My bill, if it errs, errs on the side of caution by 
banning the use of BPA in all children's products, including 
toys, dishes, baby bottles, pacifiers, you name it. If it is 
made for children, it should not have BPA in it. Specifically, 
the bill would amend the Federal Hazardous Substances Act to 
include BPA for children's products and trigger all the 
prohibitions of the Act. In that case, BPA in baby bottles and 
other children's products could not be manufactured or sold. 
Parents will not have to worry whether the products their 
children put in their mouths could cause damage.
    Let me be clear, Mr. Chairman. I think we have to look at 
eliminating BPA from a wide variety of products that all of us 
use in our daily life. If it causes harm, let us get rid of it. 
But I think it is important to focus first on children who we 
owe a duty to protect and shield from all harm, whether it is a 
sharp object or a toxic chemical. It is a similar philosophy 
that you and Senator Nelson and Senator Klobuchar, cosponsors 
of the CPSC Reform Act, took when addressing the problem of 
lead in toys. Just like lead, BPA has the potential to cause 
devastating health effects, and just like lead in children's 
toys, BPA should be banned.
    Now, I am proud to say that this act has been endorsed by 
Consumers Union, Public Citizen, the Environmental Working 
Group, First Focus, Kids in Danger, and the Consumer Federation 
of America. All are groups whose mission it is to protect our 
children. I commend them for their work and appreciate their 
support.
    Additionally U.S. PIRG has endorsed the bill, and I believe 
Ms. Hitchcock from the group is testifying before this 
Committee later this morning. And I would ask consent that 
their support letter be entered into the record.
    Senator Pryor. Without objection.
    [The information referred to follows:]

Hon. Mark Pryor,
Chairman,
U.S. Senate,
Subcommittee on Consumer Affairs, Insurance, and Automotive Safety,
Committee on Commerce, Science, and Transportation,
Washington, DC.
                                            Consumers Union
                             Consumer Federation of America
                                             Kids in Danger
                                             Public Citizen
              National Research Center for Women & Families
                        U.S. Public Interest Research Group
                                                       May 13, 2008
Dear Chairman Pryor:

    We are writing to thank you for holding a hearing this week to 
consider the effects of additives to plastics, including bisphenol-A 
(BPA) and phthalates. Our groups are deeply concerned about the 
potentially harmful health effects of both of these chemicals in 
consumer products. BPA is a common chemical found in many hard plastic 
products, including baby bottles, and phthalates are a family of 
chemicals used in toys, cosmetics, food packaging, and medical devices. 
We believe that the potential health and safety hazard associated with 
BPA and phthalates have escaped the scrutiny of our Federal regulators 
for far too long.
BPA
    We know that bisphenol-A can leach from plastic containers and cans 
and into food and beverages, generating potentially significant human 
exposures. A recent study released by the U.S. Centers for Disease 
Control and Prevention (CDC) found that BPA was in the blood of 93 
percent of Americans aged 6 and older. BPA raises particularly 
troubling health questions because it can affect the endocrine system, 
mimicking the effects of estrogen in the body. Experiments in animals 
and with human cells strongly suggest exposures typical in the U.S. 
population may increase susceptibility to breast and prostate cancer, 
reproductive system abnormalities, and, for exposure in the womb and 
early childhood, a host of developmental problems. Concerns about early 
life exposures also extend to early onset of puberty in females, 
potential prostate problems in males, and obesity.
    In May 1999, Consumer Reports magazine reported that BPA from 
polycarbonate plastic baby bottles leached into infant formula after 
the bottles were heated during testing. Based on these results, 
Consumer Reports scientists estimated that babies fed formula 
sterilized by heating in the bottle could be exposed to a BPA dose of 
about 4 percent of the amount that has adversely affected test animals 
in experiments conducted by Professor Frederick vom Saal at the 
University of Missouri, Columbia. The magazine pointed out that, 
although those levels may sound very low, safety limits for infant 
exposure can be set as low as 0.1 percent of the level that has 
adversely affected animals.
    In the decade since Consumer Reports originally published this 
article, many new studies have substantiated the work of Professor vom 
Saal, as documented in recent reviews by expert committees at the 
National Toxicology Program and the Health Ministry of Canada. Unlike 
the Canadian government, which recently announced plans to ban major 
sources of BPA exposure, U.S. regulatory agencies have yet to act to 
protect the public.
    The current U.S. Environmental Protection Agency daily upper limit 
for BPA, 50 micrograms per kilogram of body weight, is based on 
industry-sponsored experiments conducted in the 1980s. Some animal 
studies show adverse health affects from exposure of only 0.025 
micrograms per kilogram of body weight, yet a polycarbonate baby bottle 
with room temperature water can leach 2 micrograms of BPA per liter. A 
3-month-old baby drinking from a polycarbonate bottle may be exposed to 
as much as 11 micrograms per kilogram of body weight daily.
    Aside from polycarbonate plastic bottles, BPA is also a food 
additive approved by the Food and Drug Administration (FDA), commonly 
used in the coatings for the inside of food cans. But a recent report 
by the National Toxicology Program (NTP) questioned previous FDA 
findings that BPA is safe for such applications. Their report, issued 
on April 15, 2008, expressed ``some concern'' based on animal studies 
that BPA might affect the neurological systems and behavior of infants 
and children. Among its conclusions, the NTP report states that, ``the 
possibility that human development may be altered by bisphenol-A at 
current exposure levels cannot be dismissed.''
    Our organizations recently endorsed a bill introduced by Senator 
Charles Schumer recently, S. 2928, the ``BPA-Free Kids Act of 2008.'' 
This bill will prohibit the use of BPA in all children's products, 
effective 180 days after its enactment. It will also require the CDC to 
study the health effects of BPA exposure in all age groups and pregnant 
women. We support this effort and feel it should focus on the products 
that have the greatest potential for causing human harm. Particularly 
due to the possible increased risks to small children and pregnant 
women, we strongly urge the removal of BPA from all products intended 
to contact food.
    With such high consensus within the independent scientific 
community on the strength of evidence for adverse health effects 
associated with BPA exposure, we believe it is prudent--at a minimum--
to remove BPA from children's products, until science can prove its 
safety.
Phthalates
    Phthalates may be linked to developmental and reproductive health 
risks. The industry says that phthalates are safe, but some companies 
have removed them from cosmetics, for example, in response to public 
concern. California has also passed legislation banning phthalates in 
children's products.
    In 2005, the CDC reported that it had found breakdown chemicals 
from two of the most common cosmetic phthalates in almost every member 
of a group of 2,782 people it examined. In rodent studies, phthalates 
have caused testicular injury, liver injury, and liver cancer. Another 
report in 2003 found that men with higher concentrations of two 
phthalate breakdown products in their urine were more likely to have 
low sperm count or low sperm motility.
    With such serious concerns about the impact of phthalates on our 
health, and because of the ubiquity of these chemicals in our products, 
we believe Federal agencies must also examine and act upon independent, 
unbiased science about all of the potential harms associated with 
phthalates in order to protect the public health.
    Again, we appreciate your Subcommittee's work in examining BPA and 
phthalates. We look forward to continuing to work with you and the 
members of the Subcommittee in the future.
            Sincerely,
Donald L. Mays
Senior Director, Product Safety and Technical Public Policy
Consumers Union

Ami Gadhia
Policy Counsel
Consumers Union

Nancy A. Cowles
Executive Director
Kids in Danger

David Arkush
Director, Congress Watch
Public Citizen

Ellen Bloom
Director, Federal Policy
Consumers Union

Rachel Weintraub
Director of Product Safety and Senior Counsel
Consumer Federation of America

Elizabeth Hitchcock
Public Health Advocate
U.S. Public Interest Research Group

Paul Brown
Government Relations Manager
National Research Center for Women & Families

    Senator Schumer. These groups have told me that the BPA-
Free Kids Act of 2008 is a huge step in the right direction of 
protecting children from potential neurological or reproductive 
harm.
    We will hear from others, I am sure, who are going to say 
today that BPA is safe and this entire outcry has been blown 
way out of proportion. And my response is that Congress should 
not gamble with our children's health. If there is a 
significant chance that this may cause harm, particularly in 
children, then we ought to err on the side of caution.
    In closing, I believe that we in Congress owe it to parents 
to give them the peace of mind that this bill would provide. 
There are alternative chemicals and other products that can be 
used, as shown by the speed by which companies like Nalgene and 
Wal-Mart and Toys ``R'' Us moved, and I hope, Mr. Chairman, 
that in the coming months, this Committee will have the 
opportunity to mark up this bill and it will be passed into 
law. Obviously, I look forward to working with you and the 
Committee to move our legislation, make improvements that you 
might see fit.
    And last but certainly not least, I want to thank you and 
the Ranking Member for allowing me the opportunity to speak 
here today.
    Senator Pryor. Well, thank you, Senator Schumer. It is 
always good to have you here, and thank you for your interest 
in this and your leadership.
    I do not have any questions about your legislation at this 
point. Do you?

               STATEMENT OF HON. JOHN E. SUNUNU, 
                U.S. SENATOR FROM NEW HAMPSHIRE

    Senator Sununu. No, I have no questions. I certainly want 
to thank the Senator for being here and thank the Chairman for 
putting together the hearing.
    There is no question that we need to understand the role 
and responsibility of the agencies that are entrusted with the 
protections Senator Schumer talked about, the FDA, the Consumer 
Product Safety Commission, their role and responsibility in 
understanding the impact and effects of not just BPA, but any 
additives and chemicals that are included in plastics, 
especially those intended for products that are used by 
children. They are the most vulnerable population. They are the 
ones who are most likely to be affected by even low dosages or 
low levels of exposure.
    We also want to make sure that we are doing everything 
possible at the Federal level to better understand those 
impacts, whether it is research that is funded through agencies 
like the NIH, or research that is being encouraged or funded in 
the private sector. We need to have an honest, clear-headed 
assessment of what the health effects are, and what the risks 
are even if the risks are small. Oftentimes even small risks 
warrant taking action as an insurance policy against our lack 
of knowledge.
    So I thank the Senator for being here and look forward to 
the testimony of our key witnesses.
    [The prepared statement of Senator Sununu follows:]

              Prepared Statement of Hon. John E. Sununu, 
                    U.S. Senator from New Hampshire
    Mr. Chairman, thank you for holding today's hearing.
    Lately, many Americans have heard and read a lot about phthalates 
and bisphenol A (BPA), but for most, these two chemicals generate a 
tremendous amount of confusion.
    There are scientific studies that conclude both are perfectly safe, 
and other studies that indicate possible concern.
    Consumers see retail giants Wal-Mart and Toys ``R'' Us tell their 
suppliers that they will no longer sell toys with phthalates and baby 
bottles with BPA and they wonder: if they're taking action, then maybe 
there is some health impact after all. Or, are they responding to 
market forces.
    American consumers want to know:

   Are these chemicals safe?

   Are calls for their removal from products justified?

   Are there alternatives that are safer and more effective?

    Consumers are receiving conflicting data over what's safe for their 
families, and they want to be able to separate fact from fiction.
    The sheer ubiquity of plastics in our society necessitates a closer 
look; to make sure the products consumers are purchasing, and 
particularly, eating and drinking from, are not harmful.
    It is my hope we are able to shed some light on this important 
issue today, and I am quite interested to hear what our witnesses have 
to say.
    Thank you, Mr. Chairman.

    Senator Pryor. Thank you.
    Senator Schumer. I thank both of you.
    Senator Pryor. Thank you, Senator Schumer.
    With that, what we will do is we will call up our second 
panel, and that would be the two government witnesses. And I 
will just do a very, very brief introduction. If you all want 
to come up and take your seats and get your microphones 
adjusted there, that would be great.
    First we will have Dr. Norris Alderson, Associate 
Commissioner for Science, the Food and Drug Administration, and 
second we will have Dr. Marilyn Wind, Deputy Associate 
Executive Director for Health Sciences, Consumer Product Safety 
Commission. Dr. Alderson, do you want to go first?

            STATEMENT OF NORRIS E. ALDERSON, Ph.D.,

              ASSOCIATE COMMISSIONER FOR SCIENCE,

                 FOOD AND DRUG ADMINISTRATION,

            DEPARTMENT OF HEALTH AND HUMAN SERVICES

    Dr. Alderson. Good morning, Chairman Pryor and Members of 
the Subcommittee. I am Dr. Norris Alderson, Associate 
Commissioner for Science at FDA. Thank you for providing an 
opportunity to discuss the FDA's ongoing work regarding the 
safety of bisphenol A, or BPA.
    Last month, FDA Commissioner Andrew von Eschenbach formed 
an agency-wide BPA Task Force, which I chair, to conduct a 
review of the concerns raised in recent risk assessments of 
BPA. That task force is undertaking a cross-agency review of 
current research and information on the safety of BPA.
    Although our review is ongoing at this time, we have no 
reason to recommend that consumers stop using products 
containing BPA. A large body of evidence indicates that 
currently marketed products containing BPA, such as baby 
bottles and food containers, are safe and that exposure levels 
to BPA from these products are well below those that may cause 
health effects.
    I will note, however, that individuals who, nonetheless, 
have concerns about BPA may turn to alternative products in the 
marketplace. For example, alternatives to polycarbonate baby 
bottles such as those made from glass are widely available.
    I also want to emphasize that research on the safety of BPA 
is a very active area. If FDA's review leads us to a 
determination that the use of BPA is not safe, we will not 
hesitate to take the action needed.
    Bisphenol A is used in the manufacture of two types of 
polymers used in food contact articles. Polycarbonate plastics 
are used in products such as water and infant bottles, while 
epoxy-based enamels and coatings are widely used in inner 
linings of food and beverage cans. These food contact 
substances have been regulated by FDA for many years and are 
enforced by sections under Title 21.
    Small residual amounts of trace BPA can remain in polymers 
and may migrate into food during use of the product. For this 
reason, FDA's safety assessments include a consideration of 
likely consumer exposure. We have determined that dietary 
exposure to BPA from these uses is in the very low parts per 
billion range.
    The task force is looking at all products that FDA 
regulates, not just the ones I have mentioned. We are already 
focusing on specific concerns raised by reports of the National 
Tox Program at NIH.
    In November 2007, NTP's Center for the Evaluation of Risks 
to Human Reproduction released a report by a panel of experts. 
The opinion reached by the experts was that they had some 
concerns for children regarding neural and behavioral effects. 
They also had minimal concern for BPA exposure to these 
populations for the effects on the prostate gland, mammary 
gland, and early female puberty.
    NTP subsequently issued a draft report, and they iterated 
the same thing relative to the behavior, but they also raised 
their concern on the mammary gland and the early female 
puberty.
    These included new data which we are all continuing to 
review. And these lead us to conclusions that the currently 
available evidence provides little evidence that there are 
issues, but it also raises a number of uncertainties which the 
NTP brief identified.
    We have studied the reports and conclusions of NTP's expert 
panel and we are actually reviewing the draft. In fact, members 
of the BPA Task Force will be meeting with the NTP staff this 
week to discuss their findings and get a better understanding 
of how they came to their conclusions.
    Also, I should tell you, Senator, FDA's National Center for 
Tox Research is discussing with the NTP staff yesterday and 
today both BPA and phthalates.
    Although the FDA has been actively surveying data on BPA 
for many years, this form of assessment began in early 2007. We 
initially focused on the low-dose effects and have concluded 
that the current exposure to adults and infants is safe. 
Although FDA's reliance on these studies have been questioned 
because they were funded by industry, they were considered 
pivotal by FDA in our review of the data for a number of 
reasons. FDA's findings thus far are underscored by the 
conclusions of two risk assessments by the European Food Safety 
Authority and the Japanese National Institute of Advanced 
Industrial Science and Technology.
    Let me briefly mention phthalates, which are also a concern 
to this Subcommittee. FDA does not now have a comprehensive 
inventory of products that contain phthalates. We do know it is 
a component of the compounds used in certain medical products 
and that brings risk-benefit factors into play. FDA primarily 
through NCTR is conducting research to address uncertainties in 
our understanding of the potential health risks posed by 
exposure to phthalates.
    In conclusion, let me re-emphasize that current evidence 
indicates that BPA exposure from food contact materials is well 
below the levels that may cause health effects. But FDA's 
conclusions on the safety of chemical compounds or the products 
in which they are found are never set in stone. They are always 
subject to review or revision when new data or a better 
analysis become available. At the end of the day, FDA's goal is 
always to act within our authority and protect the public 
health.
    Thank you for the opportunity to testify today, and I will 
be happy to answer any questions you may have.
    [The prepared statement of Dr. Alderson follows:]

Prepared Statement of Norris E. Alderson, Ph.D., Associate Commissioner 
  for Science, Food and Drug Administration, Department of Health and 
                             Human Services
Introduction
    Good morning, Chairman Pryor and Members of the Subcommittee. I am 
Dr. Norris Alderson, Associate Commissioner for Science at the U.S. 
Food and Drug Administration (FDA or the Agency), part of the 
Department of Health and Human Services (HHS). FDA appreciates the 
opportunity to discuss our ongoing work regarding the safety of 
bisphenol-A (BPA).
    In light of recent reports and statements from the National 
Toxicology Program (NTP) at the National Institutes of Health and 
Health Canada, as well as interested public health advocates, FDA 
believes it is important that consumers have accurate and up-to-date 
information about BPA. We have established a link on our home page, at 
http://www.fda.gov, where consumers can find such information.
    On April 17, 2008, FDA Commissioner Andrew von Eschenbach formed an 
agency-wide BPA Task Force, which I chair, to conduct a review, 
encompassing all FDA-regulated product lines, of the concerns raised 
about BPA. The task force is undertaking a broad review of current 
research and information on BPA. In addition to looking at the food and 
beverage containers that have been the focus of recent concerns as well 
as our regulatory efforts over the years, the task force is conducting 
an inventory of all products regulated by FDA's food and medical 
products centers to better understand other potential routes of 
exposure. We are already looking at the specific concerns raised by NTP 
in its recent Draft Brief and the draft risk assessment released by 
Health Canada last month.
    At this time, FDA is not recommending that consumers discontinue 
using food contact materials that contain BPA. Although our review of 
the NTP reports is continuing, a large body of available evidence 
indicates that food contact materials containing BPA currently on the 
market are safe, and that exposure levels to BPA from these materials, 
including exposure to infants and children, are below those that may 
cause health effects. We also acknowledge that BPA research is an 
extremely active area, and we want to assure you that if FDA's review 
of data leads us to a determination that uses of BPA are not safe, the 
Agency will take action to protect the public health.
Regulation of Components of Food Contact Materials Containing BPA
    Section 409 of the Federal Food, Drug, and Cosmetic Act (FD&C Act) 
requires that chemicals undergo pre-market approval by FDA if they are 
reasonably expected to migrate to food. BPA is used in the manufacture 
of two types of polymers used in food contact articles, specifically, 
polycarbonate polymers and epoxy-based enamels and coatings. These food 
contact substances have been regulated for many years pursuant to 
regulations published in Title 21 of the Code of Federal Regulations 
(CFR). Polycarbonate (PC) polymers, which are found in products such as 
water and infant bottles, are regulated in 21 CFR  177.1580. Epoxy-
based enamels and coatings, which are widely used as inner linings for 
food cans, are regulated in 21 CFR  175.300(b)(3)(viii), 21 CFR  
177.1440 and 21 CFR  177.2280. Because no polymeric reactions go 
entirely to completion, small residual amounts of BPA can remain in 
polymers and may migrate into food during use of the product. For this 
reason, FDA's safety assessments include a consideration of likely 
consumer exposure. The Agency has determined that dietary exposure to 
BPA from these uses is in the very low parts per billion range, which 
is well below the levels that would cause adverse health effects. 
Further, it is important to emphasize that as new data and reviews of 
BPA have become available, FDA's review of the safety of BPA has been 
an ongoing process.
Evaluation of BPA Safety
    Although FDA has been actively surveying data on BPA for many 
years, the Agency began a formal reassessment of BPA in early 2007. 
This reassessment initially focused on possible ``low-dose'' effects 
for BPA but, in the fall of 2007, we added an evaluation of the 
endpoints identified by an expert panel of the NTP's Center for the 
Evaluation of Risks to Human Reproduction (CERHR) after the CERHR 
meeting in August 2007.
    In evaluating the safety of food contact articles or their 
constituents, such as BPA, FDA's safety assessment relies on evaluating 
probable consumer exposure as a result of the proposed use and other 
authorized uses, and ensuring that the probable consumer exposures are 
supported by the available toxicological information. With regard to 
consumer exposure, FDA found that the small amounts of BPA that 
migrated into food from the use of PC-based polymers and BPA-based 
epoxy coatings result in a cumulative daily intake for adults of 11 
micrograms per person per day (mg/person/day).
    This estimate is based on: (1) the migration levels of BPA into 
food, or into food-simulating solvents, under the most severe 
conditions of use (i.e., time and temperature), and (2) information on 
the types of food contacted, the fraction of the diet that would come 
into contact with that type of food contact material, and whether the 
finished food contact article would be intended for single or repeated 
use. FDA's evaluation also considered that the use of can enamels in 
infant formula packaging and the use of PC baby bottles results in an 
estimated daily intake of 7 mg/infant/day. These estimates relied on 
data generated by FDA laboratories or the regulated industry, or 
available in the open literature, on BPA levels in canned food and in 
food contacting PC articles.
    In conducting this evaluation, FDA was aware that higher migration 
levels had been reported in some studies available in the literature. 
Many of those studies were conducted under very unrealistic conditions, 
such as the use of aggressive solvents or extremely high temperatures 
that are not reflective of how the products were intended to be used by 
consumers. Those studies were deemed to not be representative of actual 
use conditions. In our evaluation of consumer exposure, we used 
exposure assumptions that were based on realistic, but still 
conservative, use scenarios for both adults and infants.
    FDA's reassessment of possible ``low-dose'' effects of BPA 
concluded that the current level of exposure to adults and infants is 
safe as defined in 21 CFR  170.3(i). This conclusion was based on our 
review of the most relevant data available at that time, including our 
analyses, completed in July 2007, of two pivotal multi-generational 
oral studies performed under applicable regulatory guidelines. The 
studies included the examination of reproductive and some developmental 
endpoints and a large range of exposures, including low doses. These 
studies include a two-generation reproductive toxicity test in mice and 
a three-generation reproductive toxicity test in rats.
    These studies were considered pivotal in our review of the existing 
data for a number of reasons. These include: (1) they were conducted in 
a manner that FDA would recommend to a stakeholder seeking an approval 
for a new use (i.e., they follow recommended guidelines) including 
extended parameters allowing for the examination of issues that were 
controversial to BPA at the time; (2) they were submitted to the Agency 
with supporting information (raw data) allowing for our independent 
evaluation of the findings; and (3) they both included a large range of 
exposures, including a range of high and low doses which allowed for 
the examination of dose response curves. With regard to FDA's 
evaluation of BPA, these studies are often given more weight than 
publications in the public literature that examine the same endpoints 
because the publications often lack details and supporting data that 
would be necessary for an independent evaluation of the underlying data 
by Agency scientists. In addition, many of the published studies on BPA 
have numerous protocol limitations, including the animal model 
utilized, the method of BPA measurement, the statistical analysis of 
the data, the lack of multiple/correctly spaced doses in the 
experimental protocol, and the route of administration.
    By comparing the ``no observed effect'' level (5 milligrams per 
kilogram of body weight per day) derived from the reproductive and 
developmental endpoints examined in these pivotal studies to the 
estimated daily intake of BPA, FDA determined that an adequate margin 
of exposure exists to reach a conclusion of ``reasonable certainty of 
no harm under the intended conditions of use,'' the standard set forth 
in 21 CFR  170.3(i). That margin of exposure is approximately 7,000 
fold for infants--that is, the levels of exposure to BPA at which any 
effects would be observed in infants is about 7,000 times higher than 
our estimates of actual exposure.
    In addition, FDA has completed a summary of the pharmacokinetic 
data on BPA in multiple species. FDA has determined that understanding 
the species differences and the differences in how metabolic systems 
handle BPA administered via various routes of exposure, such as oral 
versus subcutaneous, are also pivotal to examining the safety of BPA.
    FDA's findings thus far are underscored by the conclusions of two 
risk assessments for BPA from 2006, conducted by the European Food 
Safety Authority's Scientific Panel of Food Additives, Flavourings, 
Processing Aids and Materials in Contact with Food, and the Japanese 
National Institute of Advanced Industrial Science and Technology. Each 
of these documents considered the possibility of a low-dose effect and 
concluded that no health risk exists for BPA at the current exposure 
level. Neither of these risk assessments disagrees with FDA's current 
position of the safe use of BPA at the current exposure level.
BPA Task Force Review
    FDA has carefully studied the review and conclusions of the expert 
panel convened by CERHR, released on November 26, 2007. The CERHR 
expert panel found that, based on current BPA exposure levels, ``some 
concern'' exists for pregnant women and fetuses and infants and 
children for exposure to BPA causing neural and behavioral effects. The 
expert panel also concluded that there was ``minimal concern'' for BPA 
exposure in these populations for effects in the prostate gland, 
mammary gland, and an earlier age for puberty in females.
    The NTP Draft Brief released on April 14, 2008, reiterated the 
conclusions of the CERHR panel with regard to neural and behavioral 
effects. However, the NTP Draft Brief departed from the expert panel in 
concluding that ``some concern'' exists for effects in the prostate 
gland, mammary gland, and an earlier age for puberty in females for BPA 
exposure to fetuses, infants and children. These analyses emphasized 
relatively new data and emerging or difficult-to-interpret endpoints in 
toxicology and considered the fact that the studies currently available 
provide limited evidence and contain numerous uncertainties. It is 
noteworthy that the increase in concern from ``minimal'' to ``some'' 
from the conclusion from CERHR's expert panel to NTP's Draft Brief 
reflects numerous studies that have appeared in the literature only in 
the past several months. Although the NTP Draft Brief discusses ``some 
concern'' for developmental exposure and mammary and prostate gland 
cancer, it also highlights the uncertainties regarding these data and 
states that the evidence is not sufficient to conclude that BPA is a 
rodent carcinogen for these endpoints or that BPA presents a cancer 
hazard to humans.
    Neural and behavior development effects were also the focus of a 
recent draft risk assessment released by Health Canada and Environment 
Canada on April 18, 2008. Both the NTP Draft Brief and the Canadian 
draft risk assessment are reviews of existing and recently developed 
data. Both discuss animal studies on neural, behavioral, and 
developmental effects and both assessments point out that these studies 
provide only limited evidence for concern for human exposure to BPA. 
Finally, both suggest that more research is needed to better understand 
their implications for human health.
    FDA has not yet completed its review of concerns raised by the 
CERHR expert panel last fall or the NTP Draft Brief released last 
month. Therefore, those concerns are under active consideration by FDA 
and the BPA Task Force, and we will take appropriate action, if 
warranted, at the completion of our review.
Conclusion
    Although the Agency's review of the newly available reports is 
continuing, a large body of available evidence indicates that 
currently-marketed food contact materials containing BPA are safe, and 
that exposure to BPA from food contact materials, including exposures 
for infants and children, are below the levels that may cause health 
effects.
    We are actively reviewing the data on BPA and will continue to 
consider the relevance of new data and studies as they appear. FDA's 
work in assessing the safety of these products is never truly final, 
and if our continuing review of all available data leads us to a 
determination that the current levels of exposure to BPA are not safe, 
we will take appropriate action to protect the public health. Thank you 
for the opportunity to testify today, and I would be happy to answer 
any questions.

    Senator Pryor. Thank you.
    Dr. Wind?

 STATEMENT OF DR. MARILYN L. WIND, DEPUTY ASSOCIATE EXECUTIVE 
              DIRECTOR FOR HEALTH SCIENCES, U.S. 
               CONSUMER PRODUCT SAFETY COMMISSION

    Dr. Wind. Good morning, Mr. Chairman and Members of the 
Subcommittee. My name is Dr. Marilyn Wind and I am the Deputy 
Associate Executive Director for Health Sciences at the U.S. 
Consumer Product Safety Commission. I am pleased to come before 
this Committee today to testify and to answer your questions 
regarding phthalates and bisphenol A.
    Phthalates are chemicals used to soften PVC and make it 
flexible. PVC is found in a number of consumer products.
    CPSC's regulatory authority over phthalates comes from the 
Federal Hazardous Substances Act, or the FHSA. Under the FHSA, 
CPSC must consider both the toxicity of, as well as the 
exposure to, a product in order to designate it a hazardous 
substance. Children's products containing a hazardous substance 
are automatically banned by operation of law.
    Since the early 1980s, the CPSC has investigated, 
researched, and monitored phthalates used in consumer products 
under the agency's jurisdiction. In the early 1980s, the 
primary phthalate used in children's products was di-(2-
ethylhexyl) phthalate, or DEHP. After a National Toxicology 
Program bioassay indicated that DEHP caused cancer in rodents, 
the Toy Manufacturers of America representing their member 
companies agreed to voluntarily cease using DEHP in toys 
intended to be mouthed, and subsequently, a ban of DEHP was 
incorporated into the ASTM toy standard. DEHP was replaced with 
another phthalate, diisononyl phthalate, or DINP.
    Chronic studies on DINP were completed by the chemical 
industry in 1997 and 1998. In 1998, CPSC staff completed a risk 
assessment on DINP. While staff concluded that few, if any, 
children were at risk of liver or other organ toxicity from 
mouthing teethers, rattles, and other PVC toys that contain 
DINP, staff also indicated that there were a number of 
uncertainties. As a result of these uncertainties, a voluntary 
agreement was reached with industry in December 1998 to stop 
the use of DINP in teethers, rattles, and pacifiers.
    Additionally, staff at that time recommended that the 
commissioners convene a Chronic Hazard Advisory Panel, or CHAP, 
to evaluate whether there are chronic hazards associated with 
exposure to DINP and what, if any, risk is posed. The staff 
further recommended: one, that the Commission conduct an 
extensive observation study of children's mouthing behavior to 
better understand the exposure issues; two, to develop a better 
laboratory method to measure the migration of DINP from 
products; and three, to test additional products intended for 
children under 3 years of age for phthalates. The Commission 
approved all of these staff recommendations.
    A CHAP was convened and issued its report to the Commission 
on June 15, 2001. Staff also completed all the studies that the 
Commission had approved by 2002. Taking all of this information 
together, CPSC staff estimated that the daily DINP exposure 
from toys on the market at that time for children up to 3 years 
of age would not pose a health risk. Based upon this analysis, 
the Commission voted 3 to 0 on February 21, 2003 to deny a 
petition which requested the ban of PVC in all toys and other 
products intended for children 5 years of age and under.
    I would like to note that the legislation currently under 
consideration by Congress would ban certain phthalates down to 
0.1 percent. Because phthalates are ubiquitous, the level of 
0.1 percent would be a contamination or background level and 
not the result of phthalates being intentionally added to the 
product. When CPSC staff tested toys, we found that phthalates 
were present in the range of 13 to 39 percent. That is what is 
needed to make toys flexible. For toys containing multiple 
phthalates, it could be extremely difficult to measure down to 
the level of less than 0.1 percent.
    With regard to bisphenol A, or BPA, this is a chemical used 
in the manufacture of polycarbonate plastics and epoxy resins. 
The greatest potential for human exposure to BPA is from 
contact items. The recent in-depth peer review conducted by the 
National Toxicology Program Center for the Evaluation of Risks 
to Human Reproduction stated that diet accounts for the vast 
majority, 99 percent, of human exposure. If BPA migrates out of 
a food contact surface into food, it is considered an indirect 
food additive and would be under the jurisdiction of the Food 
and Drug Administration.
    Polycarbonate used in pacifier shields, helmets, protective 
gear such as goggles and chin guards, as well as other 
products, would fall under CPSC's jurisdiction. Polycarbonate 
is used in these products because it is very hard, unbreakable, 
and a sturdy plastic. There would be no exposure expected from 
helmets, goggles, other protective gear, compact disks, or 
electronics. The use of polycarbonate in pacifier shields 
prevents the shield from shattering when a child falls. 
Polycarbonates used in protective gear prevents head, eye, and 
bodily injury. Beneficial uses of polycarbonates such as these 
should be considered when acting to ban bisphenol A from 
children's products.
    I am pleased to have the opportunity to testify today and 
welcome your questions.
    [The prepared statement of Dr. Wind follows:]

 Prepared Statement of Dr. Marilyn L. Wind, Deputy Associate Executive 
 Director for Health Sciences, U.S. Consumer Product Safety Commission
    Good Morning, Mr. Chairman:

    My name is Dr. Marilyn Wind, and I am the Deputy Associate 
Executive Director for Health Sciences at the U.S. Consumer Product 
Safety Commission (CPSC). I am pleased to come before the Committee 
today to testify and to answer your questions regarding phthalates and 
bisphenol A.
    Phthalates are chemicals used to soften polyvinyl chloride (PVC) 
and make it flexible. PVC is found in a number of consumer products. 
CPSC's regulatory authority over phthalates comes from the Federal 
Hazardous Substances Act (FHSA), and since the early 1980s, the CPSC 
has investigated, researched, and monitored phthalates used in consumer 
products under the agency's jurisdiction.
    In regulating a product under the FHSA, the CPSC must consider not 
only the toxicity of the product under consideration but also the 
exposure to that product under reasonably foreseeable handling and use. 
If such a product may cause substantial personal injury or substantial 
illness during or as a proximate result of any customary or reasonably 
foreseeable use by children and is a toy or other article for use by 
children, it would be considered a hazardous substance and is 
automatically banned by operation of law.
    In the early 1980s the primary phthalate used in children's 
products was di-(2-ethylhexyl) phthalate or DEHP. A National Toxicology 
Program 2-year bioassay indicated that DEHP caused cancer in rodents. 
Because of concern about these results, the industry removed DEHP from 
pacifiers, rattles, and teethers. A ban of the use of DEHP in 
pacifiers, rattles and teethers was subsequently incorporated into ASTM 
F-963, the voluntary Standard Consumer Safety Specification on Toy 
Safety. DEHP was replaced with another phthalate, diisononyl phthalate 
or DINP.
    Chronic toxicity studies on DINP were completed by the chemical 
industry in 1997 and 1998. In 1998 CPSC staff completed a risk 
assessment on DINP. While staff concluded that few, if any, children 
were at risk of liver or other organ toxicity from mouthing teethers, 
rattles, and other PVC toys that contain DINP, staff also indicated 
that there were a number of uncertainties, primarily regarding 
exposure. As a result of these uncertainties, a voluntary agreement was 
reached with industry in December 1998 to stop the use of DINP in 
teethers, rattles, and pacifiers.
    Additionally, CPSC staff at that time recommended that the 
Commissioners convene a Chronic Hazard Advisory Panel (CHAP) to 
evaluate whether there are chronic hazards associated with exposure to 
DINP and what, if any, risk is posed.\1\ The staff further recommended: 
(1) that the Commission conduct an extensive observation study of 
children's mouthing behavior to better understand the exposure issues; 
(2) develop a better laboratory method to measure the migration of 
DINP; and (3) test additional products intended for children under 3 
years of age to determine if they contain phthalates. The Commission 
approved all of these staff recommendations.
---------------------------------------------------------------------------
    \1\ A CHAP is an independent panel of seven scientists chosen by 
the Commission from scientists recommended by the National Academy of 
Sciences. A CHAP is required under the Consumer Safety Act before the 
Commission may regulate a chronic hazard.
---------------------------------------------------------------------------
    In its report to the Commission on June 15, 2001, the CHAP 
concluded that for DINP to pose a risk of injury to young children, 
they must routinely mouth DINP-plasticized toys for 75 minutes per day 
or more. For the majority of children, they concluded that exposure to 
DINP from DINP-containing toys would be expected to pose a minimal to 
non-existent risk of injury and, at the levels to which children were 
exposed, there was no carcinogenic, reproductive or developmental 
risks.
    CPSC's behavioral observation study took place in 2000 and 2001. It 
was not completed in time for the CHAP to utilize the results when 
reaching their conclusions. In the behavioral observation study, 
trained observers monitored the behavior of 169 children between the 
ages of 3 and 36 months. The study found that the daily mouthing times 
of toys and teethers were much lower than expected. Based upon this 
observation study, staff concluded that it is very unlikely that 
children will mouth soft plastic toys for the 75 minutes a day that the 
CHAP identified as a minimum level of concern.
    In a separate study, CPSC staff measured the level of migration of 
DINP from 41 children's products purchased from retail stores. The 
scientific experiments conducted in this study measured the amount of 
DINP that would leach from a representative sample of toys when 
children placed them in their mouths. Taking all of this information 
together, the CPSC staff estimated that the daily DINP exposure from 
toys on the market at that time for children up to 3 years of age would 
not pose a health risk.
    In November 1998, a group of organizations petitioned the 
Commission to ban children's products made from PVC. Based upon the 
extensive scientific and technical investigations described above, 
staff concluded in its briefing package to the Commissioners that there 
is no demonstrated health risk posed by PVC toys or other products 
intended for children 5 years of age and under, and thus, no 
justification for banning PVC use in toys and other products for 
children 5 years of age and under. On February 21, 2003, the Commission 
voted 3-0 to deny the request to ban PVC in all toys and other products 
intended for children 5 years of age and under. A copy of the petition 
denial letter, Record of Commission Action, and Commissioners' 
statements are attached,
    I would like to note that the legislation currently under 
consideration by Congress would ban certain phthalates down to 0.1 
percent. Because phthalates are ubiquitous, the level of 0.1 percent 
would be a contamination level and not the result of phthalate being 
intentionally added to the product. When we tested toys, we found that 
phthalates were present in the range of 13 to 39 percent; that is what 
is needed to make toys flexible. For toys containing multiple 
phthalates, it could be extremely difficult to measure down to the 
level of less than 0.1 percent.
    With regard to bisphenol A, or BPA, this is a chemical used in the 
manufacture of polycarbonate plastics and epoxy resins. Small amounts 
of BPA may be released as the plastic or resin breaks down. Examples of 
consumer products using polycarbonate plastics include eyeglass lenses, 
protective eyewear, protective gear such as helmets and shin guards, 
glazing, electronics, compact disks and labware. Epoxy resins are used 
in paints, coatings, adhesives, and as linings for canned foods.
    Polycarbonate used in pacifier shields, helmets, protective gear 
such as goggles and shin guards, as well as other products, would fall 
under CPSC's jurisdiction. However, since polycarbonates are expensive, 
it is our understanding that polycarbonate is used in only those 
consumer products where there is a need for a very hard, unbreakable, 
sturdy plastic. Polycarbonate is used in pacifier shields (that prevent 
the nipple from being swallowed) so that when a child falls, the shield 
does not shatter, breaking into small parts and injuring the child. 
There would be no exposure expected from helmets, goggles, other 
protective gear, compact disks, or electronics. If there is no 
exposure, there is no health risk. Polycarbonate plays a very important 
role in its use in helmets and other protective gear. The helmets 
prevent children from receiving serious head injuries while engaging in 
many sports. This beneficial use of polycarbonate should be considered 
when acting to ban bisphenol A from children's products. Such a ban 
could result in less effective protection of children from head, eye, 
or bodily injury.
    The greatest potential for human exposure to BPA is from food 
contact items. The recent in-depth peer review conducted by the 
National Toxicology Program (NTP) Center for the Evaluation of Risks to 
Human Reproduction (CERHR) stated that diet accounts for the vast 
majority, 99 percent, of human exposure. If BPA migrates out of a food 
contact surface into food, it is considered an unintentional food 
additive and would be under the jurisdiction of the Food and Drug 
Administration (FDA). I am pleased to have the opportunity to testify 
with Dr. Alderson from FDA today, and I welcome your questions.
                                 ______
                                 
                    U.S. Consumer Product Safety Commission
                                                     Washington, DC
Record of Commission Action
Commissioners Voting by Ballot*

Commissioners Voting:
Chairman Hal Stratton
Commissioner Thomas H. Moore
Commissioner Mary Sheila Gall
Item:
    Petition (HP 99-1) Requesting Ban of Use of PVC in Products 
Intended for Children Five Years of Age and Under
Decision:
    The Commission voted unanimously (3-0) to deny petition HP 99-1 and 
issue a denial letter as drafted (copy attached). The petition requests 
a ban of polyvinyl chloride (PVC) in all toys and other products 
intended for children 5 years of age and under and requests that the 
Commission issue a national advisory warning of health risks associated 
with soft plastic vinyl toys.
    Commissioners Gall and Moore each submitted statements to accompany 
their votes. The petition denial letter and the Commissioners' 
statements are attached.
            For the Commission:
                                         Todd A. Stevenson,
                                                         Secretary.
    *Ballot vote due February 20, 2003.
                                 ______
                                 
                    U.S. Consumer Product Safety Commission
                                  Washington, DC, February 26, 2003
Mr. Jeffrey Becker Wise,
Policy Director,
National Environmental Trust,
Washington, DC.

    Re: Petition Requesting Ban of Use of Polyvinyl Chloride (PVC) in 
Products Intended for Children Five Years of Age and Under (briefing 
package date corrected as noted in italic)

Dear Mr. Wise:

    As requested in your letter of November 19, 1998 I am communicating 
through you to advise the petitioners that on February 21, 2003, the 
Consumer Product Safety Commission voted 3-0 to deny the requests from 
the National Environmental Trust and eleven other organizations that 
the Commission:

   immediately ban polyvinyl chloride (PVC) in all toys and 
        other products intended for children 5 years of age and under; 
        and

   issue a national advisory on the health risks that have been 
        associated with soft plastic vinyl toys to inform parents and 
        consumers about the risks associated with PVC toys currently in 
        stores and homes.

    The submission from the petitioners gave as the primary reason for 
these requests the toxicity of diisononyl phthalate (DINP), a 
plasticizer in PVC, and the toxicity of lead and cadmium in PVC.
    The requested ban on PVC in all toys and other products intended 
for children 5 years of age and under was docketed as a petition for 
rulemaking under section 3(j) of the Federal Hazardous Substances Act 
(FHSA) on December 7, 1998 (Petition No. HP 99-01). 15 U.S.C.  
1262(j). The request that the Commission issue a national advisory on 
the health risks that have been associated with soft plastic vinyl toys 
was not docketed because it would not require rulemaking to implement.
    To take the requested regulatory action, the Commission would have 
to declare under the FHSA that products containing PVC intended for use 
by children of 5 years old and younger were ``hazardous substances.'' 
This would require the Commission to find that such PVC products met 
the FHSA's definition of hazardous substance, which requires in this 
instance not only that the product be toxic, but that it ``may cause 
substantial personal injury or substantial illness during or as a 
proximate result of any customary or reasonably foreseeable handling or 
use, including reasonably foreseeable ingestion by children.'' 15 
U.S.C.  1261(f)(1)(A).
    In making a decision whether to grant a petition and commence 
rulemaking, the Commission is to consider, inter alia, the following 
factors:

   Whether the product involved presents an unreasonable risk 
        of injury.

   Whether a rule is reasonably necessary to eliminate or 
        reduce the risk of injury.

   Whether failure of the Commission to initiate the rulemaking 
        proceeding requested would unreasonably expose the petitioner 
        or other consumers to the risk of injury which the petitioner 
        alleges is presented by the product.

16 CFR  1051.9

    The ban rulemaking would be conducted under section 3(a) of the 
FHSA.\1\ Section 3(a)(2) of the FHSA requires that a rulemaking such as 
the one requested be conducted in accordance with section 701(e) of the 
Federal Food, Drug, and Cosmetic Act (FDCA).\2\ Under section 701(e), 
for the Commission to proceed to rulemaking, the petition must set 
forth ``reasonable grounds'' for the requested action. The United 
States Court of Appeals for the District of Columbia Circuit has held 
that ``reasonable grounds'' for a petition under the FHSA ``are grounds 
from which it is reasonable, to conclude that the Commission would be 
able to make the findings required to issue the requested rule and to 
support those findings with substantial evidence on the record.'' \3\
---------------------------------------------------------------------------
    \1\ 15 U.S.C.  1262(a).
    \2\ 21 U.S.C.  371(e).
    \3\ Consumer Federation of America v. CPSC, 883 F.2d 1073, 1076 
(D.C. Cir. 1989).
---------------------------------------------------------------------------
    The Commission considered the petition and the materials submitted 
with it; the June 15, 2001 final report of the Chronic Hazard Advisory 
Panel (CHAP) on DINP convened in accordance with sections 28 and 31 of 
the Consumer Product Safety Act, 15 U.S.C.  2077, 2080; a CPSC staff 
behavioral observation study to determine how much time young children 
actually spend mouthing objects and the types of objects they mouth; 
the November 1997 Commission staff report entitled, CPSC Staff Report 
on Lead and Cadmium in Children's Polyvinyl Chloride (PVC) Products; 
the 488 public comments received on the petition; the staff briefing 
package dated August 13, 2002; information presented by the staff 
during an oral briefing on November 8, 2002; comments received on the 
staff briefing package; and other information.
    The staff briefing package recounts the extensive scientific and 
technical investigations that have been carried out by the CPSC and 
others on the issue of PVC in products intended for children and 
concludes as follows.

        Based upon the scientific data presented in this briefing 
        package, the staff believes that there is no demonstrated 
        health risk posed by PVC toys or other products intended for 
        children 5 years of age and under and thus, no justification 
        for either banning PVC use in toys and other products intended 
        for children 5 years of age and under or for issuing a national 
        advisory on the health risks associated with soft plastic toys.

Memorandum from Marilyn L. Wind, Ph.D., Deputy Associate Executive 
Director, Directorate for Health Sciences, to the Commission, Response 
to Petition HP 99-1, August 13, 2002, at 16-17.

    That conclusion is based in part on the finding of the DINP CHAP 
that, ``[f]or the majority of children, the exposure to DINP from DINP-
containing toys would be expected to pose a minimal to non-existent 
risk of injury.'' Report to the U.S. Consumer Product Safety Commission 
by the Chronic Hazard Advisory Panel on Diisononyl Phthalate (DINP), 
June 2001, Executive Summary item 17. The new data from the recent CPSC 
behavioral observation study reported in the staff briefing package, 
which was not available at the time of the CHAP's deliberations, 
confirm this conclusion and demonstrate that children are exposed to 
DINP at even lower levels than the CHAP assumed when they reached their 
conclusion. Further, the recent survey of toys mouthed by children 
under the age of three also reported in the staff briefing package 
shows that not all soft plastic toys contain DINP. Therefore, exposure 
would be even less than the CHAP predicted because children mouth these 
toys for less time per day than the CHAP estimated, and the average 
amount of DINP in toys mouthed by children under the age of three is 
less than the CHAP estimated. If the risk to children under the age of 
three is not sufficient to warrant action, then based upon the data 
collected in the staff's behavioral observation study, and the data 
available in published literature, which indicate that mouthing 
declines as children age, there is no basis for the findings necessary 
under the CPSC regulations governing grant or denial of petitions or 
the FHSA for the Commission to take the requested actions with respect 
to DINP in PVC toys and other products intended for children 5 years of 
age and under.
    With respect to lead and cadmium, in November 1997, the Commission 
staff issued a report entitled, CPSC Staff Report on Lead and Cadmium 
in Children's Polyvinyl Chloride (PVC) Products. That report detailed 
the results of testing the Commission staff conducted on children's 
products that Greenpeace had alleged contained hazardous levels of lead 
and cadmium. Although some of the vinyl products identified by 
Greenpeace and tested by CPSC staff contained lead or cadmium, further 
testing and evaluation revealed that hazardous amounts of lead or 
cadmium were not released from the products. This means that children 
would not be exposed to hazardous levels. The report concluded that 
children would not be exposed to hazardous levels of lead or cadmium 
when the products are handled or used in a reasonably foreseeable 
manner. Thus, there is no basis for the findings necessary under the 
CPSC regulations governing grant or denial of petitions or the FHSA for 
the Commission to take the requested actions with respect to lead or 
cadmium in PVC toys and other products intended for children 5 years of 
age and under.
    In sum, as a result of consideration of the extensive research and 
analysis summarized herein, the Commission has denied the petition and 
declined to issue the requested national health advisory.
            Sincerely yours,
                                         Todd A. Stevenson,
                                                         Secretary.
    Copy to:

Nancy Chuda
Director
Children's Health Environmental Coalition

Mary Ellen Fise
General Counsel
Consumer Federation of America

Rick Hind
Legislative Director
Toxics Campaign
Greenpeace USA

Justine Maloney
Washington Representative
Learning Disabilities Association

Sheila McCarron
Program Director
National Council of Catholic Women

Sammie Moshenberg
Director (Washington Office)
National Council of Jewish Women

Philip Clapp
President
National Environmental Trust

Robert K. Musil, Ph.D.
Executive Director
Physicians for Social Responsibility

Jaydee Hanson
Assistant General Secretary
United Methodist Church--General Board of Church and Society

Pamela Spar
Executive Secretary
United Methodist Church--Women's Division

Gene Karpinski
Executive Director
U.S. Public Interest Research Group

Ed Hopkins
Vice President
Environmental Working Group
      
                                 ______
                                 
                    U.S. Consumer Product Safety Commission
                                  Washington, DC, February 20, 2003
Statement of the Honorable Mary Sheila Gall on Vote to Deny Petition 
        Requesting a Ban of Polyvinyl Chloride in Toys and Products 
        Intended for Children Five and Under
    Today I voted to deny a petition submitted by a group of 
organizations that asked the Commission to ban Polyvinyl Chloride (PVC) 
in all toys and other products intended for children aged 5 years and 
under. The Commission staff gave extensive consideration to the 
allegations of the petition and thoroughly examined all of the health 
effects alleged to be caused by children's mouthing of products made of 
PVC. The staff paid particular attention to products that used diisonyl 
phthlate (DINP) as a plasticizer. This thorough examination revealed 
that there is no risk posed by PVC that rises even remotely to that 
specified by the Federal Hazardous Substances Act (FHSA), the statute 
under which the Commission regulates this type of risk. Accordingly, 
the petition must be denied.
    The Commission and its staff gave careful attention to the 
allegations of the petition, as they properly should when claims of 
detrimental health effects to children are made. A previous Commission 
staff risk assessment concluded that the lead and cadmium in PVC 
products posed no risk of injury to children and the petitioners 
submitted no evidence that called into question the results of that 
risk assessment. Assessing the risk posed by DINP in PVC involved work 
beyond that contained in the earlier risk assessment. The Commission 
went to great lengths to assess all the risks that might be posed by 
DINP. The staff used a method validated by two international 
interlaboratory studies of measuring the quantity of DINP that migrates 
from PVC products. The staff then used that method to estimate the 
amount of DINP that actually entered a child's body when a PVC product 
was mouthed. The Commission then convened a Chronic Hazard Advisory 
Panel (CHAP), which reviewed extensive toxicological data about DINP. 
The CHAP concluded that for the vast majority of children the exposure 
to DINP from PVC-containing products posed a minimal to non-existent 
risk of injury. Data from a subsequent Commission staff study of 
exposure times of children mouthing products revealed that children 
were exposed to even less DINP than the CHAP had assumed in making its 
finding. The chance that children are being injured from mouthing 
products made from PVC is de minimus. There is simply nothing in the 
record that remotely justifies any finding that PVC products intended 
for children constitute a hazardous substance within the meaning of the 
FHSA.
    While the Commission has no legal authority to ban PVC products 
intended for use by children, there is toxicity data showing that it is 
a carcinogen in rodents, although it is a type of cancer not usually 
associated with humans. As least partially in response to these 
toxicity findings, in 1998 the toy industry and large retail chain 
stores in the U.S. voluntarily agreed not to sell items made out of PVC 
designed to be placed in the mouth (e.g., teethers, rattles and 
pacifiers). The European Union and Japan reached a similar result 
through their own regulatory processes.
    Chronic hazards are among the most technically difficult product-
safety problems that the Commission considers. Unlike acute hazards, 
where the effects occur very quickly and are easily observable, chronic 
hazards involve health effects that may occur many years after exposure 
and which may be difficult to trace to exposure to any particular 
substance. Considerable scientific expertise must be brought to bear on 
any allegations of chronic hazards and the result must always reflect a 
judgment call.' This may be subject to revision if more is learned 
about the toxicity or exposure of a specific substance. In the case of 
PVC, however, consumers may have a high level of assurance that soft 
plastic products pose no risk to children.
                                 ______
                                 
                    U.S. Consumer Product Safety Commission
                                  Washington, DC, February 21, 2003
Statement of the Honorable Thomas H. Moore on the Petition to Ban 
        Polyvinyl Chloride in Products Intended for Children Five Years 
        of Age and Under
    I am voting to deny the petition to ban polyvinyl chloride in 
products intended for children 5 years of age and under. The clear 
weight of the evidence produced by staff supports the conclusion that 
children are not at risk from mouthing products currently on the market 
that contain diisononyl phthalate (DINP). This evidence consists of new 
exposure studies showing how long children mouth various objects, the 
migration rates of phthalates from products on the market, an 
Acceptable Daily Intake that has an extremely large uncertainty/
adjustment factor and a scientific consensus that DINP is nongenotoxic 
and that the cancer caused by peroxisomal proliferation by DINP in the 
liver of rodents is not relevant to humans. As these are the best and 
most current scientific opinions, I believe the Commission must bow to 
that judgment. Our staff has done extraordinary work on this petition--
by far the most comprehensive work done to date anywhere in the world. 
I congratulate them on their achievement. Both their work, and the work 
of the scientists who participated in the Chronic Hazard Advisory Panel 
on DINP, should calm parents' fears about the potential harm to young 
children from children's products currently on the market that contain 
DINP.
    I am concerned, however, that the staffs conclusions could be the 
basis for industry to use phthalates in products that they have 
voluntarily agreed not to use them in, namely rattles, teethers and 
pacifiers. One area in which we do not have concrete information is the 
migration rate of DINP from these three types of children's products. 
Our assumption about the migration rate of phthalates from these 
products could prove to be too low. We also are not completely sure how 
much phthalates very young children are exposed to from other sources 
in their environment. This background exposure, coupled with the 
uncertainty of the rate of migration, made me consider voting to defer 
action on the petition until we see what happens in the marketplace as 
a result of the staffs conclusions. If phthalates were to be used in 
teethers, rattles or pacifiers in the future, the uncertainties 
mentioned above could cause us to be petitioned again in this area. I 
decided that I would not vote based on speculation of what might 
happen. All I can vote on today is the current state of the marketplace 
and of scientific knowledge, both of which lead to the conclusion that 
the ingestion of DINP by young children from the children's products on 
the market poses no risk of harm to America's children.

    Senator Pryor. Thank you.
    Dr. Alderson, let me start with you, if I may. Is it your 
view that the FDA should do more testing at this point?
    Dr. Alderson. Senator, the meeting that I referred to 
yesterday at NCTR was between staff of FDA as well as staff of 
the National Tox Program. FDA and particularly NCTR is what I 
call a partner in the NTP program, as we are one of the 
participating agencies which the NTP program serves in terms of 
the products we identify we need more information on.
    So the meeting ends today at noon, but I can tell you on 
the agenda the first thing yesterday morning was BPA. That was 
the first agenda item. They reviewed a number of proposed 
studies that will be considered, particularly in the 
pharmacokinetic studies to look at these low-dose issues that 
you referred to earlier in your statement. There were other 
things considered that need more review.
    But the short answer to your question is, yes, we will be 
doing additional research on BPA directed by the things that 
have been identified as uncertainties in the NTP draft report.
    Senator Pryor. Now, for clarification, let me just make 
sure that we understand your testimony, and that is, you said 
at the present time, there is no reason to stop using BPA 
because I guess the risks are either not present or they are 
acceptable.
    What about on phthalates? Have you come to a decision on 
phthalates?
    Dr. Alderson. Phthalates is a little different. The Center 
for the Evaluation of Risks to Human Reproduction in early 2000 
also did a similar type of report on phthalates that we now 
have before us on BPA. In that review, the CERHR also agreed 
with FDA's current position, that other than in infant males, 
we do not have that much concern, but at NCTR today ongoing 
there is a non-human primate study looking at this issue. So we 
are addressing the issues that we know about either currently 
or they are planned.
    Senator Pryor. Please explain to the Subcommittee in 
layman's terms the low-dose issue. I have heard it called the 
low-dose hypothesis. Could you explain what we mean by that, 
and is that controversial?
    Dr. Alderson. Well, let me start with the high dose first. 
The studies that are referred to in the NTP report referencing 
to high doses--in fact, I think the NTP brief says there are no 
controversies associated with the high doses. Everyone agrees 
there are effects there that we need to be concerned about.
    But when you come to the low doses, the endpoints that are 
being considered in terms of effects, there is not agreement 
between scientists. We have a number of reviews. If you look at 
those, there are disagreements between those reviews on whether 
there are effects or there are not effects. We believe that at 
this time the recent two studies that are referred to as the 
industry-supported studies are the best regulatory approaches 
in terms of data to address the low doses.
    Now, having said that, we do not consider those to be the 
final answer. That is because, I think, we agree that there are 
some issues still remaining there in terms of the effects. 
There are uncertainties regarding these low-dose effects; i.e., 
the studies need to be conducted to address those particular 
endpoints. They need to be designed such that you would have 
enough power to reach conclusions. We do not see that in a lot 
of studies other than these two multi-generation studies, the 
most recent studies that have been referred to.
    So there are uncertainties. It is not definitive. The 
science associated with how do you address those particular 
endpoints--there is not agreement among the toxicological 
community on how to do that.
    Senator Pryor. Great. I was planning on doing one round, 
but I may reserve the balance of my time for follow-ups.
    Senator Sununu?
    Senator Sununu. Thank you very much.
    You mentioned two major intergenerational studies. How many 
studies have been done in total that you look at to draw the 
conclusion that you made that BPA is safe?
    Dr. Alderson. Senator, we have looked at all the studies in 
the literature, and there are hundreds.
    Senator Sununu. It numbers in the hundreds. I just wanted 
to get a rough idea of whether we are talking about----
    Dr. Alderson. Many hundreds.
    Senator Sununu.--a dozen or a couple of dozen, but 
certainly more than----
    Dr. Alderson. Keep in mind this is a material that has been 
on the market or been used for now probably at least 25 years. 
So there is a wealth of information out there.
    Senator Sununu. --understood.
    And approximately how many of those or what portion of 
those studies look not just at health effects, but specifically 
focus on the health effects of children?
    Dr. Alderson. I have no way of answering that, Senator.
    Senator Sununu. If you could try to get that information 
for the record just so that we have----
    Dr. Alderson. We will try to get you an answer on that.
    Senator Sununu.--a general understanding of what the target 
is.
    Second, with regard to the high and low exposure, high and 
low dose, what does that mean? When you say a high dose, what 
is the level, and when you say low dose, what is the exposure 
level relative to the higher figure?
    Dr. Alderson. I do not know whether I have it, without 
looking in the NTP report. Here are some numbers that I have. 
For high dose, I think the NTP report or brief refers to 
something greater than 50 milligrams per kilo of body weight 
per day. For a low dose, we are talking about doses equal to or 
less than 5 milligrams per kilogram per day. This is what the 
NTP report refers to.
    Senator Sununu. OK.
    What do you think the basis is for those who have opposed 
your finding? What argument are they making and how would you 
respond to their argument? Clearly, there is a difference of 
opinion here and we need to at least understand what the basis 
is for that difference.
    Dr. Alderson. It is FDA's view that the basis for this is 
what we would normally ask for to support a decision on safety 
of this type of material. We would want to see a study that is 
specifically designed to address a particular endpoint that had 
been identified in perhaps another study where we have multiple 
doses, we use the correct model, i.e., the correct species, 
there is appropriate statistical analysis conducted on it, it 
is conducted under GLP standards. There is a whole gamut of 
standards that FDA prescribes when we are looking to make a 
decision on safety, and that is the same type of information 
that we recommend to a sponsor who comes in and tells us what 
do you need.
    Senator Sununu. But you agree that there is a value in 
doing additional research and additional evaluation, including 
many of those criteria?
    Dr. Alderson. There is no question that many of the other 
studies that are out there in the literature--we would consider 
them hypothesis-testing. They are very important to us because 
they identify potential endpoints that need to be further 
evaluated, particularly as it relates to levels where we see no 
effects.
    Senator Sununu. Dr. Wind, obviously, the difference between 
a high-dose level and a low-dose level, 50--what is it?
    Dr. Alderson. Fifty milligrams per kilo.
    Senator Sununu. Fifty milligrams versus 5 milligrams. There 
is some significance there.
    You talked about the level of material that is actually 
included in products, not the exposure level or the dose, but 
the threshold of one-tenth of 1 percent phthalates in the 
products and suggested that that might be impractical to set as 
a standard, to measure as a standard because of the physical 
nature of the manufacture of the products.
    Could you speak a little bit more about that and let us 
know if we were going to set a standard in order to minimize 
the risk, or minimize the exposure, from a manufacturing or 
testing standpoint what might be more practical?
    Dr. Wind. I think that when I spoke about the amount of 
phthalate that we found in products when we tested them, that 
was the amount that is needed to make the product flexible. So 
it is intentionally added to the product. You do not add .1 
percent of phthalate to a product. Phthalates are ubiquitous 
because they're used in everything, and so that would be a 
contamination level.
    When the ASTM established their standard for di-ethylhexyl 
phthalate----
    Senator Sununu. I am sorry. When you used the phrase 
``contamination level,'' though, are you suggesting that it is 
an impractical standard because some contamination at that very 
low level is almost inevitable----
    Dr. Wind. Yes.
    Senator Sununu.--or that that is an appropriate level 
because you would not want to have contamination at that level?
    Dr. Wind. No.
    Senator Sununu. You need to be clear.
    Dr. Wind. I am suggesting that that level is impractical 
because contamination is going to occur.
    When we looked at the phthalates--at DINP, because that is 
the only one that we have done extensive work on, even with the 
high levels, you did not see a health risk.
    When ASTM set the level for the DEHP standard, they set it 
at 3 percent of intentionally added DEHP to the product. So I 
think that the intentionally added is an important concept.
    Senator Sununu. I have one more question, Mr. Chairman, and 
I apologize for going over, but I am going to have to depart 
for another hearing.
    But I do want you to address the concern you raised about 
the impact of products that are designed as protective 
products, shin guards, eye goggles, other protective gear, if 
there were a ban put into place. For those protective products, 
are there alternatives to BPA, and have you tried to quantify 
what the impact might be in terms of health or safety if there 
were a ban put in place?
    Dr. Wind. We have not tried to look at the impact at this 
point. I do not know what would be used. What I do know is that 
since there is no exposure to BPA from something like a helmet 
or safety goggles, that no exposure means no risk.
    Senator Sununu. And those products that you mentioned would 
be affected by the legislation as written----
    Dr. Wind. Yes.
    Senator Sununu.--because it bans it in all products no 
matter what the impact or exposure might be from that product.
    Dr. Wind. Yes.
    Senator Sununu. Thank you very much.
    Thank you, Mr. Chairman.
    Senator Pryor. Thank you.
    We have been joined by Senator Bill Nelson and Senator Amy 
Klobuchar. Senator Nelson, you are next.

                STATEMENT OF HON. BILL NELSON, 
                   U.S. SENATOR FROM FLORIDA

    Senator Nelson. Thank you, Mr. Chairman for holding this 
hearing on the potential risk that we see here. Mr. Chairman, I 
want to pick up exactly where Senator Sununu was going on this.
    Dr. Wind, since there is the voluntary industry standard 
called ASTM F-963 and it bans phthalate DEHP in pacifiers, 
rattles, and teethers, is the Commission going to consider not 
a voluntary standard for the industry, but a mandatory rule?
    Dr. Wind. For DEHP?
    Senator Nelson. For pacifiers, rattles, and teethers.
    Dr. Wind. Pacifiers are no longer made out of PVC. They are 
made out of latex rubber and silicone rubber.
    Senator Nelson. Anything that can go into the child's mouth 
you are going to consider mandatory?
    Dr. Wind. Our statute requires that if a voluntary standard 
is in place and is effective, that we not do a mandatory 
standard. DEHP at this point is not used in children's 
products.
    Senator Nelson. So you support the voluntary but not a 
mandatory. Is that what you said?
    Dr. Wind. No. What I am saying is DEHP is not used in 
children's products at this point. So there is no exposure to 
DEHP.
    Senator Nelson. It is not used in rattles and teethers?
    Dr. Wind. No.
    Senator Nelson. Is it used in any small items that can get 
into a child's mouth?
    Dr. Wind. Children mouth a lot of things, so it probably 
is, but they are not toys.
    Senator Nelson. Let me ask you this. We have put it as a 
mandatory standard in the Consumer Product Safety Commission.
    Dr. Wind. Right.
    Senator Nelson. Is your leadership going to support the 
position in our bill?
    Dr. Wind. Of course, whatever Congress puts in the bill we 
will support because that is what we----
    Senator Nelson. If it is the law.
    Dr. Wind. If it is the law.
    Senator Nelson. What will your agency recommend to the 
President on a veto or signing the bill since it has the 
mandatory standard?
    Dr. Wind. I am just a scientist. So I cannot answer that 
question.
    Senator Nelson. So you cannot speak for the leadership.
    Dr. Wind. Right, yes.
    Senator Nelson. OK. I am just a little country lawyer, but 
I have to speak out for my constituents and a lot of these 
little babies that get hold of these products.
    Let me ask you since you note in your testimony that the 
Commission's actions addressed phthalates during 1998 to 2003, 
but since then there have been a number of studies that have 
come out and some countries, indeed, a state that considers 
itself a country, the State of California, has banned the use 
of certain phthalates in toys--so it would seem that this ought 
to be at the top of the agenda without it all being voluntary.
    Dr. Wind. The phthalate that children are exposed to the 
most is diisononyl phthalate, DINP. That is the one that we did 
extensive work on back in the late 1990s and early 2000 and the 
one where the Commission denied the petition to ban it. There 
have not been any studies on DINP that have come out since then 
that would change the scientific information and conclusions 
that we made from that study.
    We worked with our colleagues in the European Union because 
we did not understand how they reached the conclusion that DINP 
should be banned, and we had extensive discussions with them. 
The reality was that their risk assessment came out with the 
exact same acceptable daily intake that ours did.
    The difference between the two studies was we used our 
exposure data which we derived from a very extensive behavioral 
observation study. They picked out a number that was vastly 
larger in terms of exposure that is not justified by the 
current research, and that is how they came out with a risk of 
injury.
    Senator Nelson. So you are disagreeing as a scientist with 
some of these studies that have said phthalates and BPA may not 
be suited for use in certain toys in children's products.
    Dr. Wind. I am not making a comment about BPA because----
    Senator Nelson. OK. That has got BPA in it. What do you 
think about that?
    Dr. Wind. That is Food and Drug Administration's 
jurisdiction. So I will not comment on that.
    Senator Nelson. All right. Then let me ask Dr. Alderson. 
Many of these studies have focused on the effects. So has FDA, 
EPA, CPSC, or any other agency had studies that show the 
combined impact of these chemicals on adolescent development?
    Dr. Alderson. When you say ``combined,'' I want to make 
sure I understand the question. We have studies that we have 
reviewed the literature, a lot of studies relative to each of 
these materials separately. I am not aware of any studies--that 
does not mean they do not exist, but I am not aware of any that 
we have discussed internally in FDA where there have been 
cumulative effects looked at in terms of studies that had, for 
instance, BPA and DEHP in both.
    Senator Nelson. Well, let us do not confuse the question. 
Omit--strike from the record, Mr. Chairman, the word 
``combined.'' All right. Now will you answer the question?
    Dr. Alderson. Yes, sir.
    There are ongoing considerations of the data relative to 
BPA. Recent events with two documents from NTP released last 
month, an NTP brief draft document, that will be peer-reviewed 
next month by the NTP--that is the current document that we at 
FDA are considering. We have a task force looking at the 
implications of that.
    There were two issues raised in that document of some 
concern at the low-dose levels. They in their review looked at 
all the data, as we understand it, that were available, 
including the two low-dose multi-generation studies, one in 
rats and one in mice. So there is a lot of literature relative 
to BPA.
    Senator Nelson. What are you going to do about it?
    Dr. Alderson. Well, we are taking a look at that. We also 
need to wait until the NTP peer review is completed, which will 
take place on June 11th, and they will issue their final 
monograph this fall as to whether those areas of some concern 
are sustained through the peer review process.
    Senator Nelson. What do you think CPSC ought to do about 
it?
    Dr. Alderson. What I think CPSC ought to do?
    Senator Nelson. Are you not there to protect the interests 
of the public?
    Dr. Alderson. But as it relates to the FDA regulated 
products, i.e., those food contact materials and materials in 
food cans.
    Senator Nelson. Right, affecting the consumer safety and 
health.
    Dr. Alderson. At this point, Senator, we think they 
continue to be safe. We have not seen data where we would reach 
the conclusion that they are unsafe.
    Senator Nelson. And ``they'' in this answer is who?
    Dr. Alderson. FDA.
    Senator Nelson. What products?
    Dr. Alderson. Well, we are talking about specifically food 
contact materials, i.e., baby bottles, food packaging. We are 
also talking about liners that are in metal cans.
    Senator Nelson. How about that?
    Dr. Alderson. Yes, sir.
    Senator Nelson. That is safe.
    Dr. Alderson. As far as we are concerned. Today we have no 
reason to change our position on it.
    Senator Nelson. Even though it has got BPA.
    Dr. Alderson. Even though it has got BPA.
    Senator Nelson. OK. And there are no studies that are 
saying that the BPA in there in that bottle right there is 
unsafe?
    Dr. Alderson. I do not know about that specific bottle, but 
bottles similar to that one.
    Senator Nelson. Dr. Alderson, you know what I am asking. 
Quit straining at gnats. Are there any studies?
    Dr. Alderson. The studies we have seen, studies FDA has 
conducted on leaching of this material from this type of 
product would tell us unless you would subject it to very harsh 
conditions, i.e., continuous boiling or something like that, 
that the amount of BPA that is going to leach into the food 
that may do it in that bottle is safe.
    Senator Nelson. Thank you, Mr. Chairman.
    Senator Pryor. Senator Klobuchar?

               STATEMENT OF HON. AMY KLOBUCHAR, 
                  U.S. SENATOR FROM MINNESOTA

    Senator Klobuchar. Thank you, Mr. Chairman, and thank you 
for holding this important hearing.
    Dr. Alderson, a recent article in The New York Times--one 
scientist, when looking at these studies of the plastic 
additives, was quoted as saying, ``companies and states are 
taking leadership where the Federal Government isn't.''
    And some examples of that--Senator Nelson mentioned the 
State of California. Kaiser decided the evidence that the 
phthalates were leaking into intravenous bags were enough to 
start looking for other options, and they gathered a team of 
experts to come up with medical gloves and other medical 
supplies that were free of phthalates. And as of 2004, Kaiser 
has been rolling out only PVC-free products, including 
intravenous bags and tubes.
    Many companies are not waiting for Federal regulation and 
are already selling products that conform to the stricter 
chemical standards that you find in the European Union, Canada, 
and Japan.
    My question is this. At what point should the Federal 
regulators step in? Why would companies like Kaiser make this 
decision and the Federal Government is not doing anything? What 
message are we sending to consumers when they read about BPA 
and phthalate studies, but see that the Government has not done 
anything?
    Dr. Alderson. Senator, the FDA often finds itself in this 
position. We have standards that we ask of industry to give us 
as it relates to safety and efficacy of products. In this case, 
you are talking about products that were approved many years 
ago, and because they are food additives, a manufacturer can 
take that product and start marketing it without any 
preclearance as long as it puts that material in there in 
accordance with the regulation.
    Now, having said that, as literature becomes available on 
these type of chemicals in the products, particularly food 
packaging materials, we are continuing to look at it. And where 
there are data that become available that raises our concerns 
and they meet a regulatory standard in terms of quality of that 
data where it is designed to address in this case safety, we 
will take action. But as I have said previously, at this point 
in time, the data that we have seen does not lead us to change 
our position on how we look at the safety of either BPA or 
DEHP.
    Senator Klobuchar. Another example--and I know that Senator 
Nelson was talking to you about these bottles. Nalgene has 
started phasing out the use of BPA in their water bottles--and 
this is one of those old water bottles--because of these 
studies that have come out showing this additive leaking into 
food and beverages. In their new water bottles--and actually 
one member of my staff actually just ordered this new Nalgene 
water bottle. It looks similar and, however, do not leak.
    So where this research has shown that by using boiling 
water in one of these to--which by the way, I was amused to 
find out as we prepared for this hearing--just yesterday I used 
one of these water bottles, Mr. Chair, and ran it under really 
hot water under the faucet for quite a while because I was too 
lazy to put it in the dishwasher. It did strike me that if I 
had a choice and I knew that this was going on, that this 
company was actually phasing these out, that I would probably 
not want to take the risk, that I would probably use this water 
bottle.
    So what I am thinking about is these parents with baby 
bottles and knowing that there is some risk out there. Do you 
not think that they should be somehow--at least be some 
requirement that these things be labeled so if you guys are not 
going to regulate them, that they can at least make their own 
choice based on what they are seeing in some of these studies?
    Dr. Alderson. Senator, we at FDA have put out in our 
announcements regarding this issue since this came out last 
month that there are alternatives, particularly as it relates 
to baby bottles, i.e., glass. Those are there for people to 
see. We have also pointed out how you can determine whether BPA 
is in these bottles by looking at the recycling notification on 
those bottles.
    Senator Klobuchar. That sounds really hard for a mom with a 
12-year-old and you are trying to get them off to school. We 
are supposed to look at recycling requirements?
    Dr. Alderson. That is what the current regulation and laws 
require of us.
    Senator Klobuchar. But we are looking at maybe changing the 
laws and requirements to make it easier. That is why we are 
having this hearing.
    Dr. Alderson. I do not think FDA would object.
    Senator Klobuchar. My next question is this: If these 
companies are starting to phase these out and they are 
concerned about some of this leakage themselves, should the 
Federal Government not be more concerned and moving more 
quickly to do something about it? Because maybe not every other 
company is going to start taking these off the market. They are 
just going to keep using the old ones.
    Dr. Alderson. Senator, in FDA's consideration of safety of 
products, we feel we are obligated to use the best science to 
make those decisions. The process and the science that we 
follow--we have got a prescribed way we go about determining 
safety, and it is based on the current science as it relates to 
these type of materials. It is rated to the current science on 
what is the best approach to determine safety without going to 
humans because we are not going to be able to do human studies 
to make these determinations.
    Senator Klobuchar. Does the National Toxicology report 
released this month raise some concern about the effects of BPA 
on infants and children?
    Dr. Alderson. It does. It raises concerns but that----
    Senator Klobuchar. The European Union and Canada and these 
others countries have actually done something about that, and 
we are just concerned.
    Dr. Alderson. Well, even the Canadian report, in reading 
it, they point out there are really uncertainties in the data 
that they have reviewed. They also point out the need for 
further research.
    The EU, in communications we have had with them this week--
they are raising no concerns about the NTP report or the recent 
studies. Their position is being maintained.
    Senator Klobuchar. But you are concerned about the report 
and what it says.
    Dr. Alderson. We are concerned about it. That is the reason 
at FDA we have a task force that we are looking across all the 
agencies at any of our products that have BPA in it.
    Senator Klobuchar. I am just again thinking of these 
parents. They can choose one duck or the other duck, and one 
duck has phthalates and one duck does not. I think they would 
like to make that choice themselves, and we are not giving them 
the tools to do that.
    Thank you very much.
    Senator Pryor. Thank you.
    Senator Nelson?
    Senator Nelson. Dr. Alderson, you said in my previous 
commentary with you that a bottle like this with BPA is safe. 
So you would suggest to a young mother who would have a baby 
bottle made with BPA that she wants to heat up the formula, 
that you would recommend that she can use that bottle with BPA 
as opposed to a bottle without BPA. Is that your 
recommendation?
    Dr. Alderson. I think our recommendation would be that she 
not heat the formula in that polycarbonate bottle containing 
BPA, that she heat it in another source and let it cool and 
then put it in the bottle.
    Senator Nelson. All right. Has such a recommendation been 
made by the FDA?
    Dr. Alderson. I think that recommendation is in our recent 
announcements regarding our position as we follow the NTP brief 
draft. We pointed out that those alternatives are available, 
and I think we have said--and I do not have it in front of me, 
Senator--that we talked about there are alternative ways to 
prepare this. Certainly in our research, we have pointed out 
that boiling materials in these bottles is not recommended. And 
I do not think the manufacturers even recommend that.
    Senator Nelson. But they have got a choice. A consumer has 
a choice if they know the difference between a bottle with BPA 
and one that does not have BPA. And so the question that is 
just begged that we have to ask, representing our constituents 
and wanting their safety of the very agencies that are charged 
with protection of the consumers, is, is the consumer being 
advised by the Executive Branch of Government the difference 
between the two bottles, that a young mom may go and heat up 
the baby formula?
    Dr. Alderson. Again, Senator, I do not know what the 
specific bottles that have BPA in them--how they are 
recommended for use. I can only relate back to when my two 
children were babies and I know we did not boil hot formula in 
the bottles.
    Senator Nelson. I think back when my two children were 
young and I did not know up from down.
    [Laughter.]
    Senator Nelson. All right. Well, let me ask you, Dr. Wind. 
You are a scientist. Now, one study of your agency that has 
helped set the foundation for a final determination to deny the 
petition that infants 1 to 2 years old on average--it came out 
with a conclusion that those infants 1 to 2 years old mouthed 
soft plastic toys for 1.9 minutes a day. Does that change your 
testimony at all about phthalates?
    Dr. Wind. No, because that was the very number that we used 
when we looked at the risk. We developed an acceptable daily 
intake which is the amount that you can consume for your entire 
lifetime every day that would result in no health risk. And 
then we compared the amount of time an infant would mouth these 
products. We measured how much migrates out of the products, 
and we did actual calculations where we looked at what, in 
fact, an infant would consume. And the numbers that we came up 
with were below the estimated background level that infants 
would consume from food and other things, and it was way below 
the acceptable daily intake which already has a safety factor.
    Senator Nelson. Just so I understand, then I will stop, Mr. 
Chairman. So the CPSC has concluded that a child mouthing a 
flexible plastic toy with phthalates close to 2 minutes a day, 
that they are not going to have enough of that phthalate to be 
harmful to the child.
    Dr. Wind. Yes, and in fact, the Chronic Hazard Advisory 
Panel, which consisted of seven independent scientists, 
recommended to the Commission by the National Academy of 
Science, concluded that the only children that would be at risk 
were those that mouthed phthalate-containing toys for more than 
75 minutes a day.
    Senator Nelson. Thank you, Mr. Chairman.
    Senator Pryor. Thank you.
    Let me follow up, if I may. I do not want to pick on 
Nalgene as a company. It sounds like they are trying to be 
proactive to try to get ahead of this. So I appreciate that. 
But just using them as an example, they have announced that 
they are not going to put BPA in their bottles anymore.
    Dr. Alderson, what assurance do we have that whatever 
chemical goes into the new bottle is safe?
    Dr. Alderson. If it is a chemical that has previously been 
approved and is in our regulations as approved, that chemical 
would have to be used in accordance with those regulations, and 
that way we would assume it is safe until we get additional 
information.
    If it is a totally new chemical that we have not seen 
before, it has not been approved for that use, then they would 
have to get a preclearance approval. They could not start using 
it until that approval takes place. They would have to go 
through considerable time and effort to show safety through the 
regulatory process we have talked about previously in terms of 
multigeneration studies, chronic studies, et cetera, if the 
endpoints we see in studies point to that.
    Senator Pryor. So your view is that in order to put any 
additive there, that additive has to be preapproved by you?
    Dr. Alderson. That is correct.
    Senator Pryor. Let me ask, if I may, of the CPSC, Dr. Wind. 
From your earlier testimony in your opening statement, I was 
not clear on one point. Does the CPSC have a comprehensive list 
of all products that use phthalates?
    Dr. Wind. No. We have concentrated on toys that are 
intended to be mouthed because our exposure study showed that 
those were the ones to which kids had the most exposure, and 
since there was no risk to those, then we did not pursue other 
toys, although when we were responding to the petition, we did 
pick up a variety of toys and look at them to see how much 
phthalate migrated out of them.
    Senator Pryor. All right. For phthalates, is there a level, 
sort of a magic number, that you consider safe?
    Dr. Wind. What we found when we looked at toys was that 
there was no correlation between the amount of phthalate that 
was in a toy and the amount that migrated out of it. However, 
again, I go back to our exposure study, and the levels of 
phthalates in the toys ranged up to 39 percent, and based upon 
the exposure time, we did not find that those posed a health 
risk.
    Senator Pryor. Senator Kerry has joined us. Senator Kerry?

               STATEMENT OF HON. JOHN F. KERRY, 
                U.S. SENATOR FROM MASSACHUSETTS

    Senator Kerry. Thank you very much, Mr. Chairman, for a 
hearing that I think is of incredible importance, and I am very 
appreciative to you for having it.
    I am not entirely sure of where to begin here, but let me 
get organized and then I will sort of pull that together.
    Endocrine disrupters, as we have come to know them, are 
prevalent in our society, and I know that we are looking at two 
of those specifically here, phthalates and bisphenol A. There 
is a lot of scientific evidence showing that at low exposure 
levels, these two chemicals, which we know are contained in 
everything from baby bottles to IV tubes, can have real and 
significant impacts on child development and hormone function. 
Phthalates are very common in personal care products.
    And we seem to have a different attitude in our country 
than the Europeans do about these kinds of products. I think in 
Europe they have a burden of proof on the industry to prove 
that something does not harm them. Here in America, for 
regrettable reasons, we have a burden of proof on the 
individual to prove that it does harm them. Our TSCA, which we 
passed in 1972, really gets it backward in my judgment. And I 
am very concerned, Dr. Alderson, Dr. Wind, that the agencies 
that are supposed to be protecting consumers are simply not 
doing it.
    Americans use 12 personal care products every single day. 
They contain 126 unique ingredients. And many people assume 
that simply because the Government requires tough testing for 
drugs, that the same is true for these personal care products. 
But it is not true, is it?
    Dr. Alderson. No, sir.
    Senator Kerry. They do not get any kind of real scrutiny, 
and the reality is that outside of drugs and pesticides, the 
chemicals used to manufacture many of the products that we use 
every day, cosmetics, personal care, cleaning agents, are 
actually never tested to find out if they are harmful. Is that 
not correct?
    Dr. Alderson. As it relates to personal care items, 
particularly cosmetics, the industry conducts an extensive 
evaluation of their products, but FDA does not get to see any 
of that information.
    Senator Kerry. Just the way that Chevrolet years ago did 
evaluations on the Corvair. Correct? And many other instances 
like pajamas that used to catch on fire and beds that kids fall 
through and hang themselves in. Correct?
    So somebody is supposed to stand up here and sort of 
protect people a little bit. In my judgment, the FDA could 
hardly be doing less. They do not require studies or testing 
for a cosmetic product that is put on the shelves of the 
pharmacy or grocery store. I am told that some hair 
straighteners use estrogen. Are you aware of that?
    Dr. Alderson. No, sir.
    Senator Kerry. Are you aware of that, Dr. Wind?
    Dr. Wind. That is not something in our jurisdiction, so no.
    Senator Kerry. Even if it were not in your jurisdiction, 
you are not aware of it.
    Dr. Wind. No.
    Senator Kerry. And estrogen can, in fact, have carcinogenic 
impact when it is used in a certain quantity above normal 
levels. Would it concern you to know that young women are using 
estrogen in hair products conceivably to straighten their hair 
and that that may, in fact, have an impact?
    Dr. Alderson. Without question we would want to know that, 
sir.
    Senator Kerry. Well, it is in the public domain. It seems 
to me the FDA is putting its faith in an industry to self-
police through a panel called the Cosmetic Ingredient Review. 
Surprise, surprise. The industry funded the panel of scientists 
and they have reviewed only 11 percent of the more than 10,000 
ingredients contained in cosmetics.
    The reality is that these pose risks to health. Dozens of 
studies in recent years led to the announcement in mid-April 
from the National Toxicology Program of the National Institutes 
of Health that there is ``some concern about neural and 
behavioral effects of BPA on fetuses, infants, and children.'' 
In response to this, Senator Schumer and I introduced the BPA-
Free Kids Act of 2008, which prohibits the use.
    But again, we have been slow to take this up. In fact, the 
response from the recent study of the National Toxicology 
Program has simply promised more studies, not any concrete 
action to reduce exposure.
    The media has reported that the Federal Government's 
reluctance to regulate these chemicals is based on the reliance 
of biased studies from the chemical industry itself.
    Now, I have to tell you if that is true, if it is not being 
done independently or by yourselves, but by an industry study, 
does that not cast amazing doubt on the ability of the 
regulatory system to actually protect the public?
    Dr. Alderson. Senator, at FDA all of our products that we 
approve are based on data that are prepared and conducted in 
studies by that particular manufacturer.
    Senator Kerry. But does that not bother you? That is my 
point. You do not seem to see the connection here.
    You know, my wife and I did a book. I am not here to hawk a 
book, but we wrote a book. A chapter in it is on this topic. 
Let me just read something about baby food. ``Chemicals that go 
into the manufacture of other products intended for young 
children. Polyvinyl chloride softens because of the existence 
of phthalates. It is still used in the manufacture of 
children's toys, bath books, rattles, beach balls, plastic 
raincoats, boots, even teething rings, and it can be absorbed 
from those products during use into a young child's body.''
    ``The fact is that a biomonitoring study coordinated by 
EWG, the Environmental Working Group, tested the umbilical cord 
blood from 10 babies who have been born in the United States in 
August and September of 2004. These newborns were found to have 
absorbed in the womb a combined total of 413 chemicals. At 
birth, each child carried an average body burden of 200 
chemicals, and those chemicals included pesticides, flame 
retardants, and other persistent organic compounds or 
byproducts from burning gasoline and garbage.''
    ``The EWG also tested the breast milk of 29 first-time 
mothers from across the United States for the presence of 
components of chemical flame retardants, TVs, foam furniture, 
all of which can cause thyroid toxicity, and some of which have 
been banned in Europe. And the results were very sobering. The 
breast milk of each new mother tested positive for components 
of flame retardants. The average level of brominated fire 
retardants in the milk samples was 75 times higher than the 
average for women who had been tested in Europe and were at 
levels associated with toxic effects in studies on lab 
animals.''
    You can go on and on about what is happening with 
phthalates themselves. There were some doctors who were doing 
an analysis. I think it was in Pittsburgh at the university. 
They were trying to figure out what the impact was of 
plasticizers, phthalates on creation of cancer, and before they 
even put the cancerous carcinogen into their experiment, they 
found that their base product had already turned cancerous. And 
they could not figure out why.
    So they started doing reverse analysis to figure out what 
had happened, and then they got to the point where they 
actually made telephone calls to the makers of the plastic 
tubes to find out what the ingredients were and, indeed, found 
that the phthalates within the tubes themselves were the only 
rationale for what had created the carcinogenic transformation.
    Do you read these studies? Do they not concern you?
    Dr. Alderson. Sir, we have read all the studies you are 
talking about.
    Senator Kerry. Well, why do you not ban phthalates? There 
is a movement in California to ban them now. There is a 
movement in Europe, other places. There is a lot of study in 
rats and others. Are you familiar with those studies?
    Dr. Alderson. I personally am not, but I am sure the 
scientists at FDA who review these materials every day are.
    Senator Kerry. Well, does the Commission not talk about 
this? Do you Commissioners not talk about this?
    Dr. Alderson. We talk about these issues on a regular 
basis, Senator.
    Senator Kerry. A team at Boston Tufts University, led by 
Professor Soto, studied the effects of phthalate exposure in 
rats. They exposed pregnant rats to bisphenol A, BPA, chemical, 
and the levels to which the rats were exposed mirrored levels 
that humans encounter daily. The results: by the time they 
reached puberty, rats that had received even the lowest doses 
of BPA had four times more precancerous growths in breast 
tissue than those that had not been exposed.
    You think it is OK for people to go ahead and use this 
stuff? I mean, does this not concern you?
    Dr. Alderson. Senator, it does concern us.
    Senator Kerry. Well, how much does it concern you? Enough 
that all you do is just rely on a study that comes from the 
industry itself? You should go to their website today and read 
what they say about phthalates. Completely contrary to what is 
out there in scientific journals. It is a disgrace. And it 
obviously does not concern you enough to do something about it.
    There are thousands upon thousands of chemicals; 80,000 
chemicals are out there in the marketplace today. Something 
like less than 6,000 have been properly vetted and tested. And 
we are still living with the residue of the Toxic Control 
Substances Act that was written by the industry with the burden 
of proof on our citizens to prove harm done, not on people to 
prove that it will not be done.
    And I tell you--I mean, I could go on and on. I have used 
my time here, and it is not appropriate to abuse it. But I just 
think the job is not being done, sir, I have to tell you. And I 
do not think the American public is being adequately protected, 
and I think we are going to have to find--this law has got to 
be rewritten and we have got to start to do what we are 
supposed to do, not what the industry always asks us to do.
    Do you have any response? None. You think everything is OK?
    Dr. Alderson. Senator, as the studies become available to 
us, we at FDA----
    Senator Kerry. Studies from whom become available to you?
    Dr. Alderson. Whoever. If they have been published----
    Senator Kerry. The only studies you are getting right now--
have you asked for studies from independent sources?
    Dr. Alderson. We do not normally ask for independent 
studies.
    Senator Kerry. Then you do not protect the American people 
if you do not ask for them, if you do not look beyond what is 
handed to you.
    Thank you, Mr. Chairman.
    Senator Pryor. Thank you.
    That will be all for this panel here. I want to thank you 
all for being here and providing your testimony. And just to 
let you all know, it is very possible that Senators will have 
written questions, and they will submit those for the record 
and we will keep the record open for 2 weeks to allow Senators 
to submit their questions and you all to get your answers back.
    Now I would like to introduce the third panel. You all just 
come on up and grab a microphone and grab your seats.
    First is going to be Dr. John Peterson Myers, CEO and Chief 
Scientist, Environmental Health Sciences. Next will be Ms. 
Elizabeth Hitchcock, Public Health Advocate for U.S. PIRG, and 
third will be Dr. Steve Hentges, Executive Director, 
Polycarbonate/BPA Global Group, American Chemistry Council.
    So as you all are getting situated and finding your seats, 
I want to welcome all of you to the subcommittee. And Dr. 
Myers?

    STATEMENT OF JOHN PETERSON MYERS, Ph.D., CEO AND CHIEF 
            SCIENTIST, ENVIRONMENTAL HEALTH SCIENCES

    Dr. Myers. Mr. Chairman, distinguished Members of the 
Committee, my name is Pete Myers. I am the Chief Scientist of 
Environmental Health Sciences, a not-for-profit scientific 
organization based in Charlottesville, Virginia. It is an honor 
to be here today to participate in this discussion.
    I am going to focus most of my comments on some of the 
issues that were raised by your questions earlier, specifically 
this whole high-dose versus low-dose issue because it turns out 
that the structure, the basic way that the FDA, the EPA, and 
the CPSC have gone about asking scientific questions to respond 
to Senator Kerry's concerns are based upon 16th century 
science, not upon 21st century medicine. And that has left us 
blind to exactly the types of effects that bisphenol A and the 
phthalates now are shown to have caused in a wide array of 
experiments. I will get to that.
    I first want to begin with a couple of preliminary 
comments. As Senator Kerry knows, over 10 years ago, I actually 
co-authored a book about endocrine disruption that brought this 
issue to the attention of the American public and policymakers 
for the first time. Even then, over 10 years ago, there were 
hints of risks from bisphenol A and phthalates.
    As I look at the last 10 years, the book's most important 
effect actually was to stimulate Federal investments in medical 
and scientific research on endocrine disruption, and today, 10 
years later, we are living midstream in a scientific revolution 
that has resulted from those investments, and it is truly quite 
amazing. It is changing the framework we use to think about how 
contaminants can be toxic because the old toxicology focused on 
overt damage, overt toxicity. Are mutations caused? Is there 
overt liver toxicity, et cetera?
    This new toxicology instead looks at molecular genetics, 
and it acknowledges that our genes are actually being turned on 
and off trillions of times a second every day of our life, 
every second of our life, and things like phthalates and 
bisphenol A affect that process of turning genes on and off.
    The FDA and the EPA and the CDC--their science currently 
ignores molecular genetics. It looks at old-style toxicology, 
the consequences of high doses, but we are learning that this 
new toxicology, toxicology that builds upon the last several 
decades of molecular genetic research, is really revealing that 
the changes in gene expression that can be induced through low-
level exposures in the womb can lead the developing organism 
along a path that it never would have followed and induce 
diseases in adulthood that are actually traced to what are 
called epigenetic changes caused by low-level exposures in the 
womb. That is the central issue here. We have got to move from 
16th century science to 21st century science.
    If you leave this room with just one new piece of 
information, here it is. Numerous animal studies published in 
the peer-reviewed literature show that the average person in 
America today has levels of bisphenol A in their blood that are 
higher than those sufficient to cause harm in animals. This is 
a not a case of high-dose experiments being extrapolated to the 
consequences of low-dose exposure. These are experiments using 
low doses asking what happens when animals are exposed to the 
levels that people experience. And crucially, the mechanisms of 
action of these low-dose exposures are identical. They are 
exactly the same in animals as they are in people. So the 
results of those experiments are highly relevant to predicting 
human effects.
    Last and again about bisphenol A, I want you to focus on 
another fact that has been published in the peer-reviewed 
literature. Of the studies of bisphenol A that were funded by 
Government sources, including the National Institutes of 
Health, over 90 percent of them find adverse effects on 
animals. In contrast, none of the studies funded by industry 
report adverse effects. This is the same pattern, the very same 
pattern, you will find with industry-funded studies of the 
effects of lead, pharmaceuticals, other chemicals, and tobacco.
    Now, some of you will recall the testimony in 1994 before 
Congress of the seven heads of tobacco companies who swore that 
there was no link between cigarette smoking and cancer. As you 
listen to industry interpretation of the data on bisphenol A 
and phthalates, I would encourage you to think about that.
    I would also encourage you to take a look at this new book 
by Dr. David Michaels of George Washington University. It is 
called Doubt is Their Product. It describes in detail how 
industry trade groups manipulate science to forestall action, 
regulatory action. Every delay keeps sales going and revenue 
flowing.
    But back to this larger issue of the contrast between high 
doses and low doses. I want to give you one specific example, 
which really brings this home, and it is actually about a drug 
called tamoxifen. Now, tamoxifen, as many of you know, is used 
to fight breast cancer. At high levels, it suppresses the rate 
of growth of a breast tumor. It is very good at parts per 
million, parts per thousand levels, and physicians take great 
advantage of that. But if you go down the dose-response curve, 
to a level that is literally a million times beneath the level 
where it is effective as a drug stopping breast cancer, it 
stimulates proliferation of the breast tumor. It is an estrogen 
at that level. The high-dose experiments that our regulatory 
agencies have depended upon to anticipate low-dose effects do 
not work when you are dealing with compounds that behave like 
hormones. This is a widely accepted fact in medical 
endocrinology. It is just not challenging at all.
    The question is, when are we going to bring the 
toxicological community into the 21st century of science?
    Thank you.
    [The prepared statement of Dr. Myers follows:]

    Prepared Statement of John Peterson Myers, Ph.D., CEO and Chief 
                Scientist, Environmental Health Sciences
Base Health Standards on 21st Century Medical Science, Not 16th Century 
        Dogma
    Large scientific literatures of peer-reviewed publications now 
plausibly link bisphenol A (BPA) and several phthalates to an array of 
adverse health outcomes.
    For bisphenol A these include prostate and breast cancer, loss of 
fertility (including via polycystic ovaries and uterine fibroids, as 
well as reduced sperm count and spontaneous miscarriage) and impaired 
neurological development. Numerous studies show that many of these 
effects can be caused in laboratory animals at levels beneath the 
average concentration found in American serum today.\1\
    For phthalates these include abnormalities in the male reproductive 
tract (including undescended testes, hypospadias and reduced sperm 
count) as well as heightened sensitivity and reactivity of the immune 
system, which may lead to hyperallergic reactions and asthma.
    The strength of the evidence varies for each of these potential 
effects, for both phthalates and BPA. The human data on phthalates are 
stronger; indeed for BPA there are almost no epidemiological studies. 
But the evidence from animal experiments on BPA, especially at very low 
doses within the range of common human exposure, is much more extensive 
than with phthalates. And the mechanism of action of BPA in humans is 
the same as the mechanism of action in animals. Hence the animal 
findings are highly relevant to predicting human health impacts.
    Despite this evidence, both BPA and phthalates are in widespread, 
indeed ubiquitous use in commerce today. Virtually all Americans carry 
measurable levels in their fluids and tissues. None of the relevant 
Federal agencies have taken action to reduce exposures.
    Why?
    The scientific basis of regulatory toxicology, as it is applied 
today by Federal regulators, rests upon an assumption derived from 16th 
Century dogma. That assumption, never tested in standard procedures to 
establish acceptable exposure limits, conflicts directly with 21st 
Century medical science.
    The assumption is that experiments with high doses will reveal the 
effects of low doses. It is based upon the 16th Century observation by 
Paracelsus that ``All substances are poisons; there is none which is 
not a poison. The right dose differentiates a poison from a remedy.'' 
\2\ This has been paraphrased to become ``the dose makes the poison.''
    The assumption is directly contradicted by decades of research in 
the medical science of endocrinology showing that hormonally-active 
compounds have complicated dose-response curves in which low dose 
exposures can cause effects unpredictable from high dose experiments. 
BPA and phthalates are both hormonally-active compounds, called 
endocrine disrupters (EDCs), and peer-reviewed research has reported 
these complicated dose-response curves for both substances. 
Nevertheless, the FDA and EPA continue to depend upon this flawed 
assumption, which has been repeatedly invalidated in careful scientific 
studies, in these agencies' development of public health standards for, 
and regulation of, exposures to EDCs. This misled policy is disastrous, 
as it will lead to many lost opportunities for improving public health 
that will have implications for decades, as recent research shows long-
term detrimental effects not only on exposed individuals, but even 
subsequent generations.
    Biomonitoring studies conducted by the CDC and others document that 
wherever samples have been analyzed, people are contaminated with many 
industrial chemicals, including BPA and phthalates. Of particular 
concern are the numbers and concentrations of chemicals found in human 
amniotic fluid, fetal blood, and breast milk, rendering it impossible 
for a child to be born or to be breast-fed without developmental 
exposure.
    Many of these chemicals are known to interfere with the action of 
hormones in experimental systems, hormones that are essential for 
healthy development. With a mandate from Congress, for the last decade 
the U.S. EPA has been designing regulatory tools to screen and test for 
contaminants with endocrine effects.\3\ To date, this process has 
failed to fully integrate basic endocrinological principles in its 
decision-making and instead is relying upon toxicological methods that 
are inappropriate for EDCs.\4\ This led to a significant blind-spot in 
regulatory standard setting.
    Chemical monitoring by the CDC, carefully structured to obtain 
statistically representative estimates of Americans' exposures, 
typically reveals median serum or urine concentrations well below those 
produced by dosing regimens in animal experiments used for regulatory 
toxicology. Those regimens use high doses under the assumption that the 
effects of high doses can be used to predict low dose impacts. In fact, 
the estimates of safe daily human exposure doses for chemicals derived 
from these procedures are never directly tested, even in laboratory 
animals. Yet increasingly, epidemiological analyses of biomonitoring 
data showing associations, sometimes striking, between the low 
concentrations of chemicals measured in the general public and adverse 
health conditions. Examples include phthalates and sperm defects,\5\ 
reproductive tract abnormalities,\6\ and obesity; \7\ pesticides and 
sperm count; \8\ perchlorate \9\ or PCBs 10,11,12 and 
thyroid function; and persistent organic pollutants and type 2 diabetes 
\13\ and insulin resistance.\14\
    These associations should not arise if the safety levels 
established by high-dose testing are accurate. Several factors could be 
contributing to this apparent discrepancy between prediction and 
observation. One is that epidemiological associations do not reflect 
causality. A second is that the estimate for safety has been based upon 
an insensitive endpoint. A third is the potential for additive or 
synergistic effects of mixtures. I will focus here on a fourth, because 
it challenges the core assumption of regulation toxicology, that high-
dose testing is sufficient to predict low-dose effects. A huge 
experimental literature amassed over decades of mechanistic research in 
endocrinology demonstrates that this assumption is fundamentally flawed 
and is highly vulnerable to missing important low-dose adverse effects.
    Paracelsus's observation, above, reflects an intuitively logical 
concept that the higher the exposure, the greater the impact. Testing 
with high doses, in this view, should reveal any hazards and do so more 
efficiently than testing with low doses, because the effects will be 
stronger and easier to detect. This centuries-old paradigm remains the 
central tenet of modern regulatory toxicological approaches to studying 
the health effects of chemicals.
    Paracelsus' logic holds if and only if chemicals' effects 
faithfully follow a monotonic dose-response curve. When toxicologists 
began to focus on potential health effects of chemicals classified as 
endocrine disruptors, endocrinologists began to raise questions about 
the appropriateness of assuming monotonicity in toxicological studies 
of hormonally-active chemicals used in common household products.



    The basis for this concern is that non-monotonicity is a general 
characteristic of hormones. This issue is so central to hormone action 
that it is a critical component of determining the dose required for 
hormonally active drugs; an example is Lupron used to treat 
reproductive disorders in women and prostate cancer in men, since low 
doses stimulate while high doses inhibit tumor growth.
    These non-monotonic curves can result from multiple mechanisms, 
which have been studied by endocrinologists, pharmacologists and 
neurobiologists for decades. Hormones and hormone-mimicking chemicals 
act through receptors in target cells. Very low doses can stimulate the 
production of more receptors (called receptor up-regulation), resulting 
in an increase in responses, while higher doses (within the typical 
toxicological range of testing) can inhibit receptors (called receptor 
down-regulation), resulting in a decrease in responses. The consequence 
for gene activity, which is regulated by hormone-mimicking chemicals 
binding to receptors, is that very low doses of these chemicals (in the 
case of a positively-regulated gene) can up-regulate gene expression, 
while at higher doses the same chemicals down-regulate gene 
expression.1,15 In addition, myriad hormonal feedback 
mechanisms between the brain, pituitary gland and hormone producing 
organs (thyroid gland, adrenal glands, ovaries, testes) contribute to 
the presence of non-monotonic dose-response curves. Equally important, 
at high doses, hormones and hormone-mimicking chemicals can bind to 
receptors for other hormones (e.g., estrogens can interact with 
androgen and thyroid receptors), producing entirely different effects 
from those seen at low doses where only binding to estrogen receptors 
occurs. Also, there is non-specific (non-receptor mediated) toxicity 
that can occur at high but not low doses. The consequence is that there 
are qualitative as well as quantitative differences in the effects of 
high and very low doses of endocrine disrupting chemicals.
    Notably, EDCs may also act by mechanisms that do not require direct 
mediation of classical hormone receptors. For example, they also exert 
actions upon synthesis or function of enzymes that may be responsible 
for the synthesis or degradation of hormones; on factors that interact 
or regulate receptors such as coregulatory factors; and in the case of 
neurological actions, through neurotransmitter receptors.\16\ This 
concept is important because each of these mechanisms may have a unique 
dose-response sensitivity to an EDC, adding to the complexity of the 
overall shape of the dose-response curve.
    A recently published example of a non-monotonic response in an 
animal model, with high biomedical relevance to humans, involves the 
estrogenic drug diethylstilbestrol (DES), once widely used to treat 
difficult pregnancies but removed from the market in 1971 because it 
was found to cause a rare cancer in young adult women who had received 
fetal exposure. Research has established the BPA is structurally and 
functionally very similar to DES.
    Mice exposed perinatally to relatively high doses of DES (1000 mg/
kg/day) had reduced body weight in adulthood, but a much lower dose (1 
mg/kg/day) caused adult obesity (figure to right).17,18


    The mouse on the right received the extremely low dose compared to 
the control on the left. The researchers reported no difference between 
control and experimental animals in either calories consumed or energy 
expended.
    A similar non-monotonic response has been observed for DES effects 
on the developing prostate in mice.19,20,21 A traditional 
high-dose testing regimen with DES would never have revealed these low-
dose effects.
    Just as with DES, industrial chemicals that interfere with hormone 
signaling cannot be expected to follow monotonic dose-response rules. 
Non-monotonicity has been reported repeatedly for adverse effects with 
a number of endocrine disrupting compounds, including the bisphenol A, 
the phthalate DEHP, the pesticides, dieldrin, endosulfan and 
hexachlorobenzene, the pesticide metabolite DDE, and arochlor 1242, a 
PCB mixture.\22\
    Effects include strong exacerbation of allergic reactions following 
exposure to DEHP at a concentration one thousand-fold beneath the 
current safety standard, which is based on high dose liver toxicity 
(figure below) \23\ and increased allergic responses caused by 
picomolar level exposures (parts per trillion) to several persistent 
organic pollutants.\24\ Cells exposed to concentrations of these 
pollutants a million times higher than the level producing the maximum 
response showed no effect.


    An experiment (figure below) with rats that involved administration 
of DEHP was explicitly designed to test the adequacy of high-dose 
testing.\25\ It found that a high dose increased estrogen synthesizing 
(aromatase) enzyme activity in the brains of neonatal male rats; a dose 
100-fold lower appeared to be the ``no effect dose'', which is used to 
estimate the dose deemed safe for human exposure (this enzyme is 
involved in determining sex differences in brain function).


    In the experiment above, only because the scientists broke with 
tradition and also tested lower doses did they find significant down-
regulation of aromatase at a dose 37-times lower than the putative no 
effect dose, an effect opposite to and unpredicted from only testing 
very high doses.
    Other experiments have documented non-monotonicity in rat pituitary 
cells exposed to pico- through micro-molar levels (parts per trillion 
to parts per billion) of BPA.26,27 Acting through a 
relatively recently discovered estrogen receptor on the surface of the 
cell membrane, very low picomolar concentrations of the contaminant 
increased calcium influx and activation of enzyme cascades that 
dramatically amplify a very low-dose signal into a large cellular 
response. The dose-response curve followed a strongly non-monotonic, 
`inverted-U' shape, with the strongest response at low nanomolar 
levels. The bioactive concentrations of bisphenol A in these 
experiments were actually far below the range found ubiquitously in 
human blood and urine. Another endpoint that follows a non-monotonic 
pattern is human prostate cancer cell proliferation in response to 
bisphenol A,\28\ with the peak response occurring exactly within the 
range of exposure of men to bisphenol A based on biomonitoring 
studies.1,29
    Research over the past 20 years has identified large numbers of 
endocrine disrupting contaminants that are capable of mimicking or 
disrupting hormone function. Biomonitoring studies have established 
that many are widespread contaminants in people. Yet regulatory 
toxicology as it has been practiced for decades, and as it has been 
used to set public health exposure standards, ignores non-monotonicity 
despite the fact that, similar to hormones, all should be expected to 
display non-monotonic dose-response patterns.
    To date the Congressionally-mandated effort by the EPA, called the 
Endocrine Disruptor Screening Program (EDSP), has not acknowledged 
these common, indeed standard patterns from endocrinology, and hence it 
is on course to select methodologies that will remain blind to hazards 
posed by low doses that lead to adverse effects that only direct low-
dose testing can detect.
    An effective EDSP is required to protect Americans from exposure to 
industrial chemicals that can disrupt the endocrine system, which must 
function properly for normal development to occur as well as for normal 
adult function. Significant exposure to these chemicals is through the 
food supply, which is the domain of the FDA, but exposure also occurs 
through drinking water and air, the domain of the EPA. The American 
public depends upon these regulatory agencies to set public health 
standards sufficient to avoid harmful exposures. But until the FDA and 
EPA move beyond outdated concepts, the public health standards that 
emerge from their regulatory deliberations will continue to produce a 
disconnect between what human biomonitoring, epidemiological and 
mechanistic endocrine studies in animals reveal and what their 
regulatory decisionmakers allow.
    Were the health implications of these decisions inconsequential, 
this clash between toxicology and endocrinology would appropriately 
remain buried in academia. But the range of health conditions now 
plausibly linked to endocrine-disrupting contaminants--including 
prostate cancer, breast cancer, attention deficit hyperactivity 
disorder, infertility (including both male and female reproductive 
problems), miscarriage, and most recently, hyper-allergic diseases, 
obesity and type 2 diabetes--makes it imperative that the clash between 
basic endocrinologists and regulatory toxicologists becomes public and 
addressed by regulatory agencies. These diseases are major contributors 
to American's steadily increasing disease burden and to the escalating 
cost of health care. Extensive, careful and replicable animal research 
suggests that numerous industrial chemicals to which people are exposed 
every day, but which have not been adequately studied for health 
effects in humans, may be significant contributors to these adverse 
health trends.
    As endocrine and reproductive systems are highly conserved between 
animals and humans, there is no doubt that basic research results on 
EDCs are directly applicable to human health. Modernizing relevant 
health standards by incorporating endocrinological principles could 
help reduce a significant portion of the human disease burden, but this 
will require regulatory decisionmakers to begin asking scientifically 
appropriate questions. The soaring health care crisis in the U.S. 
demands that the regulatory apparatus of Federal Government get this 
right. Blind obedience to 16th century dogma will not solve the 
problem.
References
    \1\ L.N. Vandenberg, R. Hauser, M. Marcus, N. Olea, W.V. Welshons. 
Repro. Tox. 24, 139-177 (2007).
    \2\ M.A. Gallo, History and Scope of Toxicology, in C.D. Kaassen, 
Casarett & Doull's Toxicology, 5th Ed. (McGraw-Hill, New York, NY, 
1996), p.4.
    \3\ The 1996 Food Quality Protection Act mandated establishment of 
the Endocrine Disruptor Screening Program. http://www.epa.gov/scipoly/
oscpendo/.
    \4\ A. Gore. Experimental Biol. and Medicine 233, 3 (2008).
    \5\ R. Hauser, J.D. Meeker, S. Duty, M.J. Silva, A.M. Calafat. 
Epidemiology 17, 682-691 (2006).
    \6\ S Swan et al., Environ. Health Perspect. 113, 1056-1061 (2005).
    \7\ R.W. Stahlhut, E. van Wijngaarden, T.D. Dye, S. Cook, S.H. 
Swan. Environ. Health Perspect. 115, 876-882 (2007).
    \8\ S.H. Swan et al., Environ. Health Perspect. 111, 1478-1484 
(2003).
    \9\ B.C. Blount, J.L. Pirkle, J.D. Osterioh, L. Valentin-Blasini, 
K.L. Caldwell. Environ. Health Perspect. 114: 1865-1871.
    \10\ M.E. Turyk, H.A. Anderson, V.W. Persky. Environ. Health. 
Perspect. 115, 1197 (2007).
    \11\ T. Otake et al., Environ. Res. 105, 240 (Oct, 2007).
    \12\ J.D. Meeker, L. Altshul, R. Hauser. Environ. Res. 104, 296 
(June, 2007).
    \13\ D-H. Lee, I-K. Lee, K. Song, M. Steffes, W. Toscano, B.A. 
Baker, D. R. Jacobs. Diabetes Care 29, 1638-1644 (2006).
    \14\ D-H. Lee, I-K. Lee, S-H. Jin, M Steffes, D.R. Jacobs, Jr. 
Diabetes Care 30, 662-628 (2007).
    \15\ K.L. Medlock, C.R. Lyttle, N. Kelepouris, E.D. Newman, D.M. 
Sheehan. 1991. Proc. Soc. Exp. Biol. Med. 196, 293-300 (1991).
    \16\ A.C. Gore. Introduction to endocrine-disrupting chemicals, in 
A.C. Gore, Endocrine-disrupting chemicals: From basic research to 
clinical practice (Humana Press, New Jersey), pp. 3-8 (2007).
    \17\ R.R. Newbold, E. Padilla-Banks, R.J. Snyder, W.N. Jefferson. 
Birth Defects Research (Part A) 73, 478-480 (2005).
    \18\ R.R. Newbold, W. Padilla-Banks, R.J. Snyder, W.N. Jefferson. 
Mol. Nutr. Food Res. 51, 912-917 (2007).
    \19\ F.S. vom Saal, B.G. Timms, M.M. Motano, P. Palanza, K.A. 
Thayer, S.C. Nagel et al., Proc. Natl. Acad. Sci. USA. 94, 2056-2061 
(1997).
    \20\ C. Gupta. Proc. Soc. Exp. Biol. Med. 244, 61-68 (2000).
    \21\ B.G. Timms, K.L. Howdeshell, L. Barton, S. Bradley, C.A. 
Richter, F.S. vom Saal. Proc. Natl. Acad. Sci. 102, 7014-7019 (2005).
    \22\ J.P. Myers, W. Hessler, EnvironmentalHealthNews.org, 30 April 
2007, http://www.environmentalhealthnews.org/sciencebackground/2007/
2007-0415nmdrc.html.
    \23\ H. Takano, R. Yanagisawa, K-I. Inoue, T. Ichinose, K. 
Sadakano, T. Yoshikawa. Environ. Health Perspect. 114, 1266-1269 
(2006).
    \24\ S. Narita, R.M. Goldblum, C.S. Watson, E.G. Brooks, D.M. 
Estes, E.M. Curran, T. Midoro-Horiuti. Environ. Health Perspect. 115, 
48-52 (2007).
    \25\ A.J.M. Andrade, S.W. Grande, C.E. Talsness, K. Grote, I. 
Chahoud. Toxicology 227, 185-192 (2006).
    \26\ A.L. Wosniak, N.N. Bulayeva, C.S. Watson. Environ. Health 
Perspect. 113, 431-439 (2005).
    \27\ A. Zsarnofsky, H.H. Lee, H.S. Wang, S.M. Belcher. 
Endocrinology 146, 5388-5396 (2005).
    \28\ Y.B. Wetherill, C.E. Petra, K.R. Monk, A. Puga, K.E. Knudsen, 
Molec. Cancer Therapeut. 7, 515-24 (2002).
    \29\ A.M. Calafat, X. Ye, L-Y. Wong, J.A. Reidy, L.L. Needham. 
Environ. Health Perspect., in press, doi:10.1289/ehp.10605 (2008).

    Senator Klobuchar [presiding]. Thank you, Dr. Myers.
    Ms. Hitchcock?

STATEMENT OF ELIZABETH HITCHCOCK, PUBLIC HEALTH ADVOCATE, U.S. 
                 PUBLIC INTEREST RESEARCH GROUP

    Ms. Hitchcock. Good morning. Members of the Committee, I am 
Liz Hitchcock, Public Health Advocate for the U.S. Public 
Interest Research Group. I have submitted longer written 
testimony for the record, but I would like to cover three 
important points in this hearing.
    One, the hazards of bisphenol A and phthalates are well 
documented and pose a special danger to children.
    Two, other countries, a number of states, and retailers are 
acting in the absence of Federal action on these chemicals.
    Three, the Federal Government should regulate these and 
other toxic chemicals to protect our children's health.
    To begin, we would like to commend the Committee for its 
efforts to improve U.S. product safety, including the recent 
Senate passage of the CPSC Reform Act. When reconciled with the 
House bill, it will take long overdue steps forward in 
protecting America's children from unsafe products. We 
encourage the conference committee to take the strongest parts 
of each bill. In particular, we believe that the Senate bill's 
provisions addressing the toxic hazards of lead and phthalates 
in children's products are important steps to take preventable 
hazards out of the marketplace.
    First, the hazards of bisphenol A and phthalates are well 
documented, as Dr. Myers and others have told you in their 
testimony. For 22 years, U.S. PIRG Trouble In Toyland safety 
reports have identified hazards to a population that is 
notorious for putting everything in their mouths, small 
children. We have increased our focus in the last 10 years on 
chronic hazards posed by unnecessary exposure to lead, 
phthalates, and chemicals known to be toxic.
    In 1998, we joined a number of public interest groups in 
petitioning the CPSC to ban polyvinyl chloride in all toys 
intended for children under the age of 5 because of the 
potential health hazards posed by phthalates. In 2003, the CPSC 
denied our petition.
    Phthalates are widely used and can be found in many 
children's products, including teethers, bath books, raincoats, 
and as Senator Klobuchar pointed out, rubber duckies.
    Last year, U.S. PIRG's partner organization, Environment 
California, tested five of the most popular baby bottle brands 
on the market. Our researchers found that the bottles tested 
from all five brands leached bisphenol A at levels found to 
cause harm in numerous laboratory studies. Scientists have 
linked very low doses of bisphenol A to cancers, to impaired 
immune function, to the early onset of puberty, obesity, 
diabetes, and hyperactivity, among other problems.
    Phthalates have been linked to a number of serious health 
impacts, including reproductive defects, birth deformities, 
liver and thyroid damage, neurological impacts, and even 
cancer.
    In April, the National Toxicology Program at NIH finally 
acknowledged health concerns about children's exposure to BPA.
    Given the significant health concerns associated with both 
bisphenol A and with phthalates, taking a precautionary 
approach toward the use of these chemicals just makes sense. In 
other words, if there is evidence that these chemicals cause 
harm and if we have safer alternatives with which to replace 
them, then why would we not use precaution and restrict their 
use?
    Second, other countries and a number of States and some 
manufacturers are leading the way in taking action on these 
chemicals. For example, the European Union has had a policy 
restricting the use of phthalates since 1999. At least 14 
countries have also restricted the use of phthalates to protect 
children's health. In the United States, only California and 
Washington State have enacted phthalate legislation. A Vermont 
bill is on the Governor's desk right now. But at least a dozen 
States have either introduced or are considering introducing 
legislation to restrict phthalate use.
    In the private sector, several leading manufacturers of 
toys and baby products in the U.S. have stopped using 
phthalates over the last few years. In addition, Wal-Mart and 
Toys ``R'' Us announced early this year that they will begin 
phasing out children's toys containing the chemical in the 
coming months.
    Last month, the Canadian Government declared bisphenol A 
toxic under Canadian law, triggering a ban on baby bottles with 
that chemical. There are current efforts in five State 
legislatures to restrict uses of BPA. Senator Chuck Schumer has 
introduced S. 2928 banning BPA in all products intended for 
infants and children up age 7, a bill that U.S. PIRG supports.
    Consumers cannot be expected to do it alone and cannot 
expect all industry and retailers to take the right voluntary 
steps. The Federal Government should regulate these and other 
toxic chemicals to protect our children's health.
    First, the Federal Government should take action based on 
the overwhelming weight of evidence showing that chemicals like 
phthalates and bisphenol A may harm human health.
    U.S. chemicals policy should be reformed to require 
manufacturers to provide all hazard and health impact 
information to the Federal Government so we can begin to assess 
the thousands of chemicals currently on the market for which we 
have little or inadequate data.
    And finally, the conference committee and the Congress 
should pass a final version of the CPSC reform bill that 
includes the Feinstein Amendment banning phthalates in 
children's products. The amendment will serve to significantly 
curb children's routes of exposure to these reproductive 
toxicants.
    We commend the Committee for conducting this important 
hearing and we hope that you find our comments helpful. We 
would be happy to discuss other possible actions under the 
Committee's jurisdiction to protect consumers from chronic and 
developmental hazards from unnecessary exposure to toxic 
chemicals in consumer products.
    Thank you.
    [The prepared statement of Ms. Hitchcock follows:]

  Prepared Statement of Elizabeth Hitchcock, Public Health Advocate, 
                  U.S. Public Interest Research Group
    Chairman Pryor, Senator Sununu, Members of the Committee: I am 
Elizabeth Hitchcock, Public Health Advocate for the U.S. Public 
Interest Research Group. U.S. PIRG is the federation of state PIRGs, 
which are non-profit, non-partisan public interest advocacy 
organizations with one million members across the country.
    We are pleased to present our views at this Oversight Hearing on 
Bisphenol-A, Phthalates, Consumer Products and Consumer Health. The 
state PIRGs have long been concerned with the important issues of 
toxics in consumer products, and the ability of the Federal Government 
to protect all of us, but particularly our children, from preventable 
hazards.
    Since 1986, we have conducted toy safety research and education 
projects to avoid preventable deaths and injuries. While our annual 
Trouble In Toyland toy safety reports \1\ have emphasized the hazards 
posed by choking on small parts, we have expanded the report in the 
past decade to focus on the chronic hazards posed by unnecessary 
exposure to lead,\2\ phthalates and other chemicals known to be toxic.
Summary
    First, Mr. Chairman, we commend you for your efforts to improve 
U.S. product safety, including the recent Senate passage of your bill, 
the CPSC Reform Act. When it is reconciled with the House bill, it will 
take significant and long overdue steps forward in protecting America's 
children from unsafe products. We encourage the conference committee to 
take the strongest parts of each bill.
    In particular, we believe that the Senate bill's provisions 
addressing the toxic hazards of lead and phthalates in children's 
products are important steps to take preventable hazards out of the 
marketplace.
    Recent headlines about the long overdue acknowledgement of the 
National Toxicology Program of the U.S. National Institutes of Health 
of health concerns about children's exposure to Bisphenol-A (BPA) have 
raised concerns among consumers about this and other toxic chemicals.
    In general, U.S. PIRG's policy recommendations concerning toxic 
chemicals like Bisphenol-A and phthalates are that the Federal 
Government should:

   Phase Out Dangerous Chemicals. The U.S. Environmental 
        Protection Agency should take action based on the overwhelming 
        weight of evidence showing that chemicals like phthalates and 
        bisphenol-A may harm human health.

   The U.S. should phaseout the use of Bisphenol-A, especially 
        in children's products. Due to the possible increased risks to 
        small children and pregnant women, we strongly urge the removal 
        of BPA from all products intended to contact food.

   Reform U.S. Chemicals Policy. Manufacturers should be 
        required to provide all hazard and health impact information to 
        the EPA so the agency can begin to assess the thousands of 
        chemicals currently on the market for which it has little or 
        inadequate data.

   The Consumer Product Safety Commission should protect 
        consumers, for example, by labeling these products with the 
        names of the chemicals they contain to allow parents to choose 
        less toxic products, among other protective actions.

   The conference committee and the Congress should pass a 
        final version of CPSC reform legislation including the 
        Feinstein amendment banning phthalates in children's products 
        (incorporated as Section 40 of H.R. 4040, the CPSC Reform Act, 
        as passed by the Senate).\3\
1. Phthalates Are Ubiquitous With Exposure Linked To Health Effects
    Phthalates are a family of chemicals, including diethyl phthalate 
(DEP), diethylhexyl phthalate (DEHP), dibutyl phthalate (DBP), butyl 
benzyl phthalate (BBP), diisodecyl phthalate (DIDP), diisononyl 
phthalate (DINP), di-n-octyl phthalate (DNOP), and many other distinct 
types. The polyvinyl chloride (PVC) plastic industry uses large amounts 
of phthalates as additives to improve the flexibility of its products, 
including home siding, flooring, furniture, food packaging, toys, 
clothing, car interiors, and medical equipment, including IV bags. In 
addition, other manufacturers use phthalates in personal care products 
such as soap, shampoo, deodorant, hand lotion, nail polish, cosmetics, 
and perfume, as well as industrial products like solvents, lubricants, 
glue, paint, sealants, insecticides, detergent, and ink.\4\
    Phthalates are pervasive in the environment and in human bodies. In 
2000, the Centers for Disease Control (CDC) found high levels of 
phthalates and their transformation products (known as metabolites) in 
every one of 289 adult Americans tested, including women of 
childbearing age.\5\ Larger CDC studies in 2003 \6\ and 2005 \7\ again 
found high levels of phthalates in almost every person tested.
    Numerous scientists have documented the potential health effects of 
exposure to phthalates in the womb or at crucial stages of development, 
including (but not limited to):

   Reproductive Defects. Scientists have demonstrated links 
        between exposure to phthalates in the womb with abnormal 
        genital development in baby boys and disruption in sexual 
        development.\8\ In October 2005, an independent panel of 
        scientists convened by the National Institute of Environmental 
        Health Sciences and the National Toxicology Program released 
        its review of one type of phthalate, diethylhexyl phthalate 
        (DEHP). The panel confirmed that DEHP poses a risk to 
        reproductive and developmental health.\9\

   Premature Delivery. A study published in November 2003 
        suggests a link between exposure to phthalates and pre-term 
        birth. The scientists found phthalates and their breakdown 
        products in the blood of newborn infants, with higher levels 
        leading to a higher incidence of premature delivery.\10\

   Early Onset Puberty. One study of Puerto Rican girls 
        suggests that phthalates may be playing a role in trends toward 
        earlier sexual maturity.\11\ Scientists found that levels of 
        DEHP were seven times higher in girls with premature breast 
        development than levels in normal girls.

   Lower Sperm Counts. In 2003, Drs. Susan Duty and Russ Hauser 
        of the Harvard School of Public Health published one of the 
        first studies linking phthalate exposure with harm to human 
        reproductive health.\12\ Men who had monobutyl or monobenzyl 
        phthalate in their urine tended to have lower sperm counts, 
        with the highest concentrations leading to the lowest sperm 
        counts.
2. History of Efforts to Ban Phthalates in Children's Toys and Products
    In 1998, the state PIRGs and several other environmental and 
consumer groups petitioned the Consumer Product Safety Commission, 
asking the agency to ban polyvinyl chloride (PVC) plastic in all toys 
intended for children under the age of five because of the potential 
health hazards posed by diisononyl phthalates (DINP). While noting its 
position that ``few if any children are at risk from the chemical,'' 
\13\ in December 1998 CPSC asked the toy and baby products industry to 
remove DINP from soft rattles and teethers. About 90 percent of 
manufacturers indicated at that time that they had removed or would 
remove DINP from soft rattles and teethers by early 1999. CPSC staff 
also asked the industry to find a substitute for phthalates in other 
products intended for children under 3 years old that are likely to be 
mouthed or chewed.\14\
    CPSC also convened a Chronic Hazard Advisory Panel to examine the 
existing scientific data concerning the potential risks of phthalates 
to humans. In June 2001, the panel concluded that while the majority of 
children would not be adversely affected by diisononyl phthalate, 
``there may be a DINP risk for any young children who routinely mouth 
DINP-plasticized toys for seventy-five minutes per day or more.'' \15\
    Unfortunately, in February 2003, CPSC denied the state PIRGs' 
petition to ban PVC plastic in toys for young children.\16\
    Some manufacturers are beginning to label their baby products and 
toys as ``phthalate-free,'' which should provide parents the 
information they need to make educated purchasing decisions. The U.S. 
government, however, does not regulate the ``phthalate-free'' label or 
ensure that products labeled ``phthalate-free'' actually do not contain 
phthalates. Since the U.S. government has not established any 
guidelines for what the label means, or established any standards for 
the phthalate content in children's products, consumers can only assume 
that it means phthalates are not present in the item.
    In 2005, to test the reliability of the ``phthalate-free'' label, 
U.S. PIRG commissioned STAT Analysis Corporation in Chicago, Illinois 
to test eight soft plastic toys labeled as not containing phthalates. 
Of the eight toys tested, six contained detectable levels of 
phthalates.\17\ Based on these results, we asked the Federal Trade 
Commission (FTC) to investigate whether manufacturers' use of the 
``phthalate-free'' label constitutes unfair or deceptive marketing 
practices when the product actually contains phthalates.\18\
    With the results of the FTC investigation still pending, we once 
again commissioned STAT Analysis Corporation in the fall of 2006 to 
test 10 soft plastic toys labeled as not containing phthalates.\19\ Of 
the 10 toys tested, just two contained detectable levels of phthalates. 
Some of the items that tested positive for phthalates in the first year 
did not in the second. While this may be good news for consumers, 
nothing in U.S. law has changed to hold manufacturers accountable to 
their ``phthalate-free'' label or require them to stop using 
phthalates. Consumers still have no guarantee that the ``phthalate-
free'' products they purchase truly are phthalate-free, as evidenced by 
our test results.
    A number of individual states and other countries have taken 
action, however, to protect children's health. In 1999, the European 
Union (EU) imposed temporary restrictions on the use of six phthalates 
in toys and childcare products.\20\ This ban became permanent in 
January 2006. The EU banned three phthalates classified as reproductive 
toxicants--diethylhexyl phthalate (DEHP), butyl benzyl phthalate (BBP), 
and dibutyl phthalate (DBP)--in all toys and childcare articles. The EU 
banned three other phthalates--DINP, diisodecyl phthalate (DIDP) and 
di-n-octyl phthalate (DNOP)--in toys and childcare articles intended 
for children under 3 years of age and that can be put in the mouth.\21\
    In the past year, California and Washington State have banned 
phthalates in children's products; Minnesota and Vermont both have 
bills on their Governor's desk; and Rhode Island, New York and 
Massachusetts are considering similar measures.
    In March 2008, the U.S. Senate overwhelmingly passed the CPSC 
Reform Act, with an amendment by Senator Feinstein that eliminates 
phthalates in children's products and child care articles, which will 
serve to significantly curb children's routes of exposure to these 
reproductive toxicants. We urge the conferees to retain the phthalate 
provision, and its state savings clause, in the final bill.
3. Bisphenol-A: Developmental, Neural and Reproductive Toxicant
    Scientists have linked very low doses of bisphenol-A to cancers, 
impaired immune function, early onset of puberty, obesity, diabetes, 
and hyperactivity, among other problems.
    We know that bisphenol-A can leach from plastic containers and cans 
and into food and beverages, leading to potentially significant human 
exposures. A recent study released by the U.S. Centers for Disease 
Control and Prevention (CDC) found that BPA was in the blood of 95 
percent of humans they tested. The median level of BPA found in humans 
is higher than the level that causes adverse effects in animal studies. 
BPA raises particularly troubling health questions because it can 
affect the endocrine system, mimicking the effects of estrogen in the 
body. Experiments in animals and with human cells strongly suggest 
exposures typical in the U.S. population may increase susceptibility to 
breast and prostate cancer, reproductive system abnormalities, and, for 
exposure in the womb and early childhood, a host of developmental 
problems. Concerns about early life exposures also extend to early 
onset of puberty in females, potential prostate problems in males, and 
obesity.
    Last year, U.S. PIRG's partner organization, Environment 
California, tested five of the most popular baby bottle brands on the 
market (Avent, Dr. Brown's, Evenflo, Gerber, and Playtex) to determine 
the amount of leaching from each bottle. Our researchers found that the 
bottles tested from all five brands leached bisphenol-A at levels found 
to cause harm in numerous laboratory studies.\22\
    The current U.S. Environmental Protection Agency daily upper limit 
for BPA, 50 micrograms per kilogram of body weight, is based on 
industry-sponsored experiments conducted in the 1980s. Some animal 
studies show adverse health affects from exposure of only 0.025 
micrograms per kilogram of body weight, yet a polycarbonate baby bottle 
with room temperature water can leach 2 micrograms of BPA per liter. A 
3-month-old baby drinking from a polycarbonate bottle may be exposed to 
as much as 11 micrograms per kilogram of body weight daily.
    Aside from polycarbonate plastic bottles, BPA is also a food 
additive approved by the Food and Drug Administration (FDA), commonly 
used in the coatings for the inside of food cans. But a recent report 
by the National Toxicology Program (NTP) questioned previous FDA 
findings that BPA is safe for such applications. Their report, issued 
on April 15, 2008, expressed ``some concern'' based on animal studies 
that BPA might affect the neurological systems and behavior of infants 
and children. Among its conclusions, the NTP report states that, ``the 
possibility that human development may be altered by bisphenol-A at 
current exposure levels cannot be dismissed.''
Independent Science Shows Harmful Effects from BPA, while Industry 
        Science Shows None
    A recently-published review of scientific studies shows that, in 
the last 7 years (through November 2005), 151 studies on the low-dose 
effects of BPA have been published.\23\ None of the 12 studies funded 
by the chemical industry reported adverse effects at low levels, 
whereas 128 of 139 government-funded studies found effects. These many 
studies were conducted in academic laboratories in the U.S. and abroad. 
Even the 12 industry-funded studies have flaws, however. Of the 
industry studies, two had its positive control fail--an indication that 
the entire experiment had failed, not that BPA had not caused an 
effect.
    Another industry study concluded BPA caused no effect, but an 
independent analysis of the experiment's data by scientists convened by 
the National Toxicology Program of the U.S. Department of Health & 
Human Services concluded that in fact there was an effect. Industry 
scientists had misreported their own results.
    The chemical industry relies on an incomplete review of scientific 
studies by an effort funded by the American Plastics Council at the 
Harvard Center for Risk Analysis. The panel funded by the American 
Plastics Council only considered 19 studies in concluding in 2004 that 
the weight of the evidence for low-dose effects of BPA was weak.\24\ As 
of November 2005, there were 151 published studies on the low-dose 
effects of BPA.
    The last U.S. EPA risk assessment for BPA was based on research 
conducted in the 1980s and did not consider that BPA was a chemical 
estrogen. The most recent risk assessment of BPA was based on a 
comprehensive review of the scientific literature conducted in 1998 by 
the European Union, with some selected articles added through 2001, at 
which time few of the current 151 low-dose BPA studies had been 
published. The most recent review of scientific studies shows effects 
from exposure to BPA at levels significantly below the current ``safe 
exposure'' level established by the U.S. based on experiments conducted 
prior to 1988.
4. History of Efforts to Regulate Bisphenol-A
    In April 2008, the National Toxicology Program of the U.S. National 
Institutes of Health finally acknowledged health concerns about 
children's exposure to BPA. Unfortunately, it is unclear whether this 
determination will lead to any Federal policy changes to protect 
children from BPA. On April 18th, the Canadian Government declared BPA 
``toxic'' under Canadian Law, triggering a ban on BPA baby bottles in 
Canada. There are current efforts in state legislatures in California, 
Massachusetts, Illinois, New York and Rhode Island to restrict uses of 
the chemical. On April 29, Senator Chuck Schumer introduced S. 2928 
banning BPA in all products intended for infants and children up to age 
7. Senators Boxer, Clinton, Durbin, Feinstein, Kerry and Menendez are 
co-sponsors of the bill, which U.S. PIRG supports. The U.S. Food and 
Drug Administration announced it would review its regulatory policy on 
BPA. The FDA's reliance on two industry studies finding BPA safe, 
despite over 100 independent scientific studies linking the chemical to 
an array of illnesses, including breast and prostate cancer and 
obesity, is the subject of a Congressional investigation headed by 
Chairman John Dingell of the House Energy and Commerce Committee.
    In addition, some manufacturers and retailers are taking action on 
the chemical. Playtex Infant Care announced it will stop selling 
products made with BPA by the end of the year and will give one million 
free samples of new BPA-free products to potential customers. Wal-Mart 
and CVS announced they are phasing out BPA baby bottles in U.S. stores. 
Nalgene announced it would no longer use plastic made with BPA in its 
water bottles.
5. U.S. PIRG's Policy Recommendations
    Consumers cannot be expected to do it alone--as the thousands of 
harmful and untested chemicals currently on the market pose a super-
human challenge to completely avoid exposure. The U.S. Government must 
act in a manner that assists parents, and ensure that products on the 
market are not potentially harmful for children.

        A. Phase Out Dangerous Chemicals. The U.S. Environmental 
        Protection Agency should take action based on the overwhelming 
        weight of evidence showing that chemicals like phthalates and 
        bisphenol-A may harm human health. The United States should 
        phaseout the use of these chemicals--especially in children's 
        products. Until the U.S. Government acts, state governments 
        should continue to fill the regulatory gap and support policies 
        to phaseout these chemicals as well. CPSC should ban the use of 
        phthalates in all toys and products for children 5 years old 
        and under, and the U.S. should phaseout the use of Bisphenol-A, 
        especially in children's products. The Federal Government 
        should study the health effects of BPA exposure in all age 
        groups and pregnant women, and should focus on the products 
        that have the greatest potential for causing human harm. Due to 
        the possible increased risks to small children and pregnant 
        women, we strongly urge the removal of BPA from all products 
        intended to contact food.

        B. Reform U.S. Chemicals Policy. Currently, manufacturers can 
        put chemicals on the market without proving that they are safe. 
        Manufacturers should be required to provide all hazard and 
        health impact information to the EPA so the agency can begin to 
        assess the thousands of chemicals currently on the market for 
        which it has little or inadequate data. Next, manufacturers of 
        chemicals should be required to conduct an alternatives 
        analysis to determine if they are really using the least 
        hazardous chemical for each application. Finally, EPA must have 
        the authority to ban or restrict the use of a chemical if it 
        can harm human health.

        C. Consumer Product Safety Commission Should Protect Consumers. 
        The Consumer Product Safety Commission (CPSC) has an obligation 
        to protect consumers from dangerous products. The CPSC should 
        first label these products with the names of the chemicals they 
        contain to allow parents to choose less toxic products. Second, 
        the CPSC should take the precautionary approach and require 
        manufacturers to remove chemicals that may pose a particular 
        threat to fetuses, infants and children, particularly when the 
        chemical is not necessary for the product to function according 
        to design. In addition, CPSC and the Federal Trade Commission 
        should look into manufacturers' use of the ``phthalate-free'' 
        label and take action against manufacturers that may be 
        misleading consumers.

        D. The conference committee and the Congress should pass a 
        final version of CPSC reform legislation including the 
        Feinstein amendment banning phthalates in children's products 
        (incorporated as Section 40 of H.R. 4040 as passed by the 
        Senate). The amendment will:

     Prohibit the use of phthalates (any combination of certain 
            listed chemicals in concentrations exceeding 0.1 percent) 
            in any children's product or child care article.

     Require manufacturers to use the least toxic alternative 
            to phthalates.

     Prohibit the use of certain harmful alternatives--
            including substances known to be, likely to be, or 
            suggestive of being carcinogens; and reproductive toxicants 
            identified as causing either birth defects, reproductive 
            harm, or developmental harm.

     The amendment also includes an important ``savings 
            clause'' that would prevent Federal preemption of stronger 
            state laws regulating phthalates in toys or other product 
            categories.
Conclusion
    We commend you, Mr. Chairman, for conducting this important 
hearing. We hope that you find our comments helpful. We look forward to 
working with you and your committee staff to move legislation 
addressing these concerns forward. We would also be happy to discuss 
other possible actions under the Committee's jurisdiction to protect 
consumers from the chronic and developmental hazards from unnecessary 
exposure to toxic chemicals like Bisphenol-A and phthalates in a 
variety of consumer products. Thank you.
Endnotes
    \1\ These reports and other information about toy safety are 
available at our website www.toysafety.net. Our main website is 
www.uspirg.org.
    \2\ Lead, of course, can also pose acute hazards, at the levels (up 
to 99 percent by weight) found in toy jewelry.
    \3\ The CPSC Reform Act was approved in Committee as S. 2045 
(Pryor-Inouye) and a substitute was brought to the floor as S. 2663 
(Pryor-Inouye-Stevens-Collins). The Senate bill's text was then 
substituted for that of the House bill and re-numbered on passage as 
H.R. 4040. The Feinstein phthalates amendment (Section 40) was accepted 
on voice vote on the floor.
    \4\ Phthalate Esters Panel of the American Chemistry Council, What 
are Phthalates?, downloaded from www.phthalates.org on 14 April 2004; 
Catherine Dorey, Greenpeace, Chemical Legacy: Contamination of the 
Child, October 2003.
    \5\ BC Blount et al., ``Levels of Seven Urinary Phthalate 
Metabolites in a Human Reference Population,'' Environmental Health 
Perspectives 108: 979-982, 2000.
    \6\ Manori J. Silva et al., ``Urinary Levels of Seven Phthalate 
Metabolites in the U.S. Population from the National Health and 
Nutrition Examination Survey (NHANES) 1999-2000,'' Environmental Health 
Perspectives 112: 331-338, March 2004.
    \7\ Centers for Disease Control, ``Third National Report on 
Exposure to Toxic Chemicals'', 2005.
    \8\ Shanna H. Swan et al., ``Decrease in anogenital distance among 
male infants with prenatal phthalate exposure,'' Environmental Health 
Perspectives 113: 1056-1061, August 2005; L.E. Gray et al., ``Perinatal 
Exposure to the Phthalates DEHP, BBP, and DINP, but not DEP, DMP, or 
DOTP, Alters Sexual Differentiation of the Male Rat,'' Toxicological 
Science 58: 350-365, December 2000; Vickie Wilson et al., ``Phthalate 
Ester-Induced Gubernacular Lesions are Associated with Reduced Insl3 
Gene Expression in the Fetal Rat Testis,'' Toxicology Letters 146: 207-
215, 2 February 2004; J.S. Fisher et al., ``Human `Testicular 
Dysgenesis Syndrome': A Possible Model Using in-utero Exposure of the 
Rat to Dibutyl Phthalate,'' Human Reproduction 18: 1383-1394, 2003.
    \9\ NIEHS, ``Independent Panel to Evaluate a Chemical Used in Some 
Plastics (Di (2-ethylhexyl) phthalate) for Hazards to Human Development 
or Reproduction,'' press release, October 5, 2005.
    \10\ G. Latini et al., ``In-Utero Exposure to Di-(2-ethylhexyl)-
phthalate and Human Pregnancy Duration,'' Environmental Health 
Perspectives 111:1783-1785, 2003.
    \11\ I. Colon, D. Caro, C.J. Bourdony and O. Rosario, 
``Identification of Phthalate Esters in the Serum of Young Puerto Rican 
Girls with Premature Breast Development,'' Environmental Health 
Perspectives 108: 895-900, 2000.
    \12\ S.M. Duty et al., ``Phthalate Exposure and Human Semen 
Parameters,'' Epidemiology 14: 269-277, 2003; S.M. Duty et al., ``The 
Relationship Between Environmental Exposures to Phthalates and DNA 
Damage in Human Sperm Using the Neutral Comet Assay,'' Environmental 
Health Perspectives 111: 1164-1169, 2003.
    \13\ CPSC, ``CPSC Releases Study on Phthalates in Teethers, Rattles 
and Other Children's Products,'' press release, December 2, 1998, 
accessed May 12, 2008 at www.cpsc.gov/CPSCPUB/PREREL/PRHTML99/
99031.html.
    \14\ CPSC, ``CPSC Releases Study on Phthalates in Teethers, Rattles 
and Other Children's Products,'' press release, December 2, 1998, 
accessed May 12, 2008 at www.cpsc.gov/CPSCPUB/PREREL/PRHTML99/
99031.html.
    \15\ Report to the U.S. Consumer Product Safety Commission by the 
Chronic Hazard Advisory Panel on Diisononyl Phthalate, June 2001. 
Accessed May 12, 2008 at http://www.cpsc.gov/LIBRARY/FOIA/Foia01/os/
dinp.pdf.
    \16\ CPSC, Letter to Jeffrey Becker Wise, National Environmental 
Trust, February 26, 2003, accessed May 12, 2008 at http://www.cpsc.gov/
library/foia/foia03/petition/ageunder.PDF.
    \17\ U.S. PIRG Education Fund, Trouble in Toyland: The 20th Annual 
Survey of Toy Safety, November 2005.
    \18\ Letter to the Honorable Deborah Platt Majoras, Chairman, FTC, 
November 21, 2005. On file with the author. Our petition was later 
denied.
    \19\ Eight of the toys were labeled ``phthalate-free'' on the 
packaging. One item was labeled ``phthalate-free'' on the 
manufacturer's website. For the last item, the manufacturer's website 
claimed not to use phthalates in any of its children's products.
    \20\ ``Results of Competitiveness Council, Brussels, 24th September 
2004,'' Memo/04/225.
    \21\ Bette Hileman, ``EU Bans Three Phthalates from Toys, Restricts 
Three More,'' Chemical and Engineering News, July 11, 2005.
    \22\ ``Toxic Baby Bottles: Scientific study finds leaching 
chemicals in clear plastic baby bottles'', Environment California, 2007
    \23\ vom Saal, F. and C. Hughes, An Extensive New Literature 
Concerning Low-Dose Effects of Bisphenol A Shows the Need for a New 
Risk Assessment. Environmental Health Perspectives 113:926-933 (2005).
    \24\ vom Saal, F and C Hughes, An Extensive New Literature 
Concerning Low-Dose Effects of Bisphenol A Shows the Need for a New 
Risk Assessment. Environmental Health Perspectives 113:926-933 (2005). 
(``The charge to the HCRA panel, which was to perform a weight-of-the 
evidence evaluation of available data on the developmental and 
reproductive effects of exposure to BPA in laboratory animals, led to 
an analysis of only 19 of 47 available published studies on low-dose 
effects of BPA. The deliberations of the HCRA were in 2001-2002, and 
accordingly, a cut-off date of April 2002 was selected for 
consideration of the published literature. It is regrettable that the 
relevance of the analysis was further undermined by a delay of 2.5 
years in publication of the report. During the intervening time, 
between April 2002 and the end of 2004, a large number of additional 
articles reporting low-dose effects of BPA in experimental animals have 
been published. The result is that by the end of 2004, a PubMed 
(National Library of Medicine, Bethesda, MD) search identified 115 
published studies concerning effects of low doses of BPA in 
experimental animals.'').

    Senator Klobuchar. Thank you, Ms. Hitchcock.
    Senator Kerry has to leave and wants to say a few words 
before he goes.
    Senator Kerry. I just wanted to thank the panel very much. 
I apologize that I cannot be here. I particularly want to thank 
Pete Myers, Dr. Myers, and Dianne Dumanoski and company for Our 
Stolen Future, just a superb piece of work which I wish more 
Americans were aware of. And Ms. Hitchcock, thank you for your 
testimony.
    Now, I will submit some questions in writing, if that is 
permissible, and a fair number.
    But I very much appreciate your testimony today. I 
apologize. We just have competing hearings, and I am sorry.
    Senator Klobuchar. Thank you.
    Dr. Hentges?

        STATEMENT OF STEVEN G. HENTGES, Ph.D., EXECUTIVE

           DIRECTOR, POLYCARBONATE/BPA GLOBAL GROUP,

                   AMERICAN CHEMISTRY COUNCIL

    Dr. Hentges. Thank you, Senator Klobuchar and Members of 
the Committee. The American Chemistry Council appreciates the 
opportunity to testify today and we also appreciate your 
interest in understanding the safety of plastics additives in 
consumer products.
    We have also provided written testimony, and I ask that the 
written testimony be entered into the record.
    We firmly believe that good public health policy must be 
based on facts and the best available science, and consumers 
should expect no less. Therefore, we are committed to the 
safety of our products, and last year alone, ACC member 
companies invested over $14 billion in environment, health, and 
safety programs helping to improve the understanding of our 
products.
    As you know, much of the information on chemical safety can 
be highly technical and difficult for consumers to put into 
perspective. That is why it is essential for scientific review 
processes to be thorough and transparent in order for the 
public to have confidence in assessments conducted by 
Government experts.
    Recent press reports have questioned the safety of 
phthalate esters and bisphenol A, compounds that are used in 
plastics to impart particular performance properties. Many of 
these reports have been misleading or inaccurate and have 
resulted in widespread confusion about the safety of plastics. 
In fact, both bisphenol A and phthalates have been subjected to 
numerous rigorous and comprehensive reviews by government 
agencies in the U.S. and around the world. After more than 5 
decades of use, no reliable evidence has shown bisphenol A or 
phthalates in consumer products to have caused any harm to any 
person.
    To the contrary, recent government reviews have affirmed 
the safety of bisphenol A and phthalates in common everyday 
products. The clear weight of scientific evidence provides 
reassurance that the public should not be concerned about 
everyday products that contain either bisphenol A or 
phthalates.
    Phthalates are used to soften or plasticize otherwise rigid 
PVC plastic, which is used to make many consumer products. The 
U.S. Consumer Product Safety Commission, the National 
Toxicology program, and the U.S. Centers for Disease Control 
and Prevention have found no justification for restricting the 
use of phthalates as a plasticizer in toys and children's 
products. The CPSC conducted a 5-year health risk study and 
found no demonstrated health risk from the primary phthalate 
used in PVC toys or other products intended for children 5 
years of age and younger and no justification for banning its 
use.
    International scientific agencies have come to similar 
conclusions. The European Union conducted a decade-long risk 
assessment of five phthalates and concluded that the primary 
phthalate used in children's toys was unlikely to pose a risk 
to consumers following inhalation, skin contact, or ingestion.
    In short, rigorous scientific reviews conducted by the 
government agencies responsible for regulating phthalates in 
consumer products do not support restrictions on the use of 
these materials. The science is simply not there to support 
such action.
    Bisphenol A is used primarily to make clear, shatter-
resistant polycarbonate plastic and durable epoxy resins, both 
used in a wide array of consumer products. In the past 2 years 
alone, comprehensive scientific assessments from the European 
Union, the U.S. National Toxicology Program, Health Canada, NSF 
International, and the European Food Safety Authority have all 
been undertaken, and these assessments support the continued 
safe use of consumer products made from polycarbonate plastic 
and epoxy resins.
    Very recently the FDA said we believe there is a large body 
of evidence that indicates that FDA regulated products 
containing BPA currently on the market are safe and that 
exposure levels to BPA from food contact materials, including 
for infants and children, are below those that may cause health 
effects.
    Based on the science, bisphenol A is not banned or 
restricted anywhere in the world. Although it has been claimed 
that low doses of bisphenol A may be harmful, the so-called 
low-dose hypothesis is just that, a hypothesis that has not 
been proven and has not been accepted by any of the government 
agencies that have reviewed the science on bisphenol A.
    We understand that the public wants to be assured that the 
products they use are safe and have been evaluated using the 
best available science. We agree. In the case of phthalates and 
bisphenol A, consumers can confidently rely on rich bodies of 
safety data and the comprehensive assessments from experts in 
the U.S. and around the world.
    Thank you again for the opportunity to address the 
Committee.
    [The prepared statement of Dr. Hentges follows:]

  Prepared Statement of Steven G. Hentges, Ph.D., Executive Director, 
       Polycarbonate/BPA Global Group, American Chemistry Council
Summary of Testimony
    The American Chemistry Council represents the leading business of 
chemistry. Products supplied by the chemistry sector are essential in 
manufacturing, agriculture, energy, transportation, technology, 
communications, health, education, defense, and virtually every aspect 
of our lives. Basic industrial chemicals are the raw materials for 
thousands of other products including plastics, water treatment 
chemicals, detergents, pharmaceuticals and agricultural chemicals. 
These applications include medicines and medical technologies that save 
lives, computers that expand our horizons, foods we eat, water we 
drink, cars we drive, homes in which we live, and clothes we wear.
    We understand that recent media attention has created public 
concern and confusion about some of these chemicals--a family of 
compounds called phthalate esters, and another compound called 
bisphenol A. We are pleased to present this testimony to help address 
some of the confusion.
    Bisphenol A is a single compound used primarily to make 
polycarbonate plastic and epoxy resins. It is also used to make resins 
used as dental sealants and composites. Only trace levels of residual 
bisphenol A remain in these materials and in consumer products made 
from these materials.
    Phthalate esters describe a family of compounds used in many 
applications. The largest use is as an additive to plasticize, or 
soften, polyvinyl chloride. Before the addition of a plasticizer, 
polyvinyl chloride (vinyl) is actually a hard plastic.
    These materials have been in use for decades. They have been 
subjected to extensive study worldwide, including by independent 
researchers as well as government agencies, and scientific review is 
ongoing. U.S. regulatory agencies charged with regulating these 
compounds in various applications, after reviewing the large body of 
scientific data, have reached conclusions supporting their safe use in 
important applications. The scientific evidence supports the continued 
use of these important materials.
Bisphenol A
    Bisphenol A is a chemical building block used primarily to make 
polycarbonate plastic and epoxy resins. The safety of products made 
from these materials is supported by a 50 year safety track record of 
use and an equally long history of testing.
    Polycarbonate is a lightweight, highly shatter-resistant plastic 
with optical clarity comparable to glass. Epoxy resins have an 
exceptional combination of toughness, chemical resistance and adhesion. 
The unique attributes of these materials make them ideal for use in a 
wide array of products, many of which improve the health and safety of 
consumers.
    The manufacturing processes to make polycarbonate plastic and epoxy 
resins convert virtually all bisphenol A into the plastic or resin, 
leaving behind only trace levels of residual bisphenol A, typically 
less than 50 parts per million (0.005 percent by weight), in the 
finished materials. Consumers frequently benefit from products made 
from these materials, but come into contact with very little bisphenol 
A from use of these products.

------------------------------------------------------------------------

------------------------------------------------------------------------
    Typical Products Made From Polycarbonate Plastic and Epoxy Resins
------------------------------------------------------------------------
Health Care                          Electronic
   Eyeglass lenses              Digital media (CDs and
   Incubators                 DVDs)
   Critical components of       Electronic product
 medical devices                      housings (e.g., cell
    (e.g., kidney dialyzers, blood       phones, computers)
 oxygenators,                           Printed circuit boards
    drug infusion units)              laminates
------------------------------------------------------------------------
Security                             Sports Safety
   Blast and bullet             Bicycle and football
 resistant shielding                  helmets
   Police shields               Sunglasses and visors
   Protective visors            Skiing and diving
                                      goggles
------------------------------------------------------------------------
Automotive, Marine, and Aerospace    Building and Construction
   Headlamp lenses, mirror      Roof, skylight and
 housings and                         greenhouse glazing
    bumpers                             Corrosion resistant
   Instrument panels          coatings for steel
   Primer coatings               pipes/fittings, structural
   Fiber reinforced           steel (e.g.,
 composites                              bridges), concrete
                                      reinforcement bar
                                        Decorative and
                                      industrial flooring
------------------------------------------------------------------------
Home Appliances                      Food Containers
   Components of kitchen        Baby and water bottles
 appliances (e.g.,                      Home food storage
    food processors, refrigerators)   containers and
   Electrical appliance          tableware
 housings                               Food/beverage can
                                      coatings
------------------------------------------------------------------------

    In recent years, independent government and scientific bodies 
worldwide have examined the scientific evidence supporting the safety 
of bisphenol A. In every case, these assessments support the conclusion 
that bisphenol A is not a risk to human health at the extremely low 
levels to which people might be exposed.
    Each of these assessments comprehensively examined the potential 
reproductive and developmental toxicity of bisphenol A. Based on the 
weight of evidence, these assessments uniformly demonstrate that 
bisphenol A is not a selective reproductive or developmental toxicant. 
The most recent evaluations of bisphenol A are briefly summarized below 
along with their key conclusions regarding reproductive and 
developmental toxicity.
Bisphenol A is Deemed Safe for Use by the U.S. Food and Drug 
        Administration
    FDA regulates the use of bisphenol A in food contact materials, 
such as polycarbonate used in baby bottles and water bottles, and in 
epoxy resins used to coat cans containing food products. The U.S. Food 
and Drug Administration (FDA) said in July 2007 that ``FDA is unaware 
of any specific study in which humans exposed to BPA through any food 
containers experienced miscarriages, birth defects or cancer. 
Furthermore, human exposure levels to BPA from its use in food contact 
materials is in fact many orders of magnitude lower than the levels of 
BPA that showed no adverse effects in animal studies.''
    More recently (April 2008), in response to public confusion from 
media reports about bisphenol A, FDA formed an FDA-wide task force to 
review current research and new information on bisphenol A for all FDA-
regulated products. FDA confirmed that it has been reviewing the 
emerging literature on bisphenol A on a continuous basis. FDA also 
confirmed that based on its ongoing review, it believes there is a 
large body of evidence that indicates that FDA-regulated products 
containing bisphenol A currently on the market are safe and that 
exposure levels to bisphenol A from food contact materials, including 
for infants and children, are below those that may cause health 
effects.
    FDA's position is consistent with two risk assessments for BPA 
conducted by the European Food Safety Authority (EFSA) Scientific Panel 
on Food Additives, Flavourings, Processing Aids and Materials in 
Contact with Food and the Japanese National Institute of Advanced 
Industrial Science and Technology. Each of these documents considered 
the question of a possible low-dose effect and concluded that no 
current health risk exists for bisphenol A at the current exposure 
level. FDA said in April 2008 that it is not recommending that anyone 
discontinue using products that contain bisphenol A while FDA continues 
its risk assessment process. See http://www.fda.gov/oc/opacom/
hottopics/bpa.html.
FDA's Conclusions are Consistent with Those of the European Food Safety 
        Authority
    The European Food Safety Authority (EFSA) was established by the 
European Parliament in 2002 to provide the European Commission, the 
European Parliament and the European Member States with a sound 
scientific basis for legislation and policies related to food safety. 
Included in the scope of EFSA's work are assessments of the safety of 
food packaging and other materials that contact food.
    In January 2007, EFSA released a comprehensive assessment of 
bisphenol A that was conducted by an expert panel consisting of 21 
independent scientific experts from across the European Union.\1\ The 
assessment, which builds upon and updates an earlier assessment,\2\ 
comprehensively evaluated studies on the toxicity, metabolism and 
pharmacokinetics, and dietary exposure of bisphenol A.
    In general, the findings and conclusions of the EFSA assessment are 
consistent with those of the more recent CERHR evaluation (see below). 
The assessment established a Tolerable Daily Intake (TDI) of 50 mg/kg 
bw/day and concluded that ``people's dietary exposure to BPA, including 
that of infants and children, is estimated to be well below the new 
TDI.''
    The TDI was based on the most sensitive no-effect-levels from 
multi-generation studies conducted in the rat and mouse (see below for 
more information on these studies). For both studies, the most 
sensitive no-effect-level was for systemic toxicity (e.g., liver 
effects) at 5 mg/kg bw/day. The no-effect-levels for reproductive and 
developmental effects in both studies were at a higher dose (50 mg/kg 
bw/day) that the dose at which systemic effects occurred. The EFSA 
panel further concluded that ``low-dose effects'' of bisphenol A in 
rodents have not been demonstrated in a robust and reproducible way.
Bisphenol A has been Extensively Reviewed by the NTP Center for the 
        Evaluation of Risks to Human Reproduction
    The Center for the Evaluation of Risks to Human Reproduction 
(CERHR) was established by the U.S. National Toxicology Program and the 
National Institute of Environmental Health Sciences in 1998 to serve as 
an environmental health resource to the public and to regulatory and 
health agencies. A primary function of CERHR is to assess the potential 
for adverse effects on reproduction and development caused by agents to 
which humans may be exposed. This is accomplished through rigorous 
evaluations of the scientific literature by independent panels of 
scientists.
    The CERHR evaluation comprehensively reviewed the large scientific 
database on bisphenol A, including:

   Chemistry, use and human exposure

   General toxicology and biological effects (including 
        metabolism and pharmacokinetics)

   Reproductive toxicity

   Developmental toxicity

    To reach its conclusions, the expert panel considered the quality, 
quantity, and strength of the scientific evidence that exposure to 
bisphenol A might cause adverse effects on human reproduction and/or 
development of the fetus or infant. The overall findings of the expert 
panel evaluation were announced at a public meeting in August 2007, and 
the final CERHR report was released in November 2007. Subsequently, NTP 
released a draft ``Brief'' based on the CERHR report on April 14, 
2008.\3\
    Based on the weight of scientific evidence, the expert panel found 
no serious or high level concerns for adverse effects of bisphenol A on 
human reproduction or development. The draft NTP Brief agreed with 
these conclusions: ``the NTP has negligible concern that the exposure 
of pregnant women to bisphenol A will result in fetal or neonatal 
mortality, birth defects or reduced birth weight and growth in their 
offspring,'' and ``the NTP concurs with the conclusion of the CERHR 
Expert Panel on Bisphenol A that there is negligible concern that 
exposure to bisphenol A causes reproductive effects in non-
occupationally exposed adults, and minimal concern for workers exposed 
to higher levels in occupational settings.'' For several specific 
potential health effects (regarding neural and behavioural effects, and 
effects on the prostate gland, acceleration in puberty in females, and 
the mammary gland), the NTP draft Brief expressed ``some concern,'' but 
again no serious or high level concerns. Additional research was 
suggested by the NTP draft Brief, since data is inadequate to reach a 
firm conclusion.
The European Union Risk Assessment Supports Bisphenol A's Continued 
        Safe Use
    Under the EU Existing Substances Directive, the EU conducted a 
comprehensive risk assessment of bisphenol A that was published in 
2003.\4\ An updated risk assessment is in the final stages and is 
expected to be published in early 2008.
    The EU risk assessment comprehensively evaluated studies on the 
toxicity, metabolism and pharmacokinetics, and exposure of bisphenol A. 
In general, the findings and conclusions of the EU risk assessment are 
consistent with those of the CERHR evaluation. The 2003 risk assessment 
established an overall no-effect-level of 50 mg/kg bw/day, which was 
based on the no-effect-level for reproductive and developmental effects 
in a multi-generation study conducted in the rat. The no-effect-level 
from the rat multi-generation study has subsequently been affirmed by 
the results of a multi-generation study in the mouse (see below for 
information on both multi-generation studies). The updated risk 
assessment, based on the most recent scientific information, retains 
the overall no-effect-level of 50 mg/kg bw/day, now based on both the 
rat and mouse studies.
    The 2003 EU risk assessment was reviewed by the Scientific 
Committee for Toxicity, Ecotoxicity, and the Environment (CSTEE), which 
is an independent scientific advisory committee to the European 
Commission.\5\ The CSTEE agreed with the overall no-effect-level and 
stated that ``a number of high quality studies on the reproductive and 
developmental effects of bisphenol A are already available and do not 
support low-dose effects.'' The CSTEE further stated that ``there is no 
convincing evidence that low doses of bisphenol A have effects on 
developmental parameters in offspring . . .''
The Japanese National Institute of Advanced Industrial Science and 
        Technology's Review Supports the Continued Safe Use of 
        Bisphenol A
    The Japanese National Institute of Advanced Industrial Science and 
Technology (AIST), which is affiliated with the Japanese Ministry of 
Economy, Trade and Industry is Japan's largest public research 
organization. A comprehensive human health and environmental risk 
assessment on bisphenol A, conducted by scientists at AIST's Research 
Center for Chemical Risk Management, was published in November 2005.\6\
    Based on a thorough review of the toxicological profile of 
bisphenol A combined with estimates of human exposure, AIST concluded 
that ``current exposure levels of BPA will not pose any unacceptable 
risk to human health.''
    Along with systemic toxicity, a key toxicological endpoint for the 
AIST assessment was reproductive toxicity. Similar to the EFSA 
assessment, the most sensitive no-effect-level was 5 mg/kg bw/day for 
systemic toxicity in a multi-generation study conducted in the rat. The 
no-effect-level for reproductive toxicity was 50 mg/kg bw/day, at which 
systemic effects also occurred. The AIST assessment further concluded 
that findings from studies claiming reproductive effects at much lower 
doses were not considered to be robust in comparison to the consistent 
findings from studies reporting no low-dose effects.
Health Canada's Recent Review is Supportive of Continued Use of 
        Bisphenol A
    In April 2008, Health Canada opened a comment period on a proposal 
to ban polycarbonate baby bottles. This event has been the subject of 
some confusion in the media, because the reviewing scientists concluded 
``that bisphenol A exposure to newborns and infants is below levels 
that may pose a risk.'' The Canadian government nevertheless proposed 
moving forward with a ban on polycarbonate baby bottles based on a 
policy decision that the ``gap between exposure and effect is not large 
enough.'' Canada also proposed to set limits on BPA in infant formula 
and to work with industry on alternatives for food packaging.
    Canada did not suggest that parents and caregivers stop using 
polycarbonate bottles while the proposal is being considered. Canada 
did not suggest that stores stop selling polycarbonate baby bottles 
while the proposal is being considered. Canada did recommend that 
parents and caregivers continuing to use polycarbonate baby bottles 
``do not put boiling water in them.''
Recent, High Quality Studies Animal Studies Have Been Completed on 
        Bisphenol A
    The effects of bisphenol A on fertility and reproductive 
performance have been investigated in three high quality studies in 
rats and mice using internationally validated guidelines (two-
generation and three-generation studies in the rat, two-generation 
study in mice) and in a continuous breeding study in mice. 
Developmental toxicity studies in rats and mice have also been 
conducted.

   No effect on fertility was seen in the rat two-generation 
        study at the four low-dose levels tested (0.2-200 mg/kg bw/
        day). In the rat three-generation study, a reduction in litter 
        size was seen only at the top dose of 500 mg/kg bw/day, which 
        also produced clear parental systemic toxicity (significant 
        body weight gain reduction in both sexes and renal tubule 
        degeneration in females). No effects on reproduction or 
        development were seen at the five lower doses tested (1 mg/kg 
        bw/day to 50 mg/kg bw/day) and no parental systemic effects 
        were seen at the four lowest doses (5 mg/kg bw/day and below).

   Consistent with the rat studies, bisphenol A produced 
        parental systemic toxicity in the mouse two-generation study at 
        the two highest doses tested (50 and 600 mg/kg bw/day), 
        resulting in a NOEL of 5 mg/kg bw/day. The NOEL for 
        reproductive and developmental effects was 50 mg/kg bw/day. No 
        treatment related effects were seen at the four lowest doses 
        tested (3 mg/kg bw/day to 5 mg/kg bw/day).

   In the continuous breeding study in mice, no effects on 
        fertility were seen at 300 mg/kg bw/day. Fertility effects were 
        only observed at doses of approximately 600 mg/kg bw/day and 
        above, at which parental systemic toxicity was present.

   No evidence that bisphenol A is a developmental toxicant was 
        observed in standard developmental studies in rats and mice. In 
        rats, a maternal LOAEL and fetal NOAEL of 160 and 640 mg/kg bw/
        day, respectively, were identified. In mice, maternal and fetal 
        NOAELs were 250 and 1,000 mg/kg bw/day, respectively.

    Individually and collectively, these studies, these studies 
consistently demonstrate that bisphenol A is not a selective 
reproductive or developmental toxicant.
    In addition, effects claimed to occur at low doses in small-scale 
unvalidated studies, have not been corroborated in the large-scale 
multi-generation studies conducted according to internationally 
validated guidelines. Additional detail on these studies is provided 
below.
Three-Generation Reproductive Toxicity Study in CD Sprague-Dawley Rats
    The study followed the U.S. EPA OPPTS test guideline 837.3800, with 
additional assessments beyond the guideline requirements, and was 
conducted under Good Laboratory Practice requirements.\7\ Strengths of 
the study include:

   Oral route of administration, which is most relevant for 
        human exposure.

   Wide dietary dose range (6 dose groups ranging from 0.015 to 
        7500 ppm bisphenol A in the diet, corresponding to intakes of 
        approximately 1 mg/kg bw/day to 500 mg/kg bw/day).

   Large group size (30 animals per dose level).

   Multiple endpoints examined, including a thorough histologic 
        evaluation.

    Parental systemic toxicity (a guideline requirement) was produced 
at the two highest doses, resulting in a NOAEL of 5 mg/kg bw/day. The 
NOAEL for reproductive and developmental effects was 50 mg/kg bw/day.
Two-Generation Reproductive Toxicity Study in CD-1 Swiss Mice
    The study followed the internationally accepted OECD 416 test 
guideline, with additional assessments beyond the guideline, and was 
conducted under Good Laboratory Practice requirements.\8\ The study was 
preceded by a full two-generation reproductive toxicity study on 17b-
estradiol, which was then also used as a positive control in the 
bisphenol A study. Strengths of the study include:

   Oral route of administration, which is most relevant for 
        human exposure.

   Wide dietary dose range (6 dose groups ranging from 0.018 to 
        3500 ppm bisphenol A in the diet, corresponding to intakes of 
        approximately 3 mg/kg bw/day to 600 mg/kg bw/day).

   Large group size (28 animals per dose level).

   Multiple endpoints examined, including a thorough histologic 
        evaluation.

    In addition, maternal and paternal toxicity (a guideline 
requirement) was produced at the two highest doses, additional F1 male 
offspring were retained for evaluation concurrent with F1 parental 
males, a positive control was used to demonstrate that the test system 
was responsive to a known estrogen, and two negative control groups 
were used to increase the baseline historical database in mice and to 
define the intrinsic variability in endpoints of interest.
    Consistent with the three-generation study in rats, systemic 
toxicity was identified at the two highest doses, resulting in a no 
observed effect level (NOEL) of 5 mg/kg bw/day. The NOEL for 
reproductive and development effects was 50 mg/kg bw/day. Also 
consistent with the three-generation rat study, no treatment-related 
effects were found at doses ranging from 3mg/kg bw/day to 5 mg/kg bw/
day and the study did not corroborate effects claimed to occur in this 
low dose range in small-scale studies.
Two-Generation Reproductive Toxicity Study in CD Sprague-Dawley Rats
    In a third comprehensive study, bisphenol A has been tested in a 
two-generation reproductive toxicity study in CD Sprague-Dawley 
rats.\9\ This study, which focused on low doses, followed the 
internationally accepted OECD 416 test guideline and was conducted 
under Good Laboratory Practice requirements. Strengths of the study 
include:

   Oral route of administration.

   Large group size (25 animals per dose level).

   Wide variety of hormonally sensitive endpoints examined, 
        including behavioral measurements.

    Consistent with the three-generation rat study and the two-
generation mouse study, no treatment-related effects were found in the 
low-dose range from 0.2 to 200 mg/kg bw/day and the study did not 
corroborate effects claimed to occur in this low dose range in small-
scale studies.
National Toxicology Program Continuous Breeding Study in Mice
    Bisphenol A was administered in the diet during a one-week pre-
mating period and a 14-week mating trial to groups of twenty male and 
female CD1 mice (F0 generation) at concentrations of 0, 0.25, 0.5 or 
1.0 percent; daily intakes of bisphenol A are estimated to have been 0, 
300, 600 and 1200 mg/kg bw/day in males, and 0, 325, 650 and 1300 mg/kg 
bw/day in females.\10\ In the continuous breeding phase, a 
statistically significant decrease in maternal body weight was observed 
after each litter (between 6 and 9 percent), at the top dose, on 
postnatal day 0 compared to controls. At study termination, a small but 
statistically significant decrease in body weight (4 percent) was 
observed in treated females compared to controls.
    A subsequent one generation study to further evaluate parental 
toxicity of bisphenol A to CD1 mice observed significant parental 
toxicity at doses of 650 or 1300 mg/kg bw/day.\11\ Key evidence of 
parental systemic toxicity was increased liver and kidney weights with 
hepatocellular hypertrophy and renal tubule degeneration/regeneration, 
reduced body weights and body weight gain. In the continuous breeding 
study, a statistically significant decrease compared to controls was 
observed in the number of litters produced per pair (4.5 and 4.7 
compared to 5.0 for controls), litter size (6.5 and 9.8 compared to 
12.2 for controls) and the number of live pups per litter (6.3 and 9.7 
compared to 12.1 for controls) in the high and mid-dose group. No 
effects on fertility were observed in the low-dose group. A 
statistically significant decrease in litter size (controls: 11.4, 
treated males: 9.1, treated females: 5.9) and number of live pups per 
litter (controls: 11.3, treated males: 8.4, treated females: 5.5) were 
observed in the cross-over mating. In the continuous breeding phase, a 
statistically significant decrease in live pup weight (6 percent) on 
postnatal day 0 was observed in females at the top dose after 
adjustment for litter size, including live and still births. In the 
continuous breeding phase a small but statistically significant 
decrease in body weight gain (4 percent) was only observed in treated 
females at study termination. No effect was observed on the sex ratio 
in the F1 generation. In the F1 litters used in the cross-over breeding 
experiment, post natal (day 0) pup weights were significantly increased 
in males (9-11 percent) and in females (8-10 percent) in the mid- and 
high-dose.
    This study, conducted at high doses, is superseded by the more 
recent two generation study in mice.
National Toxicology Program Developmental Toxicity Study in Mice
    Bisphenol A has been tested for developmental toxicity in a NTP 
study using CD-1 mice.\12\ Two tests were performed and as the same 
signs of maternal toxicity were observed in both tests the data were 
combined. Groups of 29-34 time-mated female mice were gavaged with 0, 
500, 750, 1000 or 1250 mg/kg bw/day in corn oil on days 6 to 15 of 
gestation. Animals were sacrificed on day 17 of gestation and the 
fetuses were subjected to routine external, visceral and skeletal 
examinations. Data were also provided on the additional dose level of 
250 mg/kg bw/day, which was used only in the first test. Some maternal 
deaths were observed at doses of 750 mg/kg bw/day and above and a 
decrease in maternal body weight gain of 4-10 percent and 32-43 
percent, for both the treatment and gestation period was observed at 
1,000 and 1,250 mg/kg bw/day, respectively. Other significant signs of 
maternal toxicity were observed at 500, 750, 1000 or 1250 mg/kg bw/day 
as well as a dose-related statistically significant increase in mean 
relative liver weight (9-26 percent) was observed in dams in all 
bisphenol A treatment groups as compared to controls. At 1250 mg/kg bw/
day a statistically significant increase was observed in percent 
resorptions per litter (40 percent as compared to 14 percent in 
controls). A dose-related decrease in mean fetal body weight per litter 
was observed in the bisphenol A treated groups that was statistically 
significant at 1,250 mg/kg bw/day when compared to the control value; 1 
percent, 1 percent, 9 percent and 14 percent at 500, 750, 1,000 and 
1,250 mg/kg bw/day, respectively. No statistically significant effect 
was observed on the number of implantation sites per dam, the number of 
live fetuses per litter and the sex ratio. Bisphenol A administration 
had no significant effect on the percent of fetuses malformed per 
litter or the percent of litters with malformations. Overall, a 
significant increase in resorptions and decrease in fetal body weight 
was observed only at 1,250 mg/kg bw/day in the presence of severe 
maternal toxicity.
National Toxicology Program Developmental Toxicity Study in Rats
    Bisphenol A was studied for developmental toxicity potential in a 
NTP study.\13\ In the main study, two trials were performed and the 
data from both tests were combined. In total, groups of 27-29 time-
mated CD rats were gavaged with 0, 160, 320, 640 or 1,280 mg/kg 
bisphenol A in corn oil on days 6 to 15 of gestation. Animals were 
sacrificed on day 20 of gestation and the fetuses were subjected to 
routine external, visceral and skeletal examination. At 1,280 mg/kg, 
deaths were observed in 7/27 females and because of this high mortality 
rate, the top dose group was not included in statistical analyses. 
Compared to controls, a statistically significant decrease in mean 
maternal body weight gain was observed in dams at all dose levels for 
the treatment period (35-54 percent) and the gestation period (11-14 
percent). No effect was observed on gravid uterine weights. When 
maternal body weight gain was corrected for gravid uterine weight a 
statistically significant decrease was still apparent at all dose 
levels (26-34 percent). Pregnancy rates were not affected by treatment 
with bisphenol A, nor was there any effect on the number of 
implantation sites per litter, percent resorptions per litter, number 
of live fetuses per litter, sex ratio, mean fetal body weight per 
litter, percent fetuses malformed per litter and percent litters with 
malformed fetuses. In conclusion, this study provides no evidence of 
developmental toxicity in the rat at exposure levels which are toxic to 
the mother. A maternal NOEL could not be identified; instead a LOAEL of 
160 mg/kg was identified for clinical signs of toxicity and a 
statistically significant decrease (26 percent) in body weight gain. No 
fetal effects were seen at the highest dose level evaluated, 640 mg/kg.
``Low-Dose'' Studies are Unvalidated
    Although bisphenol A has been shown to have some weak ``estrogen-
like'' activity in a number of in vitro and in vivo screening assays, 
molecular biology studies \14\ have demonstrated that bisphenol A does 
not act as a weak estrogen mimic but exhibits a distinct mechanism of 
action from estradiol at the estrogen receptor. Nevertheless, the 
potency of this activity in screening assays generally ranges from 3 to 
5 orders of magnitude less than that of estradiol.
    It should also be noted that many of the studies investigating 
endocrine modulating activity are essentially screening tests and many 
employ experimental protocols that have not been validated. This 
information in conjunction with the known extensive metabolism of 
bisphenol A to non-estrogenic metabolites (see below) provides a 
scientific basis for the lack of toxicological effects at low doses in 
the multi-generation studies described above. Effects claimed to occur 
at low doses in small-scale unvalidated studies have not been 
corroborated in the large-scale multi-generation studies conducted 
according to internationally validated guidelines.
    The small-scale unvalidated studies have been evaluated in the 
comprehensive assessments described above. Each of these assessments 
applied a ``weight-of-evidence'' approach to evaluate the body of 
information available for bisphenol A. Each assessment relied on the 
results of the two- and three-generation studies described above for 
its overall conclusion.
Metabolism and Pharmacokinetics Data Supports Results from Animal 
        Studies
    The potential for a substance to cause reproductive or 
developmental toxicity is substantially influenced by metabolism and 
pharmacokinetics. These parameters have been very well characterized 
for bisphenol A in numerous animal studies (i.e., rodents and primates) 
and in several human volunteer studies.
    Overall, these studies indicate that bisphenol A has a low 
potential to cause adverse health effects in humans and, in particular, 
effects mediated by an estrogenic mode of action. Key findings from 
these studies are summarized below:

   Humans Efficiently Metabolize and Eliminate Bisphenol A from 
        the Body--Human volunteer studies confirm that bisphenol A is 
        efficiently metabolized to a glucuronide conjugate after oral 
        exposure.15,16,17 Studies in animals and with isolated liver 
        cells have shown that this metabolic process occurs in the 
        intestinal wall \18\ and in the liver 19,20,21,22 
        both of which must be crossed before bisphenol A can enter into 
        circulation in the body after oral exposure.

    In the first human study, volunteers were treated with a single 5 
        mg oral dose of bisphenol A per person, which is approximately 
        1000 times greater than a typical daily intake of bisphenol A 
        (see Section 6 below). No parent bisphenol A was found in blood 
        at any time point and all bisphenol A was excreted in urine as 
        the glucuronide. The elimination half-life for the glucuronide 
        conjugate was approximately 4 hours, which means that any 
        bisphenol A to which people are exposed should virtually all be 
        eliminated from the body within approximately 24 hours.

   Bisphenol A Has Low Bioavailability and Does Not Accumulate 
        in the Body--The human volunteer studies confirm that bisphenol 
        A has very low bioavailability (i.e., very little parent 
        bisphenol A will reach target tissues) after oral exposure. The 
        rapid elimination of bisphenol A indicates that bisphenol A has 
        very low potential (if any) to bioaccumulate in the body.

    Low bioavailability, efficient metabolism of bisphenol to the 
        glucuronide, and low potential to bioaccumulate have also been 
        demonstrated in numerous studies on laboratory animals, some of 
        which are cited here.23,24,25,26,27,28,29 Included are studies 
        that demonstrate that metabolism of bisphenol A is not altered 
        during pregnancy \30\ and that neonatal animals also 
        efficiently metabolize bisphenol A from an early age in 
        neonatal life.\31\

   Bisphenol A Metabolites are Not Estrogenic--The primary 
        metabolite of bisphenol A, the glucuronide, has been shown to 
        exhibit no estrogenic activity.\32\ The bisphenol A sulfate 
        metabolite, which may be present at lower levels, has also been 
        shown to exhibit no estrogenic activity.\33\ These studies 
        indicate that bisphenol A is not likely to cause estrogenic 
        effects since the metabolites of bisphenol A that enter the 
        body have no known biological activity and, in particular, have 
        no estrogenic activity.
Bisphenol A Presents Very Low Potential for Human Exposure
    Numerous studies have been conducted to directly measure human 
exposure to bisphenol A by urinary biomonitoring and to indirectly 
estimate human exposure by analysis of potential sources of exposure. 
These data consistently indicate that human exposure to bisphenol A is 
essentially all through the diet and is extremely low. Typical human 
exposure to bisphenol A is less than 0.1 mg/kg bw/day. Key findings 
from these studies are summarized below:

   Biomonitoring Studies Confirm Extremely Low Human Exposure--
        Since the glucuronide metabolite of bisphenol A is rapidly and 
        completely eliminated into human urine, human exposure can 
        readily be estimated by urinary biomonitoring for bisphenol A 
        (after hydrolysis of conjugates). Numerous studies conducted 
        worldwide indicate that typical human exposure to bisphenol A 
        is less than 0.1 mg/kg bw/day.

    The largest study was conducted by the U.S. Centers for Disease 
        Control and Prevention as part of their NHANES 2003-2004 
        program.\34\ This study reported urinary bisphenol A data for 
        more than 2500 individuals ranging in age from 6-85. Due to the 
        study design, the data is representative of the U.S. 
        population. In this study, the median concentration of 
        bisphenol A in urine (after hydrolysis) was 2.8 ng/ml. Based on 
        this data, the typical daily intake of bisphenol A for the 
        population is estimated to be approximately 0.05 mg/kg bw/day.

    Many smaller-scale studies from Japan,35,36,37,38,39 
        Korea,40,41 Europe,\42\ and the 
        U.S.,43,44,45,46,47,48,49 have reported similar 
        results. Included are two studies in which urine samples were 
        collected over 24-hour periods.50,51

   Potential Exposure From Consumer Products is Very Low--
        Consumer products made from polycarbonate plastic or epoxy 
        resins contain only trace levels of bisphenol A, typically less 
        than 50 parts per million (0.005 percent by weight), which 
        limits potential exposure to bisphenol A from use of products. 
        Human exposure to bisphenol A is essentially all through the 
        diet \52\ and numerous studies have been conducted to examine 
        the potential for bisphenol A to migrate from polycarbonate 
        plastic or epoxy resins into a food or beverage. Of particular 
        interest are the many studies on polycarbonate baby bottles 
        53,54,55,56,57,58 and canned foods and 
        beverages.\59\

    Calculated human exposure estimates based on measured migration 
        data combined with consumption patterns 59(k),60 are 
        generally consistent with exposure estimates directly measured 
        by biomonitoring. Both confirm that human exposure to bisphenol 
        A from all sources, including from use of consumer products, is 
        extremely low.

   Exposure to Bisphenol A Is Within Government-Set Safe Limits 
        The European Food Safety Authority recently established a 
        Tolerable Daily Intake for bisphenol A of 50 mg/kg bw/day based 
        on an up-to-date scientific review.\2\ This value is identical 
        to the Reference Dose set by the U.S. Environmental Protection 
        Agency.\61\ The typical daily intake of bisphenol A is 
        approximately 1,000 times lower than these acceptable levels 
        and poses no known risks to human health.
Phthalate Esters
    The dozen or so phthalates in use today have thousands of 
applications. Their chief use is to make vinyl soft and flexible, 
without sacrificing its durability. They are used as softeners (or 
plasticizers) in toys, cars and products found in the home and in 
hospitals. For example, they are an important ingredient in life-saving 
and life-supporting vinyl medical devices. One member of the phthalate 
family is used in perfumes and other personal care products to make 
their fragrances last longer. Another type of phthalate is used in 
items such as tool handles and nail polish to help resist chipping.
    Recent discussion regarding phthalates has focused on its use in 
toys and child care items. An extensive body of research on phthalates, 
including several recently completed U.S. and EU risk assessments, 
demonstrates that the use of phthalates, and in particular diisononyl 
phthalate (DINP), as a plasticizer in toys and objects used by children 
poses little to no risk to children.
    With respect to toys and children's products, discussion typically 
focuses on the use of six phthalates: di(2-ethylhexyl) phthalate 
(DEHP), dibutyl phthalate (DBP), and butyl benzyl phthalate (BBP)--in 
the materials used in manufacturing toys or objects used by children, 
and another three--diisononyl phthalate (DINP), diisodecyl phthalate 
(DIDP) and di-n-octyl phthalate (DNOP)--in such products that children 
can put in their mouths.\62\ This discussion apparently occurs because, 
despite the conclusions of the European risk assessments on phthalates, 
the EU acted to limit the uses of these phthalates in toys before the 
risk assessments were final.
    In the late 1990s, a question arose as to whether use of phthalates 
in vinyl toys might present a health risk to children. The concern was 
based primarily on effects in rats that were treated with very high 
oral doses of phthalates, and on the knowledge that some phthalate 
could migrate out of vinyl toys if and when they were mouthed by 
children, and thus be ingested. At the time, information was sparse and 
uncertain regarding how much phthalate actually would migrate out of 
mouthed toys and the amount of time children actually mouthed toys. 
Initial calculations using very conservative assumptions for these 
parameters showed that exposure to phthalates would be lower than the 
levels at which effects are seen in animal studies, but that the margin 
of safety (MOS) might be less than considered desirable for DINP and 
DEHP.
    In 1999, the EU instituted an emergency temporary ban on DBP, BBP, 
DNOP, DEHP, DINP and DIDP in toys intended to be put in the mouths of 
children under three, and began considering more permanent legislative 
measures.\63\ At the same time, actions were initiated to bring more 
certainty to the science. The European Commission's Joint Research 
Center (JRC), the Netherlands' TNO Nutrition and Food Research 
Institute, the United States Consumer Product Safety Commission (CPSC), 
and the Canadian Ministry of Health (Health Canada) collaborated to 
develop a reliable method for measuring phthalate migration from 
mouthed vinyl toys. In the meantime, The EU was in the process of 
conducting in-depth and comprehensive risk assessments of DBP, BBP, 
DEHP, DINP and DIDP as part of its effort to evaluate and control risks 
from existing substances. In the U.S., the CPSC undertook an exhaustive 
assessment of the risks posed by DINP in children's toys, which 
included a state-of-the-art study of children's mouthing behaviors and 
migration testing using the method developed by the European/North 
American collaboration.
    By 2003, these efforts had revealed that the risk posed by the use 
of DINP in children's toys--even those that are mouthed--is 
insignificant. The CPSC found that PVC toys and other items intended 
for children under five posed ``no demonstrated health risk.'' \64\ The 
European Union's risk assessment for DINP concluded: ``The end products 
containing DINP (clothes, building materials, toys and baby equipment) 
and the sources of exposure (car and public transport interiors, food 
and food packaging) are unlikely to pose a risk for consumers (adults, 
infants and newborns) following inhalation, skin contact and 
ingestion.'' \65\
    Paradoxically, at the same time the science was providing 
reassurance about the use of phthalates in children's products, 
European politicians were urging more and more stringent restrictions 
on such use, resulting in the permanent ban in 2005 on the use DEHP, 
DBP and BBP in toys, and DINP, DIDP and DNOP in toys intended to be 
mouthed. Since 1999, the risk assessments conducted by the CPSC and the 
EU have provided high-quality scientific evidence that the use of most 
phthalate plasticizers, in particular DINP, in toys and children's 
articles poses little to no risk to children. Contrary to assertions 
made by some, there is little uncertainty about these conclusions. 
There are always remaining questions to be addressed by science; 
however, phthalates are among the best studied compounds in the world, 
and the risk assessments are based on recent, state-of-the-art studies.
    In the meantime, early concerns from the 1990s about DEHP with 
respect to carcinogenicity observed in rodents following high dosing 
were investigated and addressed following additional research. In 2000, 
based on its judgment that the rodent results were not relevant to 
humans, the arm of the World Health Organization called the 
International Agency for Research on Cancer (IARC)--the international 
authority on cancer--changed its classification for DEHP to ``not 
classifiable'' as a human carcinogen. Regulatory agencies in Europe and 
Canada have also reached the same conclusion.
    Accordingly, based on the science and the use patterns for 
phthalates, no restriction on the use of phthalates in toys and 
childcare articles is warranted at this time.
The United States Consumer Product Safety Commission Risk Assessment 
        for Vinyl Toys Containing Phthalates Found Minimal to No Risk 
        to Children Five Years of Age or Under
    In late 1998, The National Environmental Trust and other 
organizations petitioned the U.S. Consumer Product Safety Commission 
(CPSC) to ban the use of polyvinyl chloride (PVC or vinyl) in products 
intended for children 5 years of age or under. A reason asserted for 
the ban was alleged health effects from the phthalate used as a 
plasticizer in vinyl children's products--diisononyl phthalate (DINP). 
The CPSC therefore undertook an intensive investigation of the 
toxicology of DINP and of potential exposure of children to DINP from 
vinyl products.\66\
    For its review, CPSC convened a Chronic Hazard Advisory Panel 
(CHAP)--a seven-member panel of independent scientific experts who 
conducted a detailed review of the potential health hazards posed by 
DINP in products mouthed by children. The CHAP met three times over the 
course of a year and accepted voluminous comments from representatives 
of both industry and public interest groups. The 160-page CHAP report 
was published on June 15, 2001 and is available on the CPSC 
website.\67\
    The CHAP found that 120 mg/kg/day was an Acceptable Daily Intake 
(ADI) of DINP for humans--i.e., the amount of chemical a person can be 
exposed to on a daily basis over an extended period of time (up to a 
lifetime) with a negligible risk of suffering adverse effects. Based on 
this ADI, the CHAP concluded that a young child would have to routinely 
mouth DINP-plasticized toys for 75 minutes or more per day in order to 
pose a possible DINP exposure risk. However, finding no evidence that 
children mouth such toys for such extensive periods, the Report 
concluded that exposure to DINP for toys containing phthalates poses 
little or no risk of injury to children.
    To verify these conclusions, the CPSC then conducted a state-of-
the-art study of the amount of time children mouth objects, and it 
conducted additional studies of the rate of migration of DINP from 
vinyl when mouthed, using a methodology developed and validated by the 
TNO Nutrition and Food Research Institute, CPSC, Canada Health and the 
European Commission's JRC.\68\ On September 23, 2002, the CPSC released 
a briefing package, summarizing the CPSC staff investigation of the 
potential risks of DINP in children's vinyl products.\69\ The executive 
summary of that package states:

        Based upon the observation study, staff concludes it is very 
        unlikely that children will mouth soft plastic toys for more 
        than 75 minutes a day.\70\

                *          *          *          *          *          
                *          *

        The staff concurs with the CHAP conclusion that exposure to 
        DINP from DINP-containing toys would be expected to pose a 
        minimal to non-existent risk of injury for the majority of 
        children. The new data from the behavioral observation study 
        not only confirm this conclusion, but also demonstrate that 
        children are exposed to DINP at lower levels than the CHAP 
        assumed when it reached its conclusion. Also, since children 
        mouth other products even less than they mouth toys and dermal 
        exposure is expected to be negligible, there would be no 
        justification for taking action against other products intended 
        for children 5 years old and younger.

    CPSC estimated that the most highly exposed group of children 
(those aged 3-12 months) had mean exposures to DINP of 0.07 m/kg/day 
with a 95th percentile value of 0.44. This is well below the CHAP and 
CPSC conservative ADI of 120 mg/kg/day. CPSC also estimated worst case 
exposures hypothetically assuming that all toys, teethers and rattles 
were made with DINP-plasticized vinyl (in reality, only a portion of 
toys are made with soft plastic, only about a third of the soft plastic 
toys contain DINP, and no rattles or teethers contain DINP). Even under 
these conservative conditions, the estimated DINP exposures for 
children 3-12 months were 2.91 mg/kg/day (mean) and 10.71 mg/kg/day 
(95th percentile), still well below the ADI. Additional detail on the 
CPSC analysis is provided in Appendix 1.
    The overall CPSC staff risk assessment information and conclusions 
have been published in the peer reviewed literature.\71\ The authors 
conclude that ``oral exposure to DINP from mouthing soft plastic toys 
is not likely to present a health hazard to children.'' \72\
    On February 21, 2003, the CPSC Commissioners voted unanimously to 
deny the petition.\73\ As indicated in the denial letter to 
petitioners, the Commissioners denied the petition based on the finding 
of CPSC that ``there is no demonstrated health risk posed by PVC toys 
or other products intended for children 5 years of age and younger.'' 
\74\
    The CPSC evaluation considered the conditions most likely to result 
in exposures of DINP to children and used very conservative (i.e., 
health-protective) assumptions. CPSC considered children in those age 
groups that most often mouth items; it considered exposure from such 
mouthing, which would be expected to exceed that which could occur by 
dermal contact; and it conservatively evaluated situations in which 
DINP was assumed to be used to a much greater extent in children's 
products than it actually is. As explained in Appendix 1, the 
acceptable daily intake (ADI) used by CPSC also was quite 
conservative--a value 100 times below levels at which no effects have 
been observed in animal studies. Even with such conservatism, the 
potential exposures were still well below the ADI. Thus, the CPSC 
concluded no restrictions on the use of DINP in children's articles are 
warranted.
EU Risk Assessments Demonstrate That The Use of Phthalates in Vinyl 
        Toys and Childcare Articles Poses Little or No Risk to Children
    Like the CPSC assessment, the EU's risk assessments of phthalates 
support the safety of the use of phthalate esters in toys and 
children's products. As part of its existing chemicals program, the EU 
has published risk assessments for three of the six phthalates 
typically noted as of concern for children's products, DBP,\75\ DIDP 
\76\ and DINP,\77\ and has completed draft assessments of BBP \78\ and 
DEHP.\79\ The remaining of the six phthalates, DNOP, has apparently not 
been the subject of an EU risk assessment because the production of 
this particular plasticizer ceased more than 10 years ago. The EU risk 
assessments, which incorporate the most modern and up-to-date data and 
methodology available to the EU, specifically include a consideration 
of risks to children from all potential sources, including toys and 
childcare articles.
The EU Risk Assessment for DINP Concurs With the CSPC Assessment, 
        Finding No Likely Risk to Children
    The most relevant EU risk assessment--that for DINP--was published 
in 2003. Unlike the CPSC risk assessment, which was intended only to 
determine the risk to children from mouthing objects, the EU assessment 
included an investigation of the risk to newborns, infants, children 
and adults from all routes of exposure. The EU assessment explicitly 
considered exposures of newborns, infants and children from multiple 
sources, including food and food-related uses, toys and baby equipment, 
car and public transport interiors, and building material and 
furniture. The EU risk assessment found no likely risk to humans under 
any exposure scenario. As stated in the risk assessment summary 
document with respect to consumer exposures:

        The end products containing DINP (clothes, building materials, 
        toys and baby equipment) and the sources of exposure (car and 
        public transport interiors, food and food packaging) are 
        unlikely to pose a risk for consumers (adults, infants and 
        newborns) following inhalation, skin contact and ingestion.\80\

The EU risk assessment also found no likely risk to adults, children or 
infants from environmental exposures, or from combined consumer and 
environmental exposures. The EU's finding of no risk to children under 
three was based on several calculated MOSs (Margins of Safety), all of 
which are above the CSTEE's recommended MOS of at least 100. The EU 
risk assessment reported the following MOSs with respect to children:

   176 (kidney effects) and 552 (fertility effects) for infants 
        and newborns exposed to DINP from multiple consumer pathways, 
        including toys;

   107 (kidney and liver effects) and 336 (testicular effects) 
        for infants for combined environmental and consumer exposures, 
        including toys.

    Thus, the most advanced and up-to-date EU risk assessment for DINP 
concurs with that of the CPSC: DINP exposure from the mouthing of soft 
plastic toys poses no likely risk to children. Further, the EU risk 
assessment for DINP demonstrates that exposure to DINP from other 
potential sources also poses no likely health risk. Under such 
circumstances, prohibiting the use of DINP in toys and childcare 
articles, whether or not they can be mouthed, is wholly scientifically 
unfounded.
U.S. National Toxicology Program Risk Assessments Support the Use of 
        Phthalate Esters
    The National Toxicology Program's Center for the Evaluation of 
Risks to Human Reproduction (NTP) has completed extensive risk 
assessments on the six phthalates that are the subject of various 
legislative inquiries with respect to toys and children's articles. The 
NTP assessed risks to human reproduction and development by creating a 
16-member independent panel of scientific experts that reviewed the 
toxicity and exposure information related to each phthalate. After 
three public meetings at which the key studies and issues were 
discussed, the expert panel issued a report to NTP for each phthalate. 
Based on the expert panel reports, NTP then published a Brief for each 
phthalate, in which it reported its level of concern that the various 
phthalates cause developmental or reproductive effects in humans. The 
NTP Brief, expert panel report and responses to public comments were 
combined in a Monograph published for each phthalate.\81\ The NTP's 
conclusions for each phthalate were:

   For DINP, the NTP found ``minimal concern'' for 
        developmental or reproductive effects in children;

   For DIDP, the NTP found ``minimal concern'' for 
        developmental effects in fetuses and children;

   For BBP, the NTP found ``minimal concern'' for developmental 
        effects in fetuses and children;

   For DBP, the NTP did not express a concern level for fetuses 
        and children, primarily because of the low possibility of 
        exposure from toys, but found ``minimal concern'' for 
        developmental effects when pregnant women are exposed to 
        average levels of DBP;

   For DNOP, the NTP did not express a concern level for 
        fetuses and children, also based on the low possibility of 
        exposure, but expressed ``negligible concern'' for effects on 
        adult reproductive systems;

   For DEHP, the NTP expressed ``serious concern'' only for 
        critically ill male prematurely born infants with very high 
        medical exposures, ``concern'' for infants of mothers with 
        intensive medical treatments, and ``some concern'' for children 
        older than 1 year, based on very high assumed exposures from 
        all sources.

    In sum, the NTP risk assessments typically expressed minimal 
concern for adverse developmental effects in fetuses and children, in 
particular for DINP, the phthalate most commonly used in toys. The only 
concern above ``minimal'' expressed by NTP was for very high exposures 
to DEHP, which is not used in the manufacture of children's articles 
intended to be mouthed and therefore unlikely to approach these 
exposure levels.
    An extensive body of research on phthalates, including several 
recently completed U.S. and EU risk assessments, demonstrates that the 
use of phthalates as a plasticizer in toys and objects used by children 
poses little to no risk to children.
Additivity is Not a Concern
    Some have expressed concern that exposures to phthalates could be 
added up and that this total could present a health hazard. Currently, 
reports of human hazard associated with aggregate or cumulative 
exposures to phthalates are limited, and no reproducible evidence of 
human hazard has been reported. However, based on recent U.S. Centers 
for Disease Control (CDC) biomonitoring data, humans are exposed to 
extremely low levels of several phthalates simultaneously (the 
detection of multiple phthalate metabolites in the urine confirms 
exposure, but does not inform considerations of hazard or risk). 
Exposure data published by the CDC indicate that levels of phthalates 
to which humans are exposed are much lower than doses with which 
additivity has been demonstrated in rodents.
    It is also seen from the CDC data that maximum exposure in the most 
sensitive human subpopulations are still orders of magnitude less than 
doses with which additivity has been demonstrated in rodents.\82\ Since 
the current reference dose for DBP (EPA IRIS) is 0.3 mg/kg/day, the 
estimated theoretical toxicity threshold for combined exposure to the 
most potent phthalate rodent toxicants DEHP, DBP, DIBP, and BBP would 
also be orders of magnitude higher than the RfD for DBP based on the 
simple dose addition model. It should be noted that synergistic 
effects--where the presence of one chemical enhances the effects of the 
second--do not appear to be seen in tests.
Recent Human Studies Contain Serious Flaws and Do Not Suggest a Need 
        for Action
    Several recent statistical studies have been cited as supporting 
the view that phthalates may pose risks of reproductive health risks to 
humans from phthalates. These studies, however, while suggesting areas 
where additional scientific inquiry is desirable, are by no means 
dispositive, and in some cases contradict earlier findings in rodent 
studies.
Main Study
    Danish researcher Katharina Main and co-authors of the study, 
``Human Breast Milk Contamination with Phthalates and Alterations of 
Endogenous Reproductive Hormones in Infants Three Months of Age,'' have 
suggested that exposure to phthalates affect reproductive hormones in 
baby boys.\83\ Main's study involved taking breast milk samples during 
the first three post-natal months from the mothers of 130 boys and 
analyzing the samples for various phthalate esters metabolites. Sixty-
two of the boys exhibited cryptorchidism, and 68 did not. The study, 
however, does not support Main's claims because it found no association 
between phthalate monoester levels and cryptorchidism. In addition, 
there was no significant correlation between MEHP and serum samples of 
gonadotropins, sex-hormone binding globulin (SHBG), testosterone and 
inhibin B.
Hauser Study
    A second frequently cited study, conducted by Hauser et al., 
(2006), did not demonstrate an association between semen quality and 
levels of DEP metabolites in the urine.\84\ The subjects were 463 males 
from subfertile couples and a group of control men. In general, the 
above statistical study provides results that are anecdotal in nature. 
They show a statistical association between a common chemical, or class 
of chemicals often used in personal care products, and a selected 
reproductive parameter. However, there is no causal relationship 
established, and there is no evaluation of other common, non-phthalate 
environmental chemicals. The latter evaluation would be necessary to 
establish that the increases in phthalate levels were not simply a 
biomarker of exposure to environmental chemicals in general, as opposed 
to a specific toxicant.
Swan Study
    A third study which has been reported to associate phthalates with 
reproductive health risks was conducted by Shanna Swan et al.\85\ This 
study was intended to test the hypothesis that in utero exposure to 
phthalic acid diesters blocks the action of testosterone in the male 
human fetus as reflected by changes in the anogenital distance (AGD), 
adjusted for body weight. Testosterone inhibition alters this parameter 
in reproductive tract studies of laboratory animals. This study 
examines statistical associations between physical genital measurements 
in 85 boys, up to 28 months of age, and a corresponding set of 
measurements of phthalate monoester metabolites in single spot urine 
samples collected from their mothers during the pregnancy. The 
hypothesis of Swan et al. i.e., that exposures in the environment to 
several phthalates pose a hazard to male reproductive development, is 
not supported, however, due to five major flaws in the study:

        1. The urine samples collected from the pregnant women are 
        neither reliable nor valid for measuring their exposure to 
        phthalates. The samples taken were not adjusted for variable 
        fluid intake, were not adjusted for the time of day the samples 
        were taken, and otherwise did not follow standard procedures, 
        making the samples useless for obtaining accurate measurements 
        of phthalate exposures.

        2. The anogenital distance (AGD) measurement is of no known 
        significance in humans. It is not a standard measurement in the 
        practice of medicine and has never been related to any 
        reproductive system problems. It is also difficult to measure 
        accurately. Twenty percent of the boys measured were dropped 
        from the analysis because the researchers judged that reliable 
        measurements could not be obtained for those boys. It is quite 
        possible that many of the measurements on the remaining 80 
        percent also were not accurate.

        3. Converting the AGD to an anogenital index (AGI) was an 
        attempt to correct for varying weight and age, but ignores the 
        fact that while the AGD does change with those two variables, 
        the changes are not linear, and the correction is therefore 
        incorrect. Also, the researchers did not compensate for other 
        variables, like height or premature birth, in the infant's 
        history.

        4. In addition to the normal variations in weight and age, some 
        measured infants were pre-term or even premature (which could 
        well affect variables such as AGD, and genital effects), but 
        were not excluded from the study.

        5. It appears the researchers used the wrong statistical model 
        to get their results. The statistical association claimed by 
        the researchers is based on a model that predicts a relatively 
        rapid decrease in AGI at low phthalate levels and much smaller 
        decreases at higher levels. But this relationship is not 
        biologically plausible; it should be the other way around. 
        Thus, there is some question regarding the results of a study 
        based on a possibly incorrect model.

    The Swan study has been widely criticized as having significant 
flaws, and it is also noted as having been misreported by the press:

        [We] examined this study carefully and found some 
        methodological problems, as well as a clear misinterpretation 
        of the results by the press. The baby boys were not 
        ``demasculinized'' in any way: the boys had a smaller 
        anogenital index, which is a measure of the distance from the 
        anus to the scrotum, adjusted for weight. In rats, under high 
        doses of phthalates, this anatomical change also occurs, as 
        does damage to the reproductive systems of the rats. In humans, 
        no damage to the reproductive system was measured at all. And 
        the shortened anogenital distance was well within normal ranges 
        for baby boys. (See http://www.stats.org/stories/
        WSJ_gives_skewed_phtha_oct05_05.htm)
Colon Study
    A Puerto Rican study measured blood levels of a variety of 
substances--including phthalates--in young Puerto Rican girls with a 
condition called thelarche, or premature breast development.\86\ 
Reporting of the study results appeared to have caused confusion. In 
fact, the authors of the study stated that phthalate esters ``cannot be 
interpreted as the cause of premature thelarche in Puerto Rican 
girls.'' Several key points in support of this conclusion follow:

        1. Phthalates have been tested for their ability to act as 
        estrogens. The weight of the scientific evidence demonstrates 
        that these substances are not estrogenic.\2\ Without a strong 
        indication that phthalates could induce an estrogenic response 
        in laboratory animals, it is unscientific speculation to 
        suggest that estrogen-induced effects, such as thelarche, could 
        be produced by phthalates.

        2. The authors observe the possibility for multiple causes of 
        thelarche: ``It may well be that the etiology of the various 
        manifestations of premature sexual development (including 
        thelarche) on this island is multifactorial.''

        3. Thelarche has been studied for years. Researchers have 
        identified numerous possible causes and the authors themselves 
        note: ``The following have already been associated with 
        premature sexual development in Puerto Rico: the presence of 
        anabolic steroids in poultry and consumption of soy-based 
        formula with a high phytoestrogen content by Puerto Rican 
        infants.''

        4. There is a considerable body of scientific research that 
        indicates phthalates do not affect the female endocrine system. 
        In a recent review of the data on phthalates, the National 
        Toxicology Program Center for Evaluation of Risks to Human 
        Reproduction (CERHR) Expert Panel expressed no concern related 
        to developmental effects in girls from phthalate exposures.

    The apparent high incidence of thelarche in this population seems 
unusual and warrants continued investigation. The Colon study does not 
show phthalates to be a causative factor and, for the reasons stated 
above, believes it is highly unlikely that phthalates are a factor for 
thelarche.
    In general, the above statistical studies provide results that are 
anecdotal in nature. They show a statistical association between a 
common chemical, or class of chemicals used in personal care products, 
and a selected reproductive parameter. However, there is no causal 
relationship established, and there is no evaluation of other common, 
non-phthalate environmental chemicals. The latter evaluation would be 
necessary to establish that the increases in phthalate levels were not 
simply a biomarker of exposure to environmental chemicals in general, 
as opposed to a specific toxicant. Significantly, EPA has found that 
Swan and other epidemiological studies purporting to show a correlation 
between phthalate exposure and reproductive effects are unsuitable for 
use in the risk assessment process because they cannot demonstrate 
causation.\87\
Conclusion
    From a toxicological perspective, BPA and phthalates are among the 
most well defined chemicals on Earth. They have been the subject of 
hundreds of studies in lab animals and numerous government-sponsored 
assessments. Accordingly, based on the science and the use patterns for 
these compounds, no restriction on their uses in current applications 
is warranted at this time.
                               Appendix 1
Extended Summary of the United States Consumer Product Safety 
        Commission Risk Assessment of the Phthlate Ester, DINP
    In 1998, the United States Consumer Product Safety Commission 
(CPSC), in response to a petition from several organizations to ban the 
use of PVC in products intended for children 5 years of age or under, 
undertook a rigorous investigation of the toxicology of DINP and of 
potential exposure of children to DINP from vinyl products. As part of 
its investigation, CPSC convened a Chronic Hazard Advisory Panel 
(CHAP)--a seven-member panel of independent experts who conducted a 
detailed review of the potential health hazards posed by DINP in 
products mouthed by children. The CHAP report, which was published on 
June 15, 2001,\88\ came to the following conclusions regarding overall 
risk from exposure to DINP:

   ``The CHAP concludes that humans do not currently receive 
        DINP doses from DINP-containing consumer products that are 
        plausibly associated with a significant increase in cancer 
        risk.''

   ``[T]he risk to reproductive and developmental processes in 
        humans due to DINP exposure is extremely low or non-existent.''

   ``There may be a DINP risk to young children who routinely 
        mouth DINP-plasticized toys for 75 minutes per day or more. For 
        most children, exposure to DINP from DINP-containing toys would 
        be expected to pose a minimal to non-existent risk of injury.''

    The CHAP based its conclusions regarding children's risk on a 
plausible upper-bound estimate of DINP exposure of 0.28 mg/kg/day for 
0-18 month old children, assuming those children mouth soft plastic 
toys for 3 hours every day.\89\ However, in reaching its conclusion, 
the CHAP emphasized the uncertainty associated with available DINP 
migration rate data, and questioned the robustness of existing mouthing 
behavior studies relied upon to calculate the upper-bound estimate, 
stating that ``important covariates such as developmental age, physical 
condition, ethnicity, and other sociodemographic indicators are not 
reported.'' \90\ Because of these uncertainties, the CHAP described its 
estimated child DINP exposures as ``preliminary at best.'' \91\
    To more accurately estimate potential child exposures to DINP, the 
CPSC conducted an extensive, state-of-the-art study to quantify the 
cumulative time per day that young children spend mouthing all objects, 
including toys, and conducted additional migration rate studies. The 
child mouthing study, described in Greene (2002) \92\ and Kiss 
(2001),\93\ was conducted in two phases, in which more than 550 
children ranging in age from 0 through 36 months were observed and 
their mouthing behaviors recorded. In Phase 1, the mouthing behaviors 
of 491 children ages 0 through 81 months were observed and recorded to 
the nearest minute by their parents or legal guardians for four 15-
minute periods over 2 days. In Phase 2, a trained observer observed and 
recorded the mouthing behaviors of 169 children (109 of whom had 
participated in Phase I) ages 3 through 26 months for a total of 4 
hours on at least two different days. The observer conducted the 
observations at different times of the day, and if the child attended a 
child care facility outside the home, attempts were made to observe the 
child there as well. Children were selected to ensure that the subjects 
were reasonably representative of the overall population with regard to 
race, income, type of child care and gender.
    The CPSC's mouthing study revealed that for all objects other than 
pacifiers, which do not contain DINP, estimated average daily mouthing 
times were:

   70 minutes for children between 3 months and 1 year of age;

   48 minutes for children between 1 year and 2 years; and

   37 minutes for children between 2 and 3 years of age.

    For all soft plastic items other than pacifiers, which comprise the 
items that could contain DINP, estimated average daily mouthing times 
were only;

   1.3 minutes for the 3-12 month olds;

   1.9 minutes for the 1-2 year olds; and

   0.8 minutes for the 2-3 year olds.

    Significantly, these data show that for even the youngest children, 
who typically mouth the most, the average mouthing time for all objects 
other than pacifiers is below the 75 minutes per day potential risk 
threshold identified by the CHAP. More importantly, the average amount 
of time children spend mouthing soft plastic toys, the objects that 
could contain DINP, is less than 2 minutes per day--far below CHAP's 75 
minutes per day threshold, and far below prior mouthing estimates. In 
addition, these mouthing times are significantly lower than the times 
estimated by the Dutch Consensus Group study relied upon by the EU, 
which found average mouthing times for ``plastic toys'' of 17 minutes 
for 0-18 month olds.\94\ As stated by the CPSC in its Executive Summary 
``[t]hese new mouthing data are much lower than earlier estimates and 
show an even smaller risk of exposure to DINP for children mouthing and 
chewing soft plastic toys.''
    In addition to the mouthing study, the CPSC also performed a 
migration rate study \95\ using a modified head over heals (HoH) method 
developed and validated by the TNO Nutrition and Food Research 
Institute, CPSC, Canada Health and the European Commission's JRC.\96\ 
CSPC tested 41 children's products that, according to their labeling, 
could be mouthed, sucked or chewed. Using the HoH method, the release 
of DINP was found to range from 1.05 to 11.09 mg/min/10cm\2\.
    Assuming that a child mouths a typical variety of objects and toys, 
the CPSC estimated that the most highly exposed group of children 
(those aged 3-12 months) had mean exposures to DINP of 0.07 mg/kg/day 
with a 95th percentile value of 0.44 mg/kg/day. These mean and 95th 
percentile exposure levels are, respectively, more than 1,700 and 270-
fold below CHAP and CPSC's Acceptable Daily Intake (ADI) of 120 mg/kg/
day.
    The ADI is an estimate of the amount of chemical a person can be 
exposed to on a daily basis for an extended period of time (up to a 
lifetime) with a negligible risk of suffering deleterious effects. The 
ADI for DINP was calculated using a Benchmark Dose (BD05) of 
12 mg/kg/day and dividing by a 100-fold safety factor. The 
BD05 is generally considered more robust than a NOAEL, whose 
value is tied to an arbitrarily chosen dose level, because it takes 
into account all available dose response data. For DINP, the CPSC 
calculated the BD05 by fitting a mathematical model to 
pooled dose response data from two chronic exposure studies (Lington et 
al., 1997; \97\ Moore 1998 \98\). In this case, the BD05 of 
12 mg/kg/day is not only more robust than a NOAEL from a single study, 
but is more conservative, as its value is lower than either of the two 
studies' reported NOAELs. Thus, the CSPC data indicate that a typical 
child's exposure to DINP from soft plastic toys is well below the ADI, 
a conservative estimate of safe exposure levels of DINP.
    In addition to estimating exposure to a typical child, the CPSC 
also conducted a worst-case exposure estimate, hypothetically assuming 
that all toys, teethers and rattles that the children mouthed were made 
with DINP-plasticized vinyl, when in reality, only a portion of toys 
are made with soft plastic, only about a third of soft plastic toys 
contain DINP, and no rattles or teethers contain DINP. Even applying 
these very conservative assumptions, the estimated DINP exposures for 
children 3-12 months were only 2.91 mg/kg/day (mean) and 10.71 mg/kg/
day (95th percentile), still well below the CPSC's conservative ADI of 
120 mg/kg/day.
    On September 23, 2002, the CPSC released a briefing package that 
summarized the CPSC staff investigation of the potential risks of DINP 
in children's vinyl products.\99\ The executive summary of that package 
states:

        Based upon the observation study, staff concludes it is very 
        unlikely that children will mouth soft plastic toys for more 
        than 75 minutes a day.\100\

                *          *          *          *          *          
                *          *

        The staff concurs with the CHAP conclusion that exposure to 
        DINP from DINP-containing toys would be expected to pose a 
        minimal to non-existent risk of injury for the majority of 
        children. The new data from the behavioral observation study 
        not only confirm this conclusion, but also demonstrate that 
        children are exposed to DINP at lower levels than the CHAP 
        assumed when it reached its conclusion. Also, since children 
        mouth other products even less than they mouth toys and dermal 
        exposure is expected to be negligible, there would be no 
        justification for taking action against other products intended 
        for children 5 years old and younger.

    The overall CPSC staff risk assessment information and conclusions 
have been published in the peer reviewed literature.\101\ In this 
publication, the authors state that they ``conclude that oral exposure 
to DINP from mouthing soft plastic toys is not likely to present a 
health hazard to children.'' \102\
    On February 21, 2003, the CPSC Commissioners voted unanimously to 
deny the petition to ban the use of PVC in products intended for 
children 5 years of age or under.\103\ As indicated in the denial 
letter to petitioners, the Commissioners denied the petition based on 
the finding of CPSC that ``there is no demonstrated health risk posed 
by PVC toys or other products intended for children 5 years of age and 
younger.'' \104\
Endnotes
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at http://www.efsa.europa.eu/en/science/afc/afc_opinions/
bisphenol_a.html.
    \2\ European Commission. April 17, 2002. Opinion of the Scientific 
Committee on Food on Bisphenol A. Available at http://ec.europa.eu/
food/fs/sc/scf/out128_en.pdf.
    \3\ Information on the CERHR evaluation, including the April 14 NTP 
draft brief, is available at http://cerhr.niehs.nih.gov/chemicals/
bisphenol/bisphenol.html. The final report will also be posted on this 
site.
    \4\ European Union Risk Assessment Report--4,4'-
isopropylidenediphenol (Bisphenol-A). 2003. Available at http://
ecb.jrc.it/DOCUMENTS/Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/
bisphenolasum325.pdf (summary) and http://ecb.jrc.it/DOCUMENTS/
Existing-Chemicals/RISK_ASSESSMENT/REPORT/bisphenolareport325.pdf (full 
report).
    \5\ European Commission. May 22, 2002. Scientific Committee on 
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    \6\ An abstract and detailed summary of the bisphenol A risk 
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10.html.
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    \62\ Phthalates are a group of chemicals with a variety of uses, 
and not all phthalates are used in the same applications. Of the six 
phthalates typically discussed, DNOP, DEHP, DIDP and DINP are used 
principally to plasticize--i.e., soften and make less brittle--vinyl 
(or PVC). However, DNOP, DEHP and DIDP are used much less often in 
vinyl toys than DINP. Similarly, BBP also is used in vinyl products, 
but almost exclusively in vinyl flooring. Dibutyl phthalate (DBP) 
currently is not used in vinyl; it is used primarily in latex adhesives 
and cellulose plastics and as a solvent for dyes. DINP is by far the 
phthalate most commonly used in vinyl toys and children's products. 
Child safety is a primary reason for manufacturing flexible vinyl toys, 
as they are soft and durable, so will not break and form small pieces 
that are a choking hazard or have sharp edges.
    \63\ See ENDS Environment Daily, EU phthalate ban decision 
postponed, November 22, 1999, available at: www.environmentdaily.com/
articles/index.cfm?action=article&ref=6501. At that time, members of 
CSTEE questioned whether the science supported a finding of an 
immediate risk and expressed their disagreement with the imposition of 
the emergency ban.
    \64\ CPSC, Petition Denial at 3 (quoting Memorandum from Marilyn L. 
Wind to the Commission, Response to Petition HP 99-1 (August 13, 2002), 
at 16-17).
    \65\ European Chemicals Bureau (2003). 1,2-Benzenedicarboxylic 
acid, di-C8-10-branched alkyl esters, C9-rich and di-``isononyl'' 
phthalate (DINP), CAS Nos: 68515-48-0 and 28553-12-0, EINECS Nos: 271-
090-9 and 249-079-5, Summary Risk Assessment Report, Special 
Publication I.03.101, p. 18, available at http://ecb.jrc.it/.
    \66\ A more extensive summary of the CPSC report is attached to 
these comments.
    \67\ CHAP (2001). Report to the U.S. Consumer Product Safety 
Commission by the Chronic Hazard Advisory Panel on Diisononyl Phthalate 
(DINP), June 2001, available at http://www.cpsc.gov/LIBRARY/FOIA/
Foia01/os/dinp.pdf.
    \68\ See Simoneau, C. (2000) Standard Operation Procedure, 
``Determination of release of diisonylphthalate (DINP) in saliva 
stimulant from toys and childcare articles'', JRC, European Commission, 
November 11, 2000.
    \69\ CPSC (2002). Response to Petition Requesting Ban of Use of PVC 
in Products (HP 99-1). U.S. Consumer Products Safety Commission, 
Bethesda, MD, (``CPSC Risk Assessment'') available at http://
www.cpsc.gov/library/foia/foia02/brief/briefing.html (This URL takes 
you to Commission briefing packages for Fiscal Year 2002. The first 
seven links on that page are the complete staff briefing package on 
PVC/DINP. The first link (Part 1) contains the staff memo with the 
substance of their conclusions and recommendations. The remainder of 
that link and the other links provide supporting documentation.).
    \70\ CPSC's mouthing study found that children's mouthing times for 
soft plastic objects was less than 2 minutes per day. Id.
    \71\ Babich, M., Chen, S-B., Greene, M., Kiss, C., Porter, W., 
Smith, T., Wind, M. and Zamula, W. (2004). Risk assessment of oral 
exposure to diisononyl phthalate from children's products. Regulatory 
Toxicology and Pharmacology 40:151-167.
    \72\ Id. at 165.
    \73\ Letter from Todd A. Stevenson, Secretary, CPSC, to Jeffrey 
Becker Wise, Policy Director, National Environmental Trust (February 
26, 2003) (Petition Denial); available at http://www.cpsc.gov/library/
foia/foia03/petition/Ageunder.pdf.
    \74\ CPSC, Petition Denial at 3 (quoting Memorandum from Marilyn L. 
Wind to the Commission, Response to Petition HP 99-1 (August 13, 2002), 
at 16-17).
    \75\ European Chemicals Bureau, European Union Risk Assessment 
Report: Dibutyl Phthalate, CAS No: 84-74-2, EINECS No: 201-557-4, Risk 
Assessment, with Addendum to the Environmental Section--2004, 1st 
Priority List, Volume 29 (2003).
    \76\ European Chemicals Bureau, European Union Risk Assessment 
Report: European Chemicals Bureau, European Union Risk Assessment 
Report: 1,2-Benzenedicarboxylic Acid, Di-C9-11-Branched Alkyl Esters, 
C10-Rich and Di-``Isodecyl'' Phthalate (DIDP), CAS Nos: 68515-49-1 and 
26761-40-0, EINECS Nos: 271-091-4 and 247-977-1, Risk Assessment, 2nd 
Priority List, Volume 36 (2003).
    \77\ European Chemicals Bureau, European Union Risk Assessment 
Report: 1,2-Benzenedicarboxylic Acid, Di-C8-10-Branched Alkyl Esters, 
C9-Rich and Di-``Isononyl'' Phthalate (DINP), CAS Nos: 68515-48-0 and 
28553-12-0, EINECS Nos: 271-090-9 and 249-079-5, Risk Assessment, 2nd 
Priority List, Volume 35 (2003).
    \78\ European Chemicals Bureau, European Union Risk Assessment 
Report: Benzyl Butyl Phthalate, CAS No: 85-68-7, EINECS No: 201-622-7. 
Final Report of Norwegian Pollution Control Authority (2006).
    \79\ European Union Risk Assessment Report: Bis(2-ethylhexyl) 
phthalate, CAS No: 117-81-7, EINECS No: 204-211-0. Final Report of the 
Swedish Chemical Inspectorate (2006).
    \80\ European Chemicals Bureau, DINP Risk Assessment at 18.
    \81\ The NTP Monographs are available at: http://
cerhr.niehs.nih.gov/reports/index.html.
    \82\ Maximum estimated human daily exposure to one of the most 
commonly used phthalates, DEHP, was calculated from measurements in 
children aged 3-14 (3.1 mg/kg/d).
    \83\ K.M. Main et al., ``Human Breast Milk Contamination with 
Phthalates and Alterations of Endogenous Reproductive Hormones in 
Infants Three Months of Age,'' Environmental Health Perspectives 114 
(2006).
    \84\ R. Hauser et al., Altered Semen Quality in Relation to Urinary 
Concentrations of Phthalate Monoester and Oxidative Metabolites,'' 
Epidemiology 17, no 6 (2006).
    \85\ S. H. Swan et al., ``Decrease in Anogenital Distance among 
Male Infants with Prenatal Phthalate Exposure,'' Environmental Health 
Perspectives 113 (2007).
    \86\ Ivelisse Colon, Doris Caro, Carlos J. Bourdony, and Osvaldo 
Rosario, ``Identification of Phthalate Esters in the Serum of Young 
Puerto Rican Girls with Premature Breast Development,'' Environmental 
Health Perspectives, Vol. 108, No. 9 (Sept. 2000).
    \87\ See, EPA Draft Toxicological Review of Dibutyl Phthalate (Di-
n-Butyl Phthalate): In Support of the Summary Information in the 
Integrated Risk Information System (IRIS), available at: http://
oaspub.epa.gov/eims/eimscomm.getfile?p_download_id=457421.
    \88\ CHAP (2001). Report to the U.S. Consumer Product Safety 
Commission by the Chronic Hazard Advisory Panel on Diisononyl Phthalate 
(DINP), June 2001, available at http://www.cpsc.gov/LIBRARY/FOIA/
Foia01/os/dinp.pdf.
    \89\ The 3-hour upper bound exposure estimate was based on mouthing 
time data reported in a Dutch Consensus Group study. RIVM (1998). 
Phthalate Release from Soft PVC Baby Toys. National Institute of Public 
Health and Environmental Protection (RIVM), Report from the Dutch 
Consensus Group. RIVM Report 31 3320 002, Konemann W.H. (ed), 
Bilthoven, The Netherlands.
    \90\ Id. at 30.
    \91\ Id.
    \92\ Greene, M.A. (2002) Mouthing times among young children from 
observational data. U.S. Consumer Product Safety Commission, Bethesda, 
MD.
    \93\ Kiss, C. (2001) A mouth observation study of children under 6 
years. Consumer Products Safety Commission, Bethesda MD.
    \94\ See CHAP (2001). Report to the U.S. Consumer Product Safety 
Commission by the Chronic Hazard Advisory Panel on Diisononyl Phthalate 
(DINP), June 2001, p. 20.
    \95\ See Chen, S.B. (2002) Screening of toys for PVC and Phthalates 
Migration. U.S. Consumer Products Safety Commission, Bethesda MD.
    \96\ See Simoneau, C. (2000) Standard Operation Procedure, 
``Determination of release of diisonylphthalate (DINP) in saliva 
stimulant from toys and childcare articles'', JRC, European Commission, 
November 11, 2000.
    \97\ Lington A.W., Bird M.G., Plutnick R.T., Stubblefield W.A., 
Scala R.A. (1997) Chronic toxicity and carcinogenic evaluation of 
diisononyl phthalate in rats. Fundam Appl Toxicol 36: 79-89.
    \98\ Moore M.R. (1998) Oncogenicity study in mice with 
di(isononyl)phthalate including ancillary hepatocellular proliferation 
and biochemical analyses. Covance Laboratory Report 2598-105, January 
29, 1998.
    \99\ CPSC (2002). Response to Petition Requesting Ban of Use of PVC 
in Products (HP 99-1). U.S. Consumer Product Safety Commission, 
Bethesda, MD, (CPSC Risk Assessment) available at http://www.cpsc.gov/
library/foia/foia02/brief/briefing.html (This URL links to Commission 
briefing packages for Fiscal Year 2002. The first seven links on that 
page are the complete staff briefing package on PVC/DINP. The first 
link (Part 1) contains the staff memo with the substance of their 
conclusions and recommendations. The remainder of that link and the 
other links provide supporting documentation.).
    \100\ CPSC's mouthing study found that children's mouthing times 
for soft plastic objects was less than 2 minutes per day. Id.
    \101\ Babich, M., Chen, S-B., Greene, M., Kiss, C., Porter, W., 
Smith, T., Wind M. and Zamula W. (2004). Risk assessment of oral 
exposure to diisononyl phthalate from children's products. Regulatory 
Toxicology and Pharmacology 40: 151-167.
    \102\ Id. at 165.
    \103\ Letter from Todd A. Stevenson, Secretary, CPSC, to Jeffrey 
Becker Wise, Policy Director, National Environmental Trust (February 
26, 2003) (Petition Denial); available at http://www.cpsc.gov/library/
foia/foia03/petition/Ageunder.pdf.
    \104\ Petition Denial at 3 (quoting Memorandum from Marilyn L. Wind 
to the Commission, Response to Petition HP 99-1 (August 13, 2002), at 
16-17).

    Senator Klobuchar. Well, thank you very much, Dr. Hentges, 
and to all the witnesses.
    Dr. Myers, your research seems to point to the fact that we 
have a long way to go before finding out the full effect of 
certain phthalates in PVC plastic or BPA in our food and 
beverage containers. Are there any studies that you know of 
that are looking into the low dosage exposure to which you 
referred in your opening statement?
    Dr. Myers. Yes, there are studies underway, both 
experimental with animals and epidemiological studies of 
people. There is a center at the University of Rochester that 
is leading the way in both looking at the effects of exposure 
to individual phthalates as well as mixtures of phthalates and 
bisphenol A. It is a very interesting, cutting-edge area of 
science right now.
    Additionally, there are efforts underway in California with 
Stanford University and the University of Missouri also looking 
at a prediction that arises out of some very interesting 
science on bisphenol A, that there should be an association 
between low levels of bisphenol A and an increase in the rate 
of spontaneous miscarriage in people. That study is now funded 
and we are anxiously awaiting for the results.
    Senator Klobuchar. You mentioned that study. Was that the 
Center for Disease Control that showed this high amount of 
additives in individuals tested?
    Dr. Myers. No. The studies that I just referred to----
    Senator Klobuchar. It was in your opening. No, no, no. In 
your opening statement when you talk about the high amount of--
--
    Dr. Myers. Oh, when I said that the levels in people today 
are above those----
    Senator Klobuchar. Higher than animals.
    Dr. Myers.--sufficient to cause harm in animals, that is 
the result of an analysis done by 38 leading scientists on 
bisphenol A that were brought together with funding from the 
National Institutes of Health a year ago November. And as part 
of an extensive review of the BPA literature, the scientists 
there, led by a professor from the University of Missouri named 
Wade Welshons, took the existing data and did some new analyses 
asking how can we compare what is in animals when we see 
adverse effects. What is in the serum of those animals and how 
does that compare with data from the serum of people, the 
average level in Americans today? And what that analysis 
concluded--and it is published now in Reproductive Toxicology. 
It was published in August of 2007. What that study concluded 
was that the average levels in people are above those 
sufficient to cause harm in animals.
    And another interesting thing about that analysis was that 
it reveals that if you look at what is in people today, we 
cannot explain it based on known sources of exposure. Actually 
one of the things the Consumer Product Safety Commission ought 
to be looking at is the use of BPA in thermal paper. It is 
widely used in thermal paper. Those receipts you get when you 
go to the gas station, whatever. At least in some formulations 
of that thermal paper, the concentrations of bisphenol A dust 
are quite high.
    Senator Klobuchar. Can you talk about the life cycle of 
those additives in your system?
    Dr. Myers. They are metabolized.
    Senator Klobuchar. Do they go away?
    Dr. Myers. They go away relatively rapidly, and that is one 
of the challenges. If they go away as rapidly as they do, which 
they do, why is that we find the levels that we find in people? 
There are some significant sources of exposure that we have not 
yet identified. It is not just coming in from food.
    Senator Klobuchar. One of the groups came in to talk to us 
about this. They talked about how a ban on the phthalates or 
the BPA would lead manufacturers to use plastic additives that 
have not even been tested yet. What are the alternatives?
    Dr. Myers. There certainly are alternatives for some uses. 
I was in Japan last November in the Christmas shopping season, 
and bisphenol A is not allowed to be used. Manufacturers in 
Japan have chosen not to use polycarbonate plastic for kids' 
toys and they do not allow the phthalates in kids' toys. And 
there is no lack of toys in Japanese stores during Christmas 
shopping time.
    We have heard that Nalgene has committed to replacing 
bisphenol A in its bottles. They are using a couple different 
formulations, one they have used for a long time, 
polypropylene, which is, as far as we can tell, perfectly safe. 
They have now introduced two new types, one of which is 
stainless steel which looks to be fine. It is not a plastic. We 
are not sure about the other one, and some testing should be 
done on that.
    Senator Klobuchar. Dr. Hentges, did you want to comment on 
that?
    Dr. Hentges. Any specific part of it you would like?
    Senator Klobuchar. Well, I was asking him about what these 
products would be replaced with if we make a decision, as many 
manufacturers are starting to do, to make phthalate-free 
products.
    Dr. Hentges. Right. Well, if we think about why products 
are used, they are used because of the attributes, the 
properties they have. So, for example, polycarbonate plastic is 
used because it is clear. It is highly shatter-resistant, and 
it has other useful properties as well. Epoxy resins, also made 
from bisphenol A, are used because they also have a fairly 
unique set of properties.
    So to replace those, there are a couple of initial hurdles 
that have to be gone over. One is to find something that 
performs because these products perform a function. They are 
used for something. So we have to find an alternative that 
works at least as well as what we are replacing.
    But then since we are talking here about safety, we also 
have to be sure that these products really are at least as safe 
as what we are replacing. And in the case of bisphenol A, there 
are no alternatives that have been tested as thoroughly as 
bisphenol A, that have been vetted so carefully, so frequently 
by government agencies around the world.
    So we have two very big challenges in order to find 
alternatives that we can be confident are going to be better 
than what we have today.
    Senator Klobuchar. But I showed those two bottles over 
there, the Nalgene bottles, and they did one that did not have 
the BPA in it. Are you saying that is not safe then?
    Dr. Hentges. No. I am not saying it is not safe, but it is 
made from something. I do not know what it is made from. I 
cannot tell by looking at.
    Senator Klobuchar. I can give it to you.
    Dr. Hentges. Well, I still probably could not tell by 
looking at it, but it is made from something. And the question 
then is, how much data is available to know that that something 
is safe?
    Again, the benchmark that I can speak to is bisphenol A 
because we have an extraordinarily rich scientific database 
there that supports the safety of bisphenol A, and that data 
has been reviewed repeatedly around the world, leading to the 
conclusions that you have heard, that bisphenol A is safe for 
use in that kind of a product.
    Senator Klobuchar. Now, your testimony does admit to 
evidence that an infant can be harmed by phthalates if she 
mouths a plastic toy for about an hour. Would that be a correct 
characterization?
    Dr. Hentges. I think on that question, I am going to have 
to beg off. I do not have the great personal knowledge on 
phthalates, but I can commit to providing a written answer on 
that one as a follow up for the record.
    Senator Klobuchar. OK. Well, we are going to find it in 
your testimony here, if we could just take a second.
    Dr. Hentges. It is the follow up questions where I am going 
to have some difficulty because----
    Senator Klobuchar. OK, but you do remember saying that?
    Dr. Hentges. I can read what I said.
    Senator Klobuchar. It is in the written testimony.
    Dr. Hentges. Oh, the written, OK.
    Senator Klobuchar. I think here you say based on this ADI, 
it was concluded that a young child would have to routinely 
mouth the plasticized toys for 75 minutes or more per day in 
order to pose a possible DINP exposure risk.
    Dr. Hentges. I will commit to coming back with a written 
response for the record on that.
    Senator Klobuchar. OK.
    We have also heard testimony that when boiling water is 
poured into a bottle that contains BPA, it could create a 
problem.
    Dr. Hentges. That I can speak to. There are quite a few 
studies that examine polycarbonate baby bottles. Usually it is 
baby bottles that are tested to understand how much bisphenol A 
can leach out of those under a very wide range of conditions. 
And some of the best data has been published very recently. 
Several studies have been published by different institutions 
in Europe, and one of those studies specifically looked at--all 
of them together look at a wide range of real-life use 
conditions. But one of them looked, in particular, at the 
effect of temperature and, in particular, the effect of pouring 
boiling water directly into the bottle. And what these studies 
collectively found is that there are really no real-life use 
conditions that would lead to an unsafe situation where the 
level of bisphenol A could be harmful, that it could exceed a 
safe level. And in particular, even when boiling water was 
poured into the baby bottles, that did not lead to an unsafe 
condition.
    Senator Klobuchar. But is that not, as Dr. Myers was 
saying, based on these high levels of the chemical as opposed 
to some of the low-dose levels that he is talking about?
    Dr. Hentges. No.
    Senator Klobuchar. Then why would this company change their 
product in response to concerns about this?
    Dr. Hentges. Well, let me start with the first part. In 
Europe, where these studies on baby bottles were conducted, 
just about 1 year ago, the European Food Safety Authority 
published their report on the safety of bisphenol A. And this 
was a comprehensive evaluation of the available science, and it 
included--in fact, it was probably largely focused on studies 
that examined low doses, low levels of bisphenol A. Based on 
all of those studies, based on the weight of evidence from 
those studies, they established what they call a Tolerable 
Daily Intake or, in simple terms, a safe level.
    Then comparing that to the levels that came out of the baby 
bottles in those studies that I referred to, those levels are 
far lower than the safe level that was determined based on 
studies that looked at low doses of bisphenol A.
    Senator Klobuchar. Dr. Myers, do you want to respond?
    Dr. Myers. Yes. It is simply not true. The levels of 
bisphenol A that will leach out of baby bottles--and studies in 
the United States have shown this--are within the range that 
cause harm in animals at low doses. That is a matter of--it is 
in the scientific literature.
    Senator Klobuchar. Ms. Hitchcock, do you want to respond at 
all?
    Ms. Hitchcock. No.
    Senator Klobuchar. OK. Thank you very much. I appreciate 
it.
    Senator Pryor [presiding]. Thank you, Senator Klobuchar. 
Thank you for covering for me. I had to do a quick conference 
call in the back room, and I apologize for my absence.
    Let me follow up on that, if I can. There are clearly two 
strong opinions on the safety level, and I think one of the 
reasons there might be two strong opinions is--is it possible 
that you all are looking at different studies, or are you just 
interpreting the same studies differently? Do you want to take 
a stab at that?
    Dr. Myers. Sure. The studies that I am looking at typically 
are funded by the National Institutes of Health. It is very 
interesting. The studies by the National Institutes of Health 
typically do not begin with a toxicological perspective. They 
look at different endpoints, and they use much more 
sophisticated tools to get at what are the biological 
mechanisms underlying impacts that they are seeing. These are 
studies that are published in the proceedings of the National 
Academy of Sciences. They are published in Science and Nature, 
in the premier scientific journals of the world. And the bulk 
of those, over 90 percent of those studies, show adverse 
effects in animals at low levels.
    Those are the studies that I think we need to be looking at 
because they are asking--in my opening my comments, I talked 
about a new way--a new framework for thinking about toxicology 
and how the EPA and the FDA and the Consumer Product Safety 
Commission are really missing the boat on this because they are 
focused on old toxicological endpoints. They are not using 
modern molecular genetics in their work. So I am looking at new 
science. They are looking at old science.
    Senator Pryor. Do you have a comment on that?
    Dr. Hentges. Yes. Going back to where you started, are we 
looking at different studies, no, I do not think we are looking 
at different studies. We all have the same body of scientific 
information to look at, and there are, indeed, many hundreds of 
studies on bisphenol A. But those studies vary vastly in size, 
scope, quality, relevance to human health. There is no single 
study that is really going to give us the answer about whether 
bisphenol A is safe or not.
    We review all of those studies together in a weight of 
evidence fashion, and our conclusion is that bisphenol A is 
safe for use in consumer products of the type that you are 
considering. But more important than our view is the view of 
the many independent scientific and government bodies around 
the world who have also reviewed the science, who have reviewed 
all of it together and drawn a conclusion based on the full 
weight of scientific evidence. Those conclusions, more 
importantly, support the safety of consumer products made from 
bisphenol A.
    Senator Pryor. Let me, if I can, ask each of the three of 
you the same question. I will go ahead and start with you, if I 
may. That is, are you satisfied with the job the FDA and the 
CPSC have done on these chemicals that we have been talking 
about today?
    Dr. Hentges. Well, focusing on FDA and bisphenol A, because 
they regulate food contact products made from polycarbonate 
plastic or epoxy resins, we do have confidence that FDA has 
been monitoring the science quite carefully. We believe that 
they have the scientific capability and credibility to do that. 
We have, however, because there is new information available 
from the recent reports, encouraged FDA to refresh their view, 
to update, make sure they have looked at everything, and 
provide their conclusions. That is very important because 
consumers are getting a lot of confusing and conflicting 
information, and we believe that FDA has the capability to cut 
through that confusion and provide a clearer view to consumers 
about the safety of products made from bisphenol A.
    Senator Pryor. By the way, consumers and the U.S. Senate 
are getting confusing information. There is a sharp 
disagreement here.
    But Ms. Hitchcock, would you like to answer whether you 
think FDA and CPSC are doing a good job to date?
    Ms. Hitchcock. In the presence of the confusing information 
that consumers and the U.S. Senate are getting about bisphenol 
A and about phthalates, I would say no. And we would urge them 
to do a better job. I noted in my testimony that we need to 
reform U.S. chemicals policy so that we are not testing 
chemicals that are on the market on our children and on 
ourselves before we actually know what the effects are. We are 
hearing from two scientists here and we are hearing a diversity 
of opinion about the safety of these chemicals. Where there is 
a doubt, we ought not be putting them in the hands and the 
mouths of our children.
    Senator Pryor. Did you have a comment?
    Dr. Myers. My comment will not surprise you, Senator. I 
think the FDA right now is failing the American people 
miserably. We have seen that in other cases over the last year. 
It is no different here. They are not asking the right 
questions. They are not using modern scientific methods to ask 
those questions. Molecular genetics, as it has developed over 
the last 15 years, has changed the types of questions we should 
be asking about how contaminants can interfere with health. We 
used to worry about high doses causing mutations, high doses 
causing birth defects directly. Now we know that low doses, by 
interfering with how genes are being turned on and off during 
development, can have profoundly important health consequences 
that are not revealed by the procedures that the FDA, the EPA, 
and the CPSC use today.
    We have been blind-sided by these effects. These things are 
well known to endocrinologists, medical practitioners of the 
science of endocrinology. It is not something new to them. It 
is only when over the last 15 years we have learned that some 
contaminants possess characteristics like hormones that we have 
realized we have not been asking the right questions. And that 
is actually a much bigger challenge than just dealing with BPA 
and phthalates. There are probably a lot of other contaminants 
that share these characteristics. In fact, we know there are, 
and we are similarly being blind-sided on those cases as well.
    Senator Pryor. I really did not have any more questions. I 
know that some of our colleagues will have questions that they 
will submit in writing, and we would like to leave the record 
open for 2 weeks and allow Senators to ask questions and would 
love a timely response when you all receive those.
    But I do want to thank you. This is an important issue. I 
really think the sharp disagreement on this panel underscores 
the reason we had this hearing in the first place--to try to 
start the process for the Senate and the Congress to really get 
to the facts of this. It may be what you said a few moments 
ago. It may be that the Government needs to update and upgrade 
their testing capabilities, and that may solve this problem. 
Then again, it may be that these chemicals are safe, if we did 
that.
    But I do think it is important for us, the American 
Government, to get our policy right. And I do think, Ms. 
Hitchcock said something that most Senators would agree with. 
If there is a substantial risk, even if it is not exactly known 
exactly what the level is, err on the side of caution, 
especially when it comes to children. I think you are going to 
see that here in the Senate.
    So I would appreciate you all continuing to work with us 
and continuing to talk to us and our staffs about where you 
think this should be heading. We know Senator Schumer has a 
bill. We know that there are others out there who are working 
on legislation in different forms and fashion. So this is going 
to be an issue that we will continue to work through.
    So, again, I want to thank this panel and the previous 
panels for being here.
    This hearing is adjourned.
    [Whereupon, at 12:06 p.m., the hearing was adjourned.]
                            A P P E N D I X

  Response to Written Questions Submitted by Hon. Daniel K. Inouye to 
                       Norris E. Alderson, Ph.D.
    Question 1. What research is being done to determine the effects 
these chemicals have on wildlife?
    Answer. FDA's primary concern in evaluating the safety of these 
chemicals under the Federal Food, Drug, and Cosmetic Act is their 
potential for human health effects. Numerous studies in the literature 
have been conducted to evaluate the effects of these chemicals on 
assessments of both human and ecological health. Accordingly, some of 
the studies that FDA relies on in making human safety decisions could 
potentially be applied to the safety of wildlife. The Environmental 
Protection Agency (EPA) or the Department of the Interior (DOI), 
however, would be the appropriate Federal entities to address the 
effects on wildlife.

    Question 2. What are the known effects of these harmful plastic 
chemicals on wildlife?
    Answer. There are many issues with regard to the disposal of 
plastics and its potential harm to the environment, including wildlife. 
Again, although FDA considers all relevant safety data when reviewing 
uses of food additives for human consumption, either EPA or DOI is 
better suited to address these issues.

    Question 3. Is there any evidence that humans can be exposed to 
these chemicals through the food, specifically seafood, which we eat?
    Answer. Yes, consumers may be exposed to BPA and phthalates as a 
result of their authorized uses in food contact materials. We are 
limiting our comments to that exposure source.
    Bisphenol-A (BPA) is a chemical building block of epoxy-based 
enamels used in food cans. These epoxy enamels are used to coat the 
inside of food cans to impart resistance to corrosion of the metal by 
the packaged food. By controlling degradation of the can, food is 
preserved from microbiological contamination. Many foods, including 
seafood products, are packaged in cans coated with epoxy enamels. 
Consumers may be exposed to minute amounts of BPA as it may migrate 
from the epoxy coating to food during storage.
    Phthalate plasticizers are approved for use with some food wrapping 
polymers where they impart cling and flexibility properties to the 
wrap. Although phthalate plasticizers have been authorized for such 
uses for many years, FDA's research of the regulated industry indicates 
that these uses have been largely discontinued, and nearly all 
currently available commercial food wraps are either unplasticized 
polyolefin materials having no phthalates, or are materials plasticized 
with alternate materials (such as citrates). It might be possible to 
find some polyvinyl chloride or polyvinylidene chloride food wraps on 
the market that are still plasticized with phthalates, and if those 
wraps were used; some phthalate plasticizer would be transferred to the 
food. The higher the fat content of the wrapped food, the more 
phthalate plasticizer would be transferred. Accordingly, the amount of 
phthalates in the food would vary based on the wrap used to prepare 
seafood for sale and the amount of fat content in the seafood. For this 
reason some phthalates such as Di-2-ethylhexyl phthalate are restricted 
from use in contact with high fat content foods.
                                 ______
                                 
     Response to Written Questions Submitted by Hon. Mark Pryor to 
                       Norris E. Alderson, Ph.D.
    Question 1. The U.S. National Toxicology Program released a report, 
in early April, regarding the reproductive and developmental hazards 
associated with bisphenol-A (BPA). Shortly after the report was 
released the FDA announced that it would look into the safety of baby 
bottles, formula cans, and other products made with BPA. What has the 
FDA done to move this investigation forward?
    Answer. Commissioner of Food and Drugs Andrew C. von Eschenbach, 
M.D. has formed an Agency-wide BPA Task Force to conduct a review, 
encompassing all FDA-regulated product lines, of the concerns raised 
about BPA. The Task Force is undertaking a broad review of current 
research and information on BPA, and is actively reviewing the National 
Toxicology Program's (NTP) Draft Brief. Members of the Task Force have 
met with NTP staff to discuss their findings and better understand 
NTP's approach to evaluating the underlying data. Also, staff of FDA's 
National Center for Toxicological Research (NCTR) is discussing with 
NTP additional research needs relating to BPA.
    In addition to looking at the food and beverage containers that 
have been the focus of recent concerns as well as our regulatory 
efforts over the years, the Task Force is conducting an inventory of 
all products regulated by FDA's food and medical products centers and 
is reviewing other potential routes of exposure. Additionally, the Task 
Force has been talking with representatives of product manufacturers to 
better understand manufacturing and chemistry issues. Finally, the Task 
Force is considering what recommendations for further laboratory 
studies or other research may be appropriate.

    Question 2. How long do you anticipate for a final conclusion or 
ruling from the FDA regarding possible health risks caused by BPA 
exposure?
    Answer. In late summer or early fall, the BPA Task Force is 
expected to issue its draft report. At FDA's request, the FDA Science 
Board, which is an independent advisory body to FDA on scientific 
issues, is forming a subcommittee on BPA to undertake scientific peer 
review of the Task Force report. Part of that peer review process will 
be to hold a public meeting to accept input and comments from the 
public. The full Science Board will receive the findings of the 
subcommittee during its fall meeting.

    Question 3. The ``low-dose hypothesis'' claims that exposure to 
extremely low levels of certain substances could cause adverse health 
effects in humans. Some have criticized existing studies and reviews 
for looking at only high dosage exposure. Have any of the governmental 
reviews done by FDA taken into account studies showing adverse health 
effects from low-dose exposure to BPA?
    Answer. FDA's formal re-evaluation of BPA conducted over the past 
14 months has considered many studies designed to investigate so-called 
``low'' dose effects. Two of these studies, which were designed based 
on international regulatory study guidelines, and included a wide range 
of doses, including low doses, and expanded protocols, did not 
demonstrate adverse health effects in rodents from low dose 
administration of BPA. The two pivotal studies were published by Tyl et 
al., in 2002 (rat study) and 2008 (mouse study).
    Our current review effort is ongoing regarding the concerns which 
the most recently completed assessments (NTP's Center for the 
Evaluation of Risks to Human Reproduction (CERHR) Expert Panel Report, 
the NTP Draft Brief and the Health Canada Draft Screening Assessment) 
have highlighted. The BPA Task Force review is considering numerous 
additional ``low'' dose studies and will address the more recent 
concerns raised for low-dose effects.

    Question 4. The results of studies into the potential health 
effects of BPA and phthalates conducted by the government, industry, 
and some in academia seem to vary quite widely in their results. How 
would you explain these differences?
    Answer. There are various factors that may account for differences 
in study outcomes independent of the source of information, the 
performers of the study, or the sponsors of the study. Studies 
conducted in laboratories in academia are more hypothesis-driven as 
opposed to safety evaluation studies and as such, FDA has encountered 
limitations in the methodologies, reporting, or relevance of the 
endpoints of analysis with regard to their utility in safety 
assessments. FDA has published guidance on the conduct of studies for 
submission to the Agency to support the safe use of food additives 
(Toxicological Principles for the Safety Assessment of Food 
Ingredients: Redbook 2000). This guidance is intended to help ensure 
the use in safety assessments of studies that are conducted using good 
laboratory practices (GLP) and quality assurance (QA), sufficient and 
relevant dosing protocols, adequate replicates of animals for 
meaningful statistical analysis, interim analysis when applicable, and 
analysis of endpoints (organ weights, clinical chemistry, 
histopathology, etc.) which have been validated by FDA or other 
international regulatory organizations. In addition to FDA, other 
international agencies involved in regulatory toxicology also provide 
guidance that is useful for conducting safety assessments.
    A typical GLP study submitted to FDA contains all the raw data 
collected during the course of the study, thereby allowing the Agency 
to review and audit the study and reach an independent conclusion on 
the findings reported by the study author(s). As journal publications 
typically are limited in the thoroughness in which they are reported, 
FDA is ordinarily unable to validate the performance quality or data 
integrity of these studies. By contrast, FDA's standard review 
procedures for reported GLP/QA studies allow FDA to independently reach 
the authors' conclusions or arrive at alternative interpretations of 
the data and findings presented. In addition to reporting limitations, 
many of the studies in the literature fail to control for numerous 
issues that validated regulatory protocols eliminate by design. These 
shortcomings cannot be ignored in an overall weight of evidence 
analysis of a food additive's safe use.

    Question 5. Does the FDA take into account the safety of these 
chemicals when rendering its opinions?
    Answer. Yes, FDA is required by statute to judge the information 
relevant to the safety of chemicals used in food contact material 
according to the safety standard for food additives. That standard is a 
``reasonable certainty of no harm'' (see Title 21, Code of Federal 
Regulations  170.3(i)). To accomplish this, FDA requires that industry 
sponsors provide all relevant safety data (including data indicating 
potential harm) and to produce any additional data necessary to 
establish the safety of the intended use.

    Question 6. Please explain the significance of low-dose exposures 
to BPA and how it relates to the traditionally held belief of ``the 
dose makes the poison''?
    Answer. The expression ``the dose makes the poison'' refers to the 
fact that all substances can produce toxicity given a high enough dose. 
A common extreme example is hypnoatremia--a toxic effect observed in 
individuals who consume dangerously large quantities of water resulting 
in a reduction of essential minerals in the blood. For chemicals that 
enter the food supply, FDA typically estimates a safe or acceptable 
level by determining the no observed adverse effect level in animal 
testing and extrapolating to a safe level of human consumption that is 
ordinarily 100 to 2,000 times (or more) smaller. In this regard, FDA's 
approach is based on the entire body of toxicological safety testing 
research; that research generally supports the fact that increasing 
exposure to a chemical increases the toxic effect and that potential 
toxicity can be mitigated by limiting exposure to levels many times 
lower than those that show only limited toxicity in experiments.
    Exposure to residual BPA through uses in food additives is 
relatively low, at > 11 micrograms per person per day (mg/person/day). 
Traditionally, FDA's evaluation of chemical migrants to food from the 
use of food contact materials at exposures of > 150 mg/person/day 
focuses primarily on carcinogenicity and genetic toxicity as an 
indicator of carcinogenicity, unless data are available (biological or 
predictive) that indicate a concern for another endpoint of toxicity at 
this level. However, BPA has been studied for many years with regard to 
its potential ability to bind to estrogen receptors and either mimic 
estrogen or disrupt normal endocrine activity. Since estrogens and 
other hormonally active compounds with high affinities to steroid 
receptors can show effects at low doses, research has focused on BPA's 
ability to disrupt normal hormonal activity or act as a reproductive or 
developmental toxicant. However, BPA is only weakly estrogenic (several 
orders of magnitude less than estrogen) and BPA is metabolized 
extremely quickly into BPA-glucuronide (BPAG), which is estrogenically 
inactive. Although FDA's review of the most recently raised concerns 
for BPA is not complete, previous reviews have determined the margin 
between no effect levels in animal tests and human exposures to be 
acceptable based on FDA's routinely used margins of safety.

    Question 7. How is the average person exposed to phthalates? What 
is the best way to reduce exposure to phthalates?
    Answer. In terms of food contact applications, phthalates are 
primarily used as plasticizers in polyvinyl chloride (PVC) and 
polyvinylidene chloride (PVDC) polymers to increase their flexibility. 
Di-(2-ethylhexyl) phthalate (DEHP) is perhaps the most thoroughly 
studied among the phthalates. DEHP has long been used to produce highly 
flexible versions of PVC and PVDC polymers for a variety of 
applications, such as in flexible packaging film.
    FDA-authorized uses of phthalates include uses in flexible food 
packaging. Over the past decade, however, such food contact uses have 
been greatly reduced or eliminated through the replacement of PVC and 
PVDC polymers with other polymers that do not require plasticizers and 
by the use of alternative plasticizers in PVC and PVDC. FDA's Center 
for Food Safety and Applied Nutrition (CFSAN) is tracking the 
reductions in use of phthalates in food contact materials as well as 
the development of new toxicological data. CFSAN has established a 
Phthalate Task Group (PTG), whose primary focus will be to determine 
the most realistic exposure estimation and better characterize any 
potential risk associated with phthalate use in food packaging.
    There are also significant uses of phthalates in certain medical 
products, such as intravenous solution bags and medical tubing. FDA's 
Center for Devices and Radiological Health (CDRH) has looked into the 
use of polyvinyl chloride using DEHP as a plasticizer in medical 
devices. DEHP is a chemical ingredient that affords PVC many of the 
physical properties that make it optimally suited for use in many of 
today's medical devices. While toxic and carcinogenic effects of DEHP 
have been demonstrated in laboratory animals, there are no studies in 
humans that are adequate to serve as the basis for regulatory decision-
making. Further, health care professionals should not avoid performing 
certain medical procedures simply because of the possibility of health 
risks associated with DEHP exposure. In these cases, the risk of not 
doing a needed procedure is far greater than the risk associated with 
exposure to DEHP.
    Phthalates are also widely used in cosmetics, serving as solvents 
for fragrances, antifoaming and suspension agents, skin emollients, and 
plasticizers in nail products. CFSAN's Office of Cosmetics and Colors 
has conducted laboratory surveys of phthalate levels in marketed 
cosmetics. The last survey indicated that diethylphthalate (DEP) was 
the most frequently used phthalate in cosmetics and that nail enamels 
contained the highest levels of phthalates, primarily dibutylphthalate 
(DBP). Based on the results of that survey and the toxicity data 
currently available, FDA does not believe that phthalates in cosmetics 
pose a health risk. Since the survey was conducted, we have observed 
that some cosmetic products are being reformulated to remove 
phthalates. CFSAN is planning a more extensive survey of a larger 
number of cosmetic products to better determine to what extent cosmetic 
products contribute to total human exposure to phthalates. We will 
continue to monitor and evaluate all available data to ensure that 
phthalate levels in cosmetic products are not a health concern.
    FDA, primarily through NCTR, is conducting further research to 
address uncertainties in our understanding of the potential health risk 
posed by exposure to phthalates. Much of the concern on medical 
exposures to phthalates is focused on potential reproductive tract 
effects in male infants in neonatal intensive care units, a population 
exposed to high levels of DEHP at a sensitive period of development. 
NCTR studies are evaluating the metabolism and toxicity of DEHP 
following intravenous exposure in infant male nonhuman primates, a 
model that more closely resembles the human exposure of highest 
concern.

    Question 8. Please explain the significance of phthalate mixtures.
    Answer. Regarding the toxicological significance of phthalate 
mixtures, there have been reports in the literature that individual 
phthalates with a similar mode of action can induce dose-additive 
effects when administered as a mixture.

    Question 9. What are endocrine disruptors and how do they affect 
us?
    Answer. Endocrine disruptors are exogenous substances (natural or 
synthetic) that act like hormones and, by doing so, have the potential 
to either mimic or disrupt the activities of endogenous hormones. 
Studies have linked endocrine disruptors to adverse biological effects 
in animals, giving rise to concerns that low doses of these chemicals 
may cause similar effects in human beings.

    Question 10. Is there an established list of known endocrine 
disruptors?
    Answer. At this time, FDA does not have an established list of 
endocrine disruptors. However, FDA uses all available resources in 
evaluating chemicals and their relevant (to dose) modes of actions. 
This is achieved using literature searches of FDA files and public 
information as well as computer-simulated toxicology programs which can 
predict the reproductive or teratogenic potential of a chemical. For 
instance, one resource FDA is aware of is EPA's draft list of 73 
chemicals to undergo ``Tier I'' screening in the Endocrine Disruptor 
Screening Program (EDSP). The EPA list should not be construed, 
however, as a list of known or likely endocrine disruptors.

    Question 11. Are there already alternatives to BPA and phthalates? 
Are these alternatives safer than what is currently being used? What 
science or studies exists into these alternatives?
    Answer. With respect to food contact materials, there are non-
phthalate plasticizers, including several citrate esters and a 
terephthalate ester, that are commercially available and approved by 
FDA for food contact use. Our data indicate that the alternate 
plasticizers and alternate cling wrap materials have already reduced 
significantly the consumer exposure to phthalates. Similarly, the use 
of BPA in polycarbonate drinking bottles and cups seems to have been 
largely replaced by a polyester plastic recently authorized for use by 
FDA.
    The situation with BPA-containing epoxy resin can coatings is 
somewhat different in that there are no coating materials as suitable 
as the epoxy resins. Alternate coating materials approved by FDA are 
available, but none have the combination of properties (adherence, 
flexibility, chemical resistance) that make epoxy coatings so useful 
and beneficial for preserving canned food from microbiological 
contamination.
    Any alternative to BPA or phthalates would need to meet the same 
safety standard for use that the food contact materials containing BPA 
and phthalates must meet. FDA judges the safety of all food additives 
against the same safety standard of ``reasonable certainty of no harm'' 
and does not make judgments regarding whether one chemical that meets 
this standard is ``safer'' than another. The amount of data necessary 
to support the safe use of any alternatives will vary based on the 
properties and uses of those particular chemicals.
    With respect to the use of BPA in medical devices, eliminating this 
chemical would require finding one or more chemicals that have the same 
beneficial characteristics as BPA but do not raise new biocompatibility 
or manufacturability issues. In fact, it is possible that there may not 
be an equivalent to BPA.
    With respect to phthalates, there have been a number of other 
``esters'' developed to replace DEHP as a vinyl plasticizer. Examples 
include long chain esters of citric acid (CitroflexTM) and 
epoxidized soybean oil or other vegetable oils (VikoflexTM). 
However, the amount of research that has been conducted in animal and 
human studies of these vinyl plasticizers is quite small. Because the 
potential toxic effects of alternatives to phthalates require further 
study, we cannot conclude at this time that these alternatives are 
safer for use in medical devices.

    Question 12. Do infants and children have the same immune and 
endocrine system as adults? Do studies take into account these 
differences?
    Answer. Infants and children do not have the same immune or 
endocrine system as adults, especially in terms of functions. These 
systems in infants and children are considered immature; this simply 
means that their immune and endocrine systems do not function in an 
equivalent manner to that of adults. Some studies, such as 
multigenerational or chronic studies with an in utero exposure period, 
are designed to take into account these differences. Toxicologists 
recognize, however, that many uncertainties remain with regard to the 
relevance of laboratory animal development as compared to human 
development, the appropriate methods for testing, and the extrapolation 
of findings in rodents to humans. For many of the endpoints which have 
recently begun to be highlighted, such as neural and neurobehavioral 
developmental endpoints, many questions exist with regard to 
implications for human safety assessment.

    Question 13. Have we seen many human studies on these chemicals? Is 
it even possible or ethical to conduct human studies?
    Answer. There are only a few studies involving human exposure 
available. These studies are retrospective epidemiology studies and 
limited to certain parameters, for instance, studies have been 
conducted on miscarriage and BPA levels. However, as commented on in 
the CERHR expert panel review, none of the currently available studies 
is sufficient to make conclusions regarding BPA's toxicity in humans. 
The Center for Disease Control and Prevention's National Health and 
Nutrition Examination Survey has and will continue to test for levels 
of BPA in human biological fluids. FDA sees this effort as extremely 
helpful in determining the actual internal dose to BPA, which is useful 
in verifying assumptions with regard to exposure and safety assessment.

    Question 14. Usually chemicals are tested one at a time. However, 
we come into contact with numerous chemicals every day. Do these 
studies simulate real world exposures and what is the best way to test 
chemicals?
    Answer. The issue with regard to mixtures and safety assessment is 
one that is extremely difficult to address, but occurs in the real 
human experience. Toxicologists know that chemicals involved in the 
same pathways may act additively, synergistically, or may inhibit one 
another. However, for risk assessment purposes, chemicals are normally 
tested individually to avoid data interpretation difficulties that may 
result from metabolic and toxicological interactions with other 
chemicals. This is usually done at much higher doses than human 
exposures for the comparison of effects observed in animal testing to 
the human estimated exposure (margin of safety). Testing chemicals at 
dose levels simulating ``real world'' exposures would require an 
extremely large number of animals to determine an effect that was not 
considered a random or chance event. Basing any conclusions on random 
or chance events relating to potential toxicity may give a false sense 
of safety. Considering all possible exposures to chemicals with known 
modes of actions is an insurmountable challenge based on current 
science. In addition, as is the case with BPA, environmental or dietary 
compounds such as phytoestrogens, which are naturally present in soy-
based food products, may also be potential confounders.

    Question 15. What about workers who are in the plants that 
manufacture phthalates and BPA. Are protections in place to make sure 
that they aren't unnecessarily exposed?
    Answer. While toxicological data and analyses that have been 
developed by FDA may be useful in assessing the effects of exposure in 
the workplace (and vice versa), issues related to workplace safety are 
under the regulatory purview of the Occupational Safety and Health 
Administration. That agency, rather than FDA, would be better 
positioned to answer this question.
                                 ______
                                 
   Response to Written Questions Submitted by Hon. John F. Kerry to 
                       Norris E. Alderson, Ph.D.
    Question 1. In light of the results of the 2007 assessment by the 
Center for the Evaluation of Risks to Human Reproduction and last 
month's draft brief from the National Toxicology Program, what actions 
is FDA taking to ensure the safety of products that contain BPA? Why is 
FDA allowing consumer products--particularly children's products--that 
contain BPA to stay on the market?
    Answer. Commissioner of Food and Drugs Andrew C. von Eschenbach, 
M.D. has formed an Agency-wide BPA Task Force to conduct a review, 
encompassing all FDA-regulated product lines, of the concerns raised 
about BPA. The Task Force is undertaking a broad review of current 
research and information on BPA, and is actively reviewing NTP's Draft 
Brief.
    Members of the Task Force have met with NTP staff to discuss their 
findings and better understand the underlying data. Also, staff of 
FDA's NCTR is discussing with NTP additional research needs relating to 
BPA.
    In addition to looking at the food and beverage containers that 
have been the focus of recent concerns, as well as our regulatory 
efforts, over the years, the BPA Task Force is conducting an inventory 
of all products regulated by FDA's food and medical products centers 
and is reviewing other potential routes of exposure. Additionally, the 
Task Force has met with representatives of product manufacturers to 
better understand manufacturing and chemistry issues. Finally, the Task 
Force is considering what recommendations for further laboratory 
studies or other research may be appropriate.
    The NTP has stated that its Draft Brief on BPA is not a 
quantitative risk assessment, nor does it supersede risk assessments 
conducted by regulatory agencies. The report stated that more research 
is needed to better understand the health implications of BPA exposure. 
Although FDA's review is ongoing, at this time we have no reason to 
recommend that consumers stop using products containing BPA. A large 
body of evidence indicates that currently-marketed products containing 
BPA, such as baby bottles and food containers, are safe, and that 
exposure levels to BPA from these products are well below those that 
may cause health effects.

    Question 2. In your written testimony, you note that FDA continues 
to monitor the safety of phthalates and BPA. How much information is 
required before FDA will make a decision that exposure to these 
chemicals is not safe? Are there established decision points for 
reevaluation?
    Answer. FDA's re-evaluation of any food additive involves a 
determination of whether the permitted use of that compound continues 
to meet the safety standard. That is the primary decision point for FDA 
to take action. There is no minimum amount of data necessary to reach 
that decision point but the data underpinning such a decision must be 
relevant to the safety assessment of the chemical. FDA's current 
consideration of the data on BPA follows.
    Information exists indicating the possibility of concern for humans 
exposed during development. That possible concern includes 
developmental toxicity effects (neural and behavioral effects, prostate 
gland, and early onset of puberty in females) and a possible 
predisposition for cancer (mammary and prostate glands) later in life. 
The data generating these concerns are rodent data and contain many 
uncertainties and limitations. For example, regarding the conclusion of 
a predisposition of cancer, for both endpoints, the NTP stated that 
``The evidence is not sufficient to conclude that bisphenol A is a 
rodent [mammary/prostate] gland carcinogen or that bisphenol A presents 
a [breast cancer/prostate] hazard to humans.''
    FDA takes the NTP and its expert panels' conclusions seriously and 
our Task Force is currently reviewing these data as they relate to the 
safety assessments of BPA-containing products that are regulated by 
FDA. The Agency's established decision points in this re-evaluation are 
to consider the information that has indicated a concern and report 
those findings with recommendations to the Commissioner for appropriate 
action. FDA's activities with regard to BPA will be conducted using 
public peer review and the FDA Science Board. At FDA's request, the FDA 
Science Board, which is an independent advisory body to FDA on 
scientific issues, is forming a subcommittee on BPA to undertake 
scientific peer review of the Task Force report. Part of that peer 
review process will be to hold a public meeting to accept input and 
comments from the public. The full Science Board will receive the 
findings of the Subcommittee during its fall meeting.
    With regard to phthalates, CFSAN's Phthalate Task Group is 
evaluating current use levels and, based on the information gathered, 
will consider what action may be necessary to establish a more 
realistic exposure estimate. Any actions necessary to modify the 
existing regulations to reflect current known practices will be 
pursued, as appropriate. Should FDA's updated assessment indicate a 
safety concern, appropriate regulatory actions will be taken to protect 
consumers.

    Question 3. News reports have indicated that the FDA relied 
exclusively on a handful of industry-funded studies of the low-dose 
effects of BPA, in the face of contrary evidence from dozens of 
scientific studies. Is this accurate?
    Answer. FDA's position on BPA is based on the consideration of 
hundreds of studies and is not derived solely from the review of the 
two industry-funded studies. However, FDA has concluded that these two 
studies are pivotal to the safety assessment of BPA, due to the design 
of the studies and the quality of the data. While we have used these 
studies in determining the current ``no observed effect level'' (NOEL) 
for BPA, this is not the same as stating that our position is entirely 
dependent on consideration of only these two studies.
    The two rodent studies that were considered pivotal were sponsored 
by the American Plastics Council and the Society of the Plastics 
Industry and were conducted by RTI International, Research Triangle 
Park, North Carolina. The studies were conducted to address questions 
concerning possible low-dose effects of BPA on endpoints that were of 
concern at that time. The industry briefed FDA and our European 
counterparts on the two studies during the planning and execution 
phases. These studies were considered pivotal in our review of the 
existing data for a number of reasons, including the following: (1) 
they were conducted in a manner that CFSAN's Office of Food Additive 
Safety would recommend to a stakeholder seeking an approval for a new 
use (i.e., they follow Agency guidelines) and included additional 
protocol considerations allowing for the examining of issues that were 
controversial to BPA at the time planned; (2) they were submitted to 
the Agency with supporting information (raw data) allowing for our 
independent evaluation of the findings; and (3) they both included a 
large range of exposures, including a range of high and low doses which 
allowed for the examination of dose response curves. These studies have 
been given more weight in FDA's evaluation of BPA, compared to 
publications in the public literature that examine the same endpoints, 
because these publications often lack details and supporting data that 
would allow Agency scientists to make an independent evaluation of the 
underlying data. In addition, many of the published studies on BPA have 
numerous protocol limitations, including the animal model utilized, the 
method of BPA measurement, the statistical analysis of the data, the 
failure to use multiple or correctly spaced doses in the experimental 
protocol, and the route of administration.

    Question 4. Do your agencies require labeling of consumer products 
that contain BPA or phthalates? Is there any control over current 
voluntary labeling of products as ``BPA-free'' or ``phthalate-free''?
    Answer. FDA does not require such labeling. Because FDA has not 
made a determination that BPA or phthalates, under current conditions 
of use, are unsafe, we do not believe that labeling for the presence of 
these chemicals would provide consumers with meaningful information on 
the safety of the products. Pursuant to our authority under the Federal 
Food, Drug, and Cosmetic Act, if FDA determined that a water bottle or 
other product containing BPA was in fact not safe, we would not address 
it through labeling; rather, we would take action to restrict or 
possibly disallow its use.
    Manufacturers are permitted to voluntarily label products as ``BPA 
free'' or ``Phthalate free'' so long as the labeling statements are 
truthful and not misleading.

    Question 5. Can you please explain the different roles for FDA, 
CPSC and EPA in the study and regulation of phthalates, BPA and other 
endocrine disrupting chemical compounds? Do the agencies share data and 
information?
    Answer. FDA is the agency responsible for the safety of food and 
medical products, and this jurisdiction includes food containers and 
packaging (food contact materials). Although BPA itself is not 
considered a food additive, it is present as an impurity in 
polycarbonate plastics and epoxy-based resins and was considered as 
part of FDA's overall review of BPA-containing food contact materials. 
Similarly, phthalates are considered as part of FDA's review of food 
contact materials when they are added to food contact polymers to help 
soften them and make them more pliable (i.e., they act as 
plasticizers).
    The Consumer Product Safety Commission (CPSC) is responsible for 
the safety of consumer articles that would not fall under the 
jurisdiction of the FDA. For example, although baby bottles and nipples 
would fall under the jurisdiction of FDA, the safety of baby pacifiers 
or toys would fall under CPSC. EPA is responsible for the effect of 
chemicals on the environment as a result of their manufacture, use, and 
disposal.
    FDA, CPSC, and EPA work closely in areas where our jurisdiction 
converges. A recent example of such cooperation is the response in 2006 
to elevated lead levels in soft-sided polyvinyl chloride (PVC) 
lunchboxes, where FDA and CPSC shared data and information. FDA was 
concerned about the potential for lead migrating into food held in the 
PVC lunchboxes while CPSC was concerned about potential exposure of 
children to the lead by touching the PVC or by putting parts of the PVC 
lunchbox in their mouths.
    Memoranda of understanding have been developed over the years to 
help facilitate cooperation between FDA and both CPSC and EPA.

    Question 6. Do we know what levels of BPA and phthalates are safe 
for human (particularly child) consumption?
    Answer. Ordinarily, FDA uses the term ``acceptable daily intake'' 
(ADI to define the estimated maximum amount of a food additive to which 
individuals in a population may be exposed daily over their lifetimes 
without an appreciable health risk. These levels are determined by 
examining endpoints from which the NOEL or no observed adverse effect 
level (NOAEL), if appropriate, is calculated in animal studies. 
However, since BPA is an impurity and not a food additive, FDA 
considers margin of safety (MOS) more appropriate in evaluating the 
safety of BPA. The MOS is compared to the typical uncertainty factors 
used for the appropriate endpoint in deeming if the substance is safe 
for the expected exposure.
    CFSAN's typical uncertainty factors are 10 for intraspecies 
variability and 10 for interspecies variability for reproductive or 
developmental effects that are reversible (which is the observation at 
the NOEL for BPA). For systemic toxicity, exposure in the applicable 
studies is less than chronic; therefore, an additional factor of 10 is 
used to extrapolate from subchronic to chronic exposure. Using this 
approach, the Agency has determined adequate safety margins for both 
infant and adult exposure to BPA, based on the NOELs identified in Tyl. 
et al. (2002, 2008) rodent studies. The lowest NOEL in both studies was 
5 mg/kg bw/day, based on the endpoint of systemic toxicity. FDA's task 
force is currently examining the additional endpoints identified in the 
recently released draft documents as they relate to the current 
exposure and the previously examined and referenced toxicity studies. 
Should FDA's updated assessment indicate a safety concern, appropriate 
regulatory actions will be initiated to protect consumers.
    FDA's approach to phthalates is similar to BPA. As noted in the 
response to your earlier question, CFSAN's Phthalate Task Group is 
currently evaluating current use levels of phthalates in food contact 
materials and based on the information obtained, FDA will reassess the 
safety of food contact materials containing phthalates. Should FDA's 
updated assessment indicate a safety concern, appropriate regulatory 
actions will be initiated to protect consumers.
                                 ______
                                 
     Response to Written Questions Submitted by Hon. Mark Pryor to 
                          Dr. Marilyn L. Wind
    Question 1. According to my information, CPSC has never done a 
comprehensive study on the effects of all phthalates. Why has CPSC not 
undertaken a thorough study? In light of recent reports, does CPSC 
intend to do a full review of possible effects of phthalate exposure?
    Answer. CPSC's primary interest in phthalates has been exposure 
levels resulting from the mouthing of children's products, especially 
pacifiers, teethers and rattles. In this regard, the CPSC conducted 
comprehensive studies of the two phthalates (DINP and DEHP) that were 
used in children's products intended to be mouthed. In regulating a 
product under the Federal Hazardous Substances Act (FHSA), the CPSC 
must consider the toxicity of a product and the consumer's exposure to 
that product under reasonably foreseeable handling and use. 
Accordingly, the CPSC prioritizes its research work related to 
phthalates by concentrating on those consumer products under the 
agency's jurisdiction where there is a concern about such toxicity and 
exposure.
    Foods and cosmetics would be the primary source of human exposure 
from phthalates other than DINP and DEHP, and those products fall under 
the jurisdiction of the Food and Drug Administration (FDA). Since 
manufacturers have removed DINP and DEHP from children's products that 
are intended to be mouthed, the CPSC has now initiated a study of 
substitutes that may be used to replace these phthalates. Additionally, 
CPSC staff continues to monitor the scientific literature on 
phthalates, including new data expected from the comprehensive National 
Research Council study on all phthalates.

    Question 2. The ``low-dose hypothesis'' claims that exposure to 
extremely low levels of certain substances could cause adverse health 
effects in humans. Some have criticized existing studies and reviews 
for looking at only high dosage exposure. Have any of the governmental 
reviews done by CPSC taken into account studies showing adverse health 
effects from low-dose exposure to BPA?
    Answer. The greatest potential for human exposure to BPA is from 
food contact items. The recent in-depth peer review conducted by the 
National Toxicology Program (NTP) stated that diet accounts for 99 
percent of human exposure. Accordingly, primary jurisdiction for BPA 
falls under the FDA. The CPSC has not conducted studies on adverse 
health effects from low-dose exposure to BPA and would defer to the 
authority and expertise of the FDA in this case. It should be noted 
that the NTP has released a comprehensive peer-reviewed report on this 
subject.

    Question 3. The results of studies into the potential health 
effects of BPA and phthalates conducted by the government, industry, 
and some in academia seem to vary quite widely in their results. How 
would you explain these differences? Does the CPSC take into account 
the safety of these chemicals when rendering its opinions?
    Answer. With regard to Bisphenol A (BPA), there are a large number 
of studies giving very varied results. Since the NTP Center for the 
Evaluation of Risk to Human Reproduction conducted a comprehensive Peer 
Review Panel of all the literature, and since BPA exposure results 
primarily from products under FDA jurisdiction, the CPSC has deferred 
to the NTP and FDA in the evaluation of BPA.
    With regard to phthalates, the European Union (EU) and the CPSC 
reached different conclusions in their risk assessments on DINP. While 
the European Union evaluated other phthalates as well, the CPSC did not 
since the primary exposure to children was from DINP. EU scientists and 
CPSC scientists discussed the differences in their respective risk 
assessments of DINP. When the CPSC was examining the health effects of 
DINP, it convened a Chronic Hazard Advisory Panel (CHAP), which is a 
panel of seven independent scientists recommended by the National 
Academy of Sciences, to review the studies and advise the Commission on 
its findings. The report from the CHAP, as well as the subsequent staff 
hazard and risk assessment, was based on a review of all available 
scientific studies. At the time of the CHAP, the results from the 
Commission behavioral observation study were not available. However, 
the CHAP concluded that there was no concern for infants who mouthed 
toys containing DINP for less than 75 minutes per day. The CPSC's 
behavioral observation study indicated that children's daily mouthing 
time of such toys is significantly less than that. Staff, therefore, 
concluded that there was not a risk of injury to children from such 
exposure. The EU risk assessment was exactly the same as the CPSC risk 
assessment, but the EU assumed an exposure that was larger than 75 
minutes per day, without doing any behavioral studies to substantiate 
such an assumption. CPSC's study showed that such an assumption was not 
justified.
    Thus, the CPSC staff's risk assessment was based upon exposure data 
developed in a well conducted behavioral observation study whereas the 
EU risk assessment was based upon an assumed exposure that was many 
fold higher than that observed in the CPSC study. As indicated 
previously, the FHSA requires that the Commission make a determination 
of risk based upon both hazard and exposure and in that way assess the 
safety of products when making its decisions.

    Question 4. Please explain the significance of low-dose exposures 
to BPA and how it relates to the traditionally held belief of ``the 
dose makes the poison''?
    Answer. As noted above, BPA falls under the primary jurisdiction of 
the FDA since diet accounts for 99 percent of human exposure. 
Accordingly, the CPSC defers to the expertise and authority of the FDA 
with regard to low-dose exposures to BPA.

    Question 5. How is the average person exposed to phthalates? What 
is the best way to reduce exposure to phthalates? Please explain the 
significance of phthalate mixtures.
    Answer. For products under CPSC's jurisdiction, the agency has been 
primarily concerned about phthalate exposure from the mouthing of 
children's products, especially pacifiers, teethers and rattles. In 
this regard, the CPSC has conducted comprehensive studies of the two 
phthalates, DINP and DEHP, where exposure to children from their use 
was a matter of concern. The staff's risk assessment also considered 
``background'' exposures from phthalates in addition to DINP; however, 
because most of the products studied by CPSC staff contained that 
single phthalate, the risk assessment focused on DINP. Most exposures 
from other phthalates were from food and other sources not regulated by 
the CPSC. As noted above, manufacturers subsequently removed DINP and 
DEHP from children's products that are intended to be mouthed, and the 
agency's current focus is on studying exposure to possible substitutes 
that may be used to replace these phthalates.

    Question 6. What are endocrine disruptors and how do they affect 
us?
    Answer. The term endocrine disruptors does not have a precise 
definition. It has been used to define endocrine active substances in 
animals as well as chemicals that bind to an estrogen or androgen 
receptor or are positive in other in vitro or in vivo tests. The 
relevance to human risk of positive results in these assays has not 
been determined and is still under considerable discussion by the 
scientific community at large.

    Question 7. Is there an established list of known endocrine 
disruptors?
    Answer. CPSC staff does not know of any such list nor is the term 
well defined.

    Question 8. Are there already alternatives to BPA and phthalates? 
Are these alternatives safer than what is currently being used? What 
science or studies exists into these alternatives?
    Answer. The scientific community does not know all the alternatives 
that are being used for phthalates. When switching from phthalates, 
manufacturers can continue to use polyvinyl chloride (PVC) containing a 
plasticizer other than a phthalate or they can use a completely 
different plastic than PVC. As noted above, the CPSC has recently 
initiated a study of phthalate substitutes. This study will determine 
what is known about the toxicity of some of these alternatives. In 
order to use a chemical in a consumer product, manufacturers are not 
required to do any particular toxicity testing. However, the FHSA 
requires that a manufacturer provide cautionary warning on products 
that meet the definition of a hazardous substance. The implementing 
regulation provides test methodologies for a manufacturer to test their 
products to determine if they meet the definition and requires warnings 
for the safe use and storage of the product. While manufacturers may do 
such testing for household chemical products, often the chemicals used 
in other types of consumer products have no toxicity information; the 
chemical may be more, less or equally toxic to the chemical it is 
replacing. Lack of toxicity data does not mean that the chemical is 
non-toxic; it just means the toxicity profile of the chemical is 
unknown. The CPSC does not have pre-market clearance authority for a 
product containing a new chemical or for a new use of an existing 
chemical. The Environmental Protection Agency (EPA) has been given 
those authorities under the Toxic Substances Control Act.

    Question 9. Do infants and children have the same immune and 
endocrine system as adults? Do studies take into account these 
differences?
    Answer. Depending upon the age of the infant/child and the 
particular system under consideration, there may be differences which 
would make the infant/child more or less sensitive than an adult. In 
some cases studies take these differences into account by using 
immature animals.

    Question 10. Have we seen many human studies on these chemicals? Is 
it even possible or ethical to conduct human studies?
    Answer. Intentional testing of chemicals for toxicity in humans is 
generally not done, precisely for the reason stated; it is not ethical. 
Epidemiological studies are sometimes conducted in which exposures are 
measured or estimated and the occurrence of adverse effects are 
recorded. Epidemiology is sometimes a powerful tool for assessing the 
toxicology of chemicals, but studies in humans are generally difficult, 
time-consuming and expensive. For example, many of the potential 
effects are ones that might occur after long-term exposure, may not be 
apparent for many years, and may have effects that are the same as 
those from other chemicals to which a person is exposed. There are a 
limited number of studies in which metabolites of phthalates have been 
looked for in the urine of humans. There are few epidemiological 
studies that exist and the effects in humans have not been clearly 
demonstrated.

    Question 11. Usually chemicals are tested one at a time. However, 
we come into contact with numerous chemicals every day. Do these 
studies simulate real world exposures and what is the best way to test 
chemicals?
    Answer. The toxicological effects of chemicals, in general, are 
tested one at a time because testing more than one chemical at a time 
would confound the results and it would be impossible to determine 
which of a group of chemicals tested together was responsible for the 
toxicologic endpoint. Because of the nearly limitless combinations of 
potential chemical exposures in the world, it is simply not possible to 
test mixtures in most cases. In certain cases, such as household 
chemical products, where one particular product contains a mixture of 
chemicals, the product generally is tested as a whole in the United 
States to determine appropriate classification and labeling. Further, 
if appropriate data are available for a given exposure scenario, a risk 
assessment could consider information about more than one chemical to 
determine the overall risk. The ``science'' of conducting risk 
assessments for mixtures is very new.

    Question 12. What about workers who are in the plants that 
manufacture phthalates and BPA. Are protections in place to make sure 
that they aren't unnecessarily exposed?
    Answer. CPSC's jurisdiction does not cover chemical exposures in 
the workplace. The Occupational Safety and Health Administration (OSHA) 
has jurisdiction over worker exposure to chemicals.
                                 ______
                                 
   Response to Written Questions Submitted by Hon. John F. Kerry to 
                          Dr. Marilyn L. Wind
    Question 1. In your written testimony, you explain the CPSC's 2003 
decision to deny the request to ban polyvinyl chloride (PVC), which 
contains phthalates. Has any new evidence surfaced since 2003 that 
would lead you to reconsider that decision?
    Answer. No new scientific evidence has surfaced since 2003 that 
would lead CPSC staff to recommend to the Commission that it reconsider 
its decision to deny the request to ban polyvinyl chloride which 
contains phthalates.

    Question 2. Do your agencies require labeling of consumer products 
that contain BPA or phthalates? Is there any control over current 
voluntary labeling of products as ``BPA-free'' or ``phthalate-free''?
    Answer. At present, the CPSC does not require labeling of products 
containing either phthalates or BPA. Under CPSC's governing statutes, 
the Commission has the authority to require labeling only if a product 
is determined to be a ``hazardous substance.'' CPSC's statutes are 
risk-based, not ``hazard-based.'' That is to say, the product in 
question must actually pose a risk of substantial illness or injury, 
not simply contain a potential toxicant. The FTC has jurisdiction over 
the labeling of products that make claims such as ``BPA-free'' or 
``phthalate-free.''

    Question 3. Can you please explain the different roles for FDA, 
CPSC and EPA in the study and regulation of phthalates, BPA and other 
endocrine disrupting chemical compounds? Do the agencies share data and 
information?
    Answer. Each regulatory agency has specific jurisdiction which is 
defined in their laws and regulations. FDA generally has responsibility 
over food, drugs, and cosmetics. EPA has broad authority over the 
manufacture of chemicals and the implementation of new uses for 
existing chemicals. The CPSC has responsibility generally over consumer 
products and their potential for substantial injury or illness in 
reasonably foreseeable use scenarios. In addition to defining their 
authority, these agencies' laws and regulations restrict certain types 
of information that can be shared outside each agency. For information 
that is not restricted, agency scientists often share scientific 
information, develop needed data together, and participate on 
interagency groups such as the National Toxicology Program and its 
committees and then process the information within their own statutory 
or regulatory framework.

    Question 4. Do we know what levels of BPA and phthalates are safe 
for human (particularly child) consumption?
    Answer. CPSC staff developed an Acceptable Daily Intake (ADI) for 
the amount of the phthalate DINP that could be ingested on a chronic 
basis and not result in an adverse health effect. CPSC staff has not 
developed ADI's for BPA or other phthalates since there were no 
exposures to these chemicals from consumer products under the agency's 
jurisdiction which would indicate that a determination of an ADI was 
warranted.
                                 ______
                                 
  Response to Written Questions Submitted by Hon. Daniel K. Inouye to 
                       John Peterson Myers, Ph.D.
    Question 1. What research is being done to determine the effects 
these chemicals have on wildlife?
    Answer. Wildlife research has received much less attention than 
potential effects of bisphenol A and phthalates on laboratory animals 
and on humans. There is very little funding available to pursue this 
line of inquiry.
    There is no published literature on phthalates and wildlife nor am 
I aware of any active research program currently studying this issue. I 
am aware of one unpublished study, carried out by Dr. Louis Guillette 
and his students (University of Florida, Gainesville), in collaboration 
with the U.S. Centers for Disease Control, finding unexpectedly and 
extremely high levels of phthalates in alligators living in the wild in 
Florida. Alligators sampled in the Everglades contained average levels 
of the phthalate MEHP in their urine of almost 100 parts per million. 
Because the CDC did the chemical analysis, and re-did their assay once 
these exceptional values were discovered, the data are credible. That 
is an extraordinarily high level to encounter in any non-experimental 
organism. Phthalate levels from alligators in central Florida are not 
quite as high, but still a cause for significant concern. The 
researchers believe that the source of exposure is the use of 
phthalates as stabilizers in herbicides being used to control aquatic 
vegetation. If that is the case, these levels might be quite 
widespread. Research examining the extent of phthalate contamination in 
wild animals and ascertaining the consequences should be a high 
priority.
    Two extensive reviews summarizing research on bisphenol A and 
wildlife have been published within the past 12 months:
    Crain, D., et al., 2007. An ecological assessment of bisphenol-A: 
Evidence from comparative biology. Reproductive Toxicology 23:225-239.
    Canadian Ministry of the Environment. 2008. Draft Screening 
Assessment for Phenol, 4,4'-(1-methylethylidene)bis- (80-05-7). 
Available for download at: http://www.ec.gc.ca/substances/ese/eng/
challenge/batch2/batch2_80-05-7.cfm.
    Because of the paucity of funding, there is no comprehensive effort 
in the U.S. to gather information about the effect of BPA on wildlife. 
Research dollars from the Federal Government into these issues have 
declined dramatically over the past decade. Almost all of the work 
underway is on aquatic organisms.
    In the U.S., the United States Geological Survey laboratory in 
Columbia, Missouri, is studying BPA and its effects on fish. Dr. Don 
Tillett and Dr. Kathy Richter are the principal scientists.
    In Japan, Dr. Koji Arizono at the University of Kumamoto is 
conducting research on BPA and fish.
    In Germany, Dr. Jorg Oehlmann at Johann Wolfgang Goethe University, 
Frankfurt, is the lead researcher on effects of BPA on marine snails.

    Question 2. What are the known effects of these harmful plastic 
chemicals on wildlife?
    Answer. To my knowledge, there are no published papers in the 
modern literature on phthalates and wildlife. This is extraordinary 
given the widespread use of phthalates as inert ingredients in 
pesticides. Given what is known about the reproductive harm caused by 
phthalates in laboratory animals, if the unpublished data from 
Guillette's lab (above) are representative, then widespread damage is 
likely to be occurring.
    Documented effects of BPA on wildlife are varied but much more 
needs to be learned. As summarized in the Canadian review (reference 
above), BPA at high doses is acutely toxic to aquatic organisms and 
considered highly hazardous. Low concentrations of BPA are sufficient 
to a range of adverse effects, especially at sensitive stages of 
development. These effects include feminization of male fish, delayed 
development of aquatic invertebrates, `super-feminization' of marine 
snails (leading to death of females), delayed emergence and mouthpart 
deformities in insects.
                                 ______
                                 
     Response to Written Questions Submitted by Hon. Mark Pryor to 
                       John Peterson Myers, Ph.D.
    Question 1. Some have pointed out the preponderance of studies 
showing the safety of these and other chemicals used in consumer 
products. It would seem that there are significantly less studies 
purporting the harm or risk of these chemicals. How do you respond to 
these criticisms?
    Answer. The reverse is true. Many more studies have been published 
that find adverse effects resulting from low levels of exposure. This 
pattern itself has been published in the peer-reviewed literature: vom 
Saal, F. and C. Hughes, 2005. An Extensive New Literature Concerning 
Low-Dose Effects of Bisphenol A Shows the Need for a New Risk 
Assessment. Environmental Health Perspectives 113:926-933. In an 
extensive review of the literature, they showed that over 90 percent of 
government-funded studies of low-dose effects found adverse effects. An 
update of their tally through July 2007 shows that 166 out of 195 (85 
percent) studies published on the effects of BPA at low doses find 
adverse consequences. Out of 14 industry-funded studies to date, none 
have found adverse effects. Out of 181 government-funded studies, 166 
(92 percent) have found adverse effects.
    There is a vital difference between industry-funded studies and 
those funded by government (mostly by NIH). The NIH-funded studies must 
meet the highest standards of scientific rigor simply to get funded. 
They use highly sophisticated and sensitive assays that incorporate the 
latest knowledge from medicine, endocrinology, reproductive 
development, neurobiology, etc. The scientists, to be competitive in 
this day and age of shrinking research budgets, must be among the best 
in the world. Their work focuses not only on the structural changes 
that are caused, but also on the genetic mechanisms underlying those 
changes. That is key, because BPA's principal mode of action is through 
altering the expression of genes.
    In contrast, industry-funded studies are using techniques dating to 
the middle of the last century, literally. They measure gross changes 
in anatomy and weight. And they do so poorly, because they usually 
involve multiple technicians with limited training to carry out the 
measurements. This use of multiple technicians introduces variability 
that makes it more difficult for them to find significant results.
    Plastic industry representatives are critical of the sample sizes 
of NIH-funded research, and use that criterion to exclude many 
excellent studies. This is a false criticism. NIH requires scientists 
to use as few animals as necessary. NIH-funded scientists respond to 
this requirement in two scientifically-tested ways. First, they perform 
a statistical power analysis which allows them to calculate, based on 
preliminary results, how large a sample will be required to achieve a 
given level of significance, if the preliminary results are valid. 
Second, they either use only one technician for crucial measurements, 
reducing variability, or they carefully examine inter-observer 
variability, and factor that into their analysis. These are standard 
NIH procedures.
    Importantly, the estimate of statistical significance factors in 
its calculation the sample size of the study. A small sample size 
requires a bigger difference between controls or experimentals, or less 
variance, or both, to achieve a given level of significance. Insisting 
upon an arbitrary sample size is not scientific and ignores basics 
statistics.
    Industry often points to the fact that its experiments follow 
``Good Laboratory Practices'' or GLP. This says nothing about the 
quality of the science, only that they followed certain standards of 
record-keeping that were established after massive fraud was found in 
the results of contract laboratories.
    The most recently published study from an industry laboratory 
purporting to find no effect of BPA on the developing mouse prostate is 
a good example of how GLP does not translate into good science:
    Tyl, R., et al., 2008. Toxicological Sciences, in press. This 
study's major failure is its inappropriate use of a positive control. 
Scientists use positive controls to demonstrate their competence at 
performing the experiment. A positive control is performed by exposing 
a group of animals to an agent known to cause an effect. In this case, 
Tyl et al.'s published data show that the strain of mice they used 
required a high dose of their positive control, estradiol. It would not 
respond to a low dose. If the strain wouldn't respond to a low dose of 
the positive control, it couldn't be expected to respond to a low dose 
of bisphenol A, which typically, for this type of effect, is 100 to 
10,000 times less powerful than estradiol. Another weakness in this 
study was the choice of which positive control to use. Estradiol was a 
highly unusual choice, which means there is no scientific literature 
against which to compare the results of the experiment and help 
understand why it required such high doses.

    Question 2. How precautionary should we be when the weight of 
evidence seems to show these chemicals are safe?
    Answer. The weight of the evidence shows that bisphenol A is not 
safe. We should immediately begin phasing out uses that lead to human 
exposure. The strongest evidence is for developing organisms. Therefore 
the highest priority should be placed on measures that will reduce 
exposures for pregnant women, infants and children. Some evidence also 
indicates risk for men with prostate cancer (it interferes with the 
standard medical treatment for prostate cancer). We should also 
invigorate investments in `green chemistry' to identify safe 
replacements.

    Question 3. Please explain the significance of low-dose exposures 
to BPA and how it relates to the traditionally held belief of ``the 
dose makes the poison''?
    Answer. Bisphenol A is a synthetic sex hormone. Endocrinologists 
have known for years that all hormones can have different effects at 
different doses. This is called a `biphasic response' or a `non-
monotonic dose response curve.' It is well established in the 
literature of medical endocrinology. This means that the effects seen 
at one dose, for example a high dose, may be completely unrelated to 
other effects seen at low doses. With bisphenol A, at very high levels 
it is toxic. For example, the experiments used to establish the current 
FDA and EPA standards showed that at relatively high doses (50 mg/kg/
day) it causes weight loss in mice. At low doses, however, BPA turns on 
genes that are responsive to estrogen. These responses and their 
effects are very different from the ones seen at the levels at which 
BPA is toxic.
    This means that tests of the effects of BPA at high doses can't be 
used to predict what will happen following a low-dose exposure. It 
directly contradicts a fundamental assumption of toxicology that 
``biological effects increase as the dose increases.'' At one dose 
level BPA will alter the expression of one set of genes while at 
another it will affect a different set. And at high levels it is 
overtly toxic, so the mechanism of impact is not through alteration of 
gene expression.

    Question 4. How is the average person exposed to phthalates? What 
is the best way to reduce exposure to phthalates?
    Answer. Exposures to phthalates come from many, indeed ubiquitous 
sources, although the type of phthalate varies significantly depending 
upon the type of product or use. Common sources of exposure include 
leaching from PVC plastic, dermal absorption of phthalates used in 
cosmetics and personal care products, exposure to phthalates in dust 
generated by abrasion of phthalate containing products, including 
carpeting and building materials.
    Phthalate exposure can be reduced by avoiding products that contain 
them. Unfortunately, products are not required to identify their 
phthalate content in labels. Some do. Two general rules of thumb: do 
not heat (including microwave) food or drinks in plastics; avoid 
unnecessary personal care products.

    Question 5. Please explain the significance of phthalate mixtures.
    Answer. Research that has been published over the past 5 years has 
drawn attention to the fact that mixtures of contaminants can have 
effects even when each of the components of the mixture is at a dose at 
which, by itself, it can cause no harm. Work by Dr. Earl Gray (U.S. 
EPA) has extended these basic findings into research on phthalates. He 
has shown that a mixture of different phthalates, each one at a level 
insufficient to cause harm, can cause dramatic harm in exposed animals.
    This is important because current regulatory assessments of 
phthalates are all evaluate phthalates one-by-one. No accounting is 
made for the fact that virtually all people are exposed to multiple 
phthalates continuously.

    Question 6. What are endocrine disruptors and how do they affect 
us?
    Answer. Endocrine disruptors are chemical contaminants that 
interfere with hormone action. There are multiple mechanisms. The best 
studied involve altering the expression of genes under the control of 
hormones, either directly or indirectly. Some endocrine disruptors, for 
example BPA, mimic the action of hormones. BPA is an estrogen mimic. It 
causes effects that resemble the effects of adding estrogen. Other 
endocrine disruptors interfere with the action of hormones. For 
example, phthalates interfere with testosterone and other androgens. 
They are deemed `anti-androgens.'
    Interfering with hormone action can cause adverse effects by 
altering the timing and pattern of gene expression. During fetal 
development, for example, it is imperative that gene expression follow 
a normal pattern; otherwise development can be adversely affected.
    Initially scientists believed that compounds like bisphenol A were 
`weak' estrogens. That was because they were focused on only one 
mechanism of action. In the last 5 years research has revealed that BPA 
and similar compounds can be just as powerful as estrogen.

    Question 7. Is there an established list of known endocrine 
disruptors?
    Answer. There have been several efforts to compile lists of 
endocrine disruptors, but none incorporate the most recent research.
    Here are several existing lists:

    IEH. 2005 Mar. Chemicals purported to be endocrine disrupters. A 
compilation of published lists. Leicester, UK: MRC Institute for 
Environment and Health. (Web Report W20). Available at: http://
www.silsoe.cranfield.ac.uk/ieh/pdf/w20.pdf.

        Abstract: [A total of 966 compounds or elements were identified 
        as having been suggested to be established or potential 
        endocrine disrupters (EDs). The list is based on the BKH (2000) 
        report; Environmental Defense--Scorecard sources; the German 
        Federal Environment Agency; the UK Institute for Environment 
        and Health; the California EPA; the Japan Chemical Industry 
        Ecology-Toxicology & Information Center and other publications. 
        Online databases Medline, Biosis, Embase, NTIS, ToxNet, 
        SciSearch, Pascal and CA Search were searched during the period 
        Jan 2000-Jan 2002. Chemicals are grossly classified into 
        General Anthropogenic (alcohols & glycols; aromatic 
        hydrocarbons; anilines & derivatives; benzene & derivatives; 
        benzophenones and derivatives; biphenyls and metabolites; 
        dioxins and metabolites; diphenyl derivatives; diphenyl ethers; 
        furans and metabolites; naphthols & naphthalenes; phenols and 
        derivatives; phthalate esters and derivatives; siloxanes; 
        styrene and derivatives; miscellaneous), Biocides (carbamates; 
        fungicides; herbicides; organochlorines; organophosphates; 
        pyrethroids; miscellaneous), Biogenic (anthraquinones; 
        flavanones; isoflavonoids; lignans; phenolic acids; plant-
        derived substances; vitamins; miscellaneous), Pharmaceuticals, 
        Inorganic & Organometals and Consumer Products. There are 6 
        tables corresponding to these categories, giving the chemical 
        name, CAS number, chemical group and/or use, references (mostly 
        from previous compilations), and Notes (type of endocrine 
        disruption activity, and/or level of concern or (un)certainty). 
        Five pages of references follow.]

    European Commission. Endocrine Disrupters website. http://
ec.europa.eu/environment/endocrine/strategy/substances_en.htm. This 
website links to the documents listed below:

    DHI. 2007 May. Study on enhancing the Endocrine Disruptor priority 
list with a focus on low production volume chemicals. Revised report to 
European Commission DG ENV. ENV.D.4/ETU/2005/0028r. 252 pp. http://
ec.europa.eu/environment/endocrine/documents/final_report_2007.pdf.

    Wrc-NSF. 2002 Nov. Study on the scientific evaluation of 12 
substances in the context of endocrine disrupter priority list of 
actions. 613 pp. http://ec.europa.eu/environment/endocrine/documents/
wrc_report.pdf.

    BKH-RPS. 2002 Nov. Study on gathering information on 435 substances 
with insufficient data. 279 pp. http://ec.europa.eu/environment/
endocrine/documents/bkh_report.pdf#page=1.

    BKH Consulting Engineers, TNO Nutrition and Food Research. 2000 Nov 
10. Toward the establishment of a priority list of substances for 
further evaluation of their role in endocrine disruption. Final Report 
(incorporating corrigenda to final report dated 21 June 2000).: 
European Commission DG ENV. M0355008/1786Q/10/11/00. PDFs (16 files) 
available at http://ec.europa.eu/environment/endocrine/strategy/
substances_en.htm, and also available at: http://europa.eu.int/comm/
environment/docum/01262_en.htm (scroll down).

         Abstract: [A list of 564 chemicals (including metals) (see 
        Annexes 9 and 10) classified as ``manmade'' were compiled from 
        other endocrine disruptor lists and classified as follows: 74 
        with high-production volume; 51 highly persistent; and 29 
        metals. The 146 chemicals discussed in the Annexes 6, 7, 12 and 
        13 refer to these three groups combined; the remainder are 
        discussed in Annex 8. For extensive references see Annexes 9 
        and 11. Chemicals listed in table 3-6 are the same as those 
        covered by Annex 14.]

    Question 8. Are there already alternatives to BPA and phthalates? 
Are these alternatives safer than what is currently being used? What 
science or studies exists into these alternatives?
    Answer. There are alternatives for many uses. For example, 
manufacturers have already brought to market plastic baby bottles that 
are not made from polycarbonate, the plastic based on BPA. One of the 
replacements is based upon a different type of chemistry that by 
definition is vastly less likely to leach anything even under 
conditions of stress. That is because of the nature of the chemical 
bonds. The bonds that bind BPA into polycarbonate are weak and dissolve 
readily. The bonds that bind polyether sulphone are exceedingly 
resistant to degradation. By definition they will be safer than BPA. 
Glass baby bottles are much safer too.
    One of the most problematic of replacements is for the use of BPA 
as an epoxy resin to line food cans. There is no perfect substitute 
available for this lining. However, Japanese manufacturers have found a 
way to reduce BPA leaching by 95 percent. And some manufactures of baby 
formula have decided that they don't need to use cans at all. Instead 
they put the formula in cardboard containers. These are available in 
the U.S. and Japan.

    Question 9. Do infants and children have the same immune and 
endocrine system as adults? Do studies take into account these 
differences?
    Answer. The fetus, infants and children are developing into adults. 
As they develop, all their physiological, neurological and immune 
systems are maturing. That has two important implications for exposure 
to endocrine disruptors. First, their developing systems are responding 
constantly to hormonal signaling that can be disrupted by endocrine 
disruptors. And the consequences of that disruption, because it alters 
how development is unfolding, can have life long consequences. Those 
developmental processes are already completed in adults, so they are 
not vulnerable in the same way. Second, fetuses and the young do not 
produce all the enzymes that adults produce. Some of these enzymes are 
essential for detoxifying toxicants that get into the blood stream. 
Without a mature set of enzymes, fetuses and the young are less able to 
defend themselves.
    This is particularly relevant to BPA. The enzyme that detoxifies 
BPA in mammals, including people, is produced at much lower levels in 
the young. That makes the young more vulnerable to the same exposure. 
It is also part of some `inside baseball' arguments over toxicity 
testing in BPA. Industry argues that because most human exposure to BPA 
is oral, only oral tests on animals are relevant. This criterion would 
eliminate some of the most striking low-dose results, which used 
injection or subcutaneous implants. However, these experiments were 
designed to mimic how a fetus experiences BPA. From the perspective of 
the fetus, it doesn't matter how the BPA gets into its mother's 
bloodstream. The National Toxicology Program in its review of the 
`expert panel' assembled by the Center for the Evaluation of Risks to 
Human Reproduction (CEHRH) agreed with this assessment, based on data. 
The experiments chose doses that fall well within the range of 
concentrations that have been measured in mother's bloodstreams. Hence 
they are highly appropriate for considering risk to humans.

    Question 10. Have we seen many human studies on these chemicals? Is 
it even possible or ethical to conduct human studies?
    Answer. There have been almost no published studies of the effects 
of BPA on humans. There is a small number of epidemiological studies of 
effects of phthalates on people. They consistently report adverse 
effects. Endpoints range from reproductive tract malformations to sperm 
abnormalities to immune system problems (asthma).
    None of these studies involve application of phthalates or BPA to 
humans. That would be unethical. They are all epidemiological studies, 
which examine how different levels of exposure alter the risk of 
specific endpoints.

    Question 11. Usually chemicals are tested one at a time. However, 
we come into contact with numerous chemicals every day. Do these 
studies simulate real world exposures and what is the best way to test 
chemicals?
    Answer. Studies that test chemicals only one at a time are 
insufficient to assess risks in the real world. We come into contact 
with hundreds, if not thousands, of chemicals every day. Sophisticated 
research that has been conducted over the past years shows with 
scientific certainty that regulations based on tests done on chemicals 
one-at-a-time can dramatically underestimate risks. What this research 
shows repeatedly is that when you have a mixture of chemicals, each one 
at a level that causes no effect, collectively they can cause severe 
damage.
    Sometimes the effects are what you would expect based on the 
mechanisms of toxicity of the components of a mixture. But some results 
indicate that mixtures can cause completely unpredictable effects, for 
example, inducing such stress that the immune system is compromised and 
the animal becomes vulnerable to a common bacteria and dies from 
bacterial meningitis. No test in use today to develop toxicological 
standards takes these possibilities into account.
    Testing of chemicals must start with an explicit requirement to 
test over a wide dose range. Current testing is usually carried out 
over a narrow and, compared to human exposure, relatively high level. 
The results of these high dose tests are then used to estimate a safe 
level of exposure, by incorporating safety factors that take a `no 
observed adverse effect level' (NOAEL) to a `reference' or acceptable 
dose, which might be 100 to 1,000 times lower than the NOAEL. That 
reference dose is never tested directly. It is assumed to be safe 
because of the assumption of toxicology that (above) ``biological 
effects increase as the dose increases.'' But hormonally-active 
compounds like BPA and phthalates can have effects at low doses that 
are completely unpredictable from effects at high doses.
    Having a complete dose-response curve is the first step in working 
with mixtures. Scientists have learned that under some circumstances 
they can combine the dose-response curves of components of a mixture to 
predict with reasonable accuracy how the mixture will behave. This 
includes examples like those described above where the levels of any 
one of the components was too low to cause an effect, but the effect of 
the mixture was very significant.
    Another vital element of testing is to remove it from pressure from 
economic interests. Experience has repeatedly shown, with chemicals 
like tobacco, pharmaceuticals, lead, vinyl chloride, chromium, 
bisphenol A, tris, etc. that data from laboratories with economic ties 
to the manufacturers of the material produce data that cannot be 
trusted.
    Another weak part of the system that leads from testing to 
regulatory standards is how regulatory agencies assess existing data. 
The overwhelming pattern is for agency assessments to give inordinate 
weight to industry data, even though industry data have clear biases. 
They often reject NIH-funded data, thus ignoring the most sophisticated 
research available. This has been the overwhelming experience with 
bisphenol A. A parallel example with another chemical was just revealed 
through investigative reporting by the Journal Sentinel (Milwaukee, 
WI), in an outstanding article published on 13 July 2008. The Journal 
Sentinel published a similar analysis of bisphenol A in 2007. Here are 
links to the two articles.
    Hazardous flame retardant found in household objects. A flame 
retardant that was taken out of children's pajamas more than 30 years 
ago after it was found to cause cancer is being used with increasing 
regularity in furniture, paint and even baby carriers, and EPA's safety 
assessment is biased toward industry, again. Milwaukee Journal 
Sentinel, Wisconsin. 13 July 2008 http://www.jsonline.com/story/
index.aspx?id=771917.
    Warning: Known to cause severe health risks to laboratory animals, 
bisphenol A is in you. Investigative reporting finds that the Federal 
Government's assurances that bisphenol A is a safe chemical are based 
on outdated and incomplete government studies and science mostly funded 
by the chemical industry. Milwaukee Journal Sentinel, Wisconsin. 2 
December 2007 http://www.jsonline.com/story/index.aspx?id=692145

    Question 12. What about workers who are in the plants that 
manufacture phthalates and BPA. Are protections in place to make sure 
that they aren't unnecessarily exposed?
    Answer. This is a matter of significant concern because permissible 
occupational exposures are based upon existing standards. They will not 
have factored in any of the considerations that are driving concerns 
about endocrine disrupting compounds. Few occupational studies are 
available on risks of phthalates, and none for bisphenol A.
                                 ______
                                 
   Response to Written Questions Submitted by Hon. John F. Kerry to 
                       John Peterson Myers, Ph.D.
    Question 1. Why are there such dramatically different results on 
the low-dose effects of BPA between the results of studies sponsored by 
the chemical industry and studies conducted by academics or government 
entities?
    Answer. Studies conducted by academics or government entities like 
the NIH use highly sophisticated methods that are at the cutting edge 
of medical science today. Industry funded studies, in contrast, still 
rely upon methods developed in the middle of the last century and use 
assays that are far weaker than those used by NIH-funded scientists. 
For example, the `debate' over prostate effects of BPA contrasts 
studies by NIH-funded scientists that began with simple measurements of 
prostate weight (in 1997) but now involve highly sophisticated 
computer-based reconstructions of prostate morphology during 
development and analyses of changes in the ways that genes are 
expressed in specific key tissues of the prostate, with those of 
industry-funded scientists who in 2008 published yet another failed 
study on prostate size. Industry research has offered no conflict with 
the more sophisticated research because they haven't conducted it. Yet 
the NIH-funded work not only shows the simple weight effect but also 
shows how it happens in exquisite microscopic detail and reveals the 
molecular mechanisms that cause it to happen.
    Industry funded studies also continue to be based on the assumption 
that ``biological effects increase as the dose increases.'' Decades of 
work in basic medical science with hormones shows that to be a false 
assumption for chemicals that behave like hormones. BPA is a synthetic 
hormone.
    An important historical point: The field of endocrine disruption, 
and specifically research on bisphenol A, has attracted many scientists 
from other fields who have brought into this research area tools and 
knowledge that have been foreign to classic toxicology. Scientists like 
Dr. Gail Prins (University of Illinois), Dr. Shuk Mei Ho (University of 
Cincinnati), Dr. Patricia Hunt (Washington State University), Dr. Anna 
Soto (Tufts University) and Dr. Frederick vom Saal (University of 
Washington) are all major players in their own fields of science, 
publishing in the leading scientific journals of the world and highly 
competitive for NIH grants. They ask questions toxicologists wouldn't 
have asked because they know that hormones and hormone like substances 
don't follow classic toxicological patterns. They bring in vastly more 
powerful techniques, newer and more sensitive assays, etc. They do 
research that is not within the ability of traditional toxicologists.

    Question 2. In light of dozens of advanced studies over the past 
several years, in conjunction with the recent assessment from the 
National Toxicology Program, do you believe that the Federal Government 
should control exposure to BPA and phthalates?
    Answer. Current science justifies regulatory action to reduce 
exposures to phthalates and bisphenol A. It is impossible for 
individual consumers to have sufficient information to make informed 
choices--especially when most of the time the content of consumer 
products is not revealed. But it should not fall to mothers to become 
chemical engineers and toxicological experts to buy toys and bottles 
for their children. For both phthalates and BPA, enough data are in 
hand to justify reducing exposure levels, first by eliminating their 
use in materials designed to hold food or water, or to purposefully 
come in contact with infants or babies mouths. Simultaneously, a 
rigorous investigation should be launched to identify other major 
sources of human exposure. While we know that levels in people today 
are higher than those sufficient to cause harm in laboratory animals, 
we do not have a comprehensive picture of the sources of human 
exposure, nor can we explain why human levels are as high as they are. 
Scientists suspect there are significant unidentified sources yet to be 
found.

    Question 3. Can consumers trust products that are currently labeled 
as ``BPA-free'' or ``phthalate-free''?
    Answer. That is an empirical question that remains to be answered 
for most instances. Glass baby bottles and stainless steel sports 
bottles do not contain BPA. It is possible to make the products that 
have been labeled ``BPA-free'' with BPA, and ``phthalate-free'' without 
phthalates, but whether individual companies are misrepresenting their 
products can only be determined through analysis.

    Question 4. What has been the experience of the European Union in 
phasing out phthalates in toys and childcare products? Has this been a 
significant logistical and manufacturing challenge for regulators and 
industry?
    Answer. I don't know the answer to that question. I do know that 
when I visited Japan in November 2008 during the Christmas shopping 
season, shelves were full of plastic toys that did not contain 
phthalates.

    Question 5. Why are low-dose effects of endocrine-disrupting 
chemicals like BPA and phthalates more dangerous than those of other 
compounds?
    Answer. This question strike to the heart of a huge blind spot in 
the current system of establishing health standards for exposures to 
chemicals.
    For many chemicals . . . perhaps even most, although scientists 
haven't asked . . . it is safe to assume that ``biological effects 
increase as the dose increases.'' This assumption is at the core of how 
risks of exposure are assessed. The problem is that endocrinologists . 
. . scientists and physicians who study hormones . . . know that the 
effects of a hormone at one dose can be completely different, and 
indeed unpredictable, from the effects at another dose. High doses can 
be overtly toxic. Intermediate doses will turn on one set of genes but 
not another. Low doses will turn on yet another set of genes. The 
responses to those doses will be very different. If the genes turned on 
by low doses cause deleterious effects, as they definitely do with 
bisphenol A, then traditional toxicology testing will be completely 
blind to the risk.
    I am including here an essay I wrote about this phenomenon with Dr. 
Frederick vom Saal. It was published in the December issue of San 
Francisco Medicine, the journal of the San Francisco Medical Society.
    http://www.sfms.org/AM/Template.cfm?Section=Home&TEMPLATE=/CM/HTM
LDisplay.cfm&CONTENTID=2506&SECTION=Article_Archives.
                                 ______
                                 

  Bringing environmental regulations up to date: Should public health 
    standards for endocrine-disrupting compounds be based upon 16th 
                 Century dogma or modern endocrinology?

                   J.P. Myers[1] and F.S. vom Saal[2]

    Health standards established in the United States for exposure to 
toxic chemicals rest upon a core assumption: high-dose testing 
procedures used in regulatory toxicology adequately predict potential 
low-dose effects. Scientific discoveries over the past decade have 
profoundly challenged that assumption as information has grown about 
the commonness of contaminants that behave like hormones.
    Endocrinologists long ago discovered that hormones have effects at 
low serum concentrations that can differ dramatically, and 
unpredictably, from those caused at high levels.\1\ Indeed, sometimes 
they can be diametrically opposed. This endocrinological reality stands 
in direct conflict with any assumption that high dose studies predict 
low dose impacts. If contaminants with hormonal characteristics, known 
as endocrine disruptors, behave similarly, then the regulatory tests 
used to establish safety standards may be blind to important impacts.
    A growing body of research now confirms that endocrine disruptors, 
like hormones, can also contradict the expectations of traditional 
regulatory testing. This creates the strong likelihood that some health 
standards currently used to set exposure limits for the American public 
are too weak.
    To the non-endocrinologist, it seems logical that higher doses 
would lead to larger effects. This assumption has been at the core of 
toxicology for centuries, beginning with Paracelsus's 16th century 
observation that ``All things are poison and nothing is without poison, 
only the dose permits something not to be poisonous.'' His quote has 
been paraphrased to ``the dose makes the poison'' and is generally 
interpreted to mean that the higher the exposure, the greater the 
impact.
    For many contaminants, toxins, poisons and pharmaceuticals, this 
assumption has helped protect public health. But substantial evidence 
is now in hand showing that people are exposed to hundreds of 
chemicals, if not more, that can behave like hormones.
    Some endocrine-disrupting chemicals are produced in very high 
volumes. The compounds of greatest concern include plastic monomers and 
plasticizers used widely in common consumer goods, leading to virtual 
ubiquitous exposure in the U.S. and other developed countries. For 
example, the plastic monomer, bisphenol A (BPA) was discovered to be an 
estrogen in the 1930s, but now it is used as the basic chemical 
building block for polycarbonate plastic and an epoxy resin used to 
line most food cans sold in U.S. supermarkets today.
    The chemical characteristics of polycarbonate and the epoxy resin 
guarantee that normal use will contaminate food and water that comes 
into contact with BPA-based materials, especially if heated. Most 
plastic baby bottles are made with polycarbonate and baby formula cans 
are lined with the resin. This will result in substantial, unavoidable 
exposures for infants fed warmed formula.
    Many studies have now shown that BPA is capable of causing a wide 
range of adverse effects in laboratory studies at serum concentrations 
beneath the median level found in people throughout the developed 
world.\2\ The adverse effects caused by fetal exposure and infant 
exposure to BPA in animal experiments include breast cancer, prostate 
cancer, impaired fertility, cystic ovaries, uterine fibroids, 
hyperactivity and obesity. The current EPA and FDA health standards for 
BPA, however, are based upon traditional toxicological testing 
conducted in the 1980s. Modernizing the BPA standard based on current 
science would require lowering acceptable exposures by a factor of at 
least 5,000-fold and would require elimination of BPA from many common 
products.
    Driven by a need to be cost-effective, regulatory toxicology has 
applied the `dose makes the poison' concept in practice by testing 
first at high doses and then testing at successively lower doses until 
no response, or little response, is seen. Often only 3 or 4 doses are 
used and for the vast majority of chemicals these rarely if ever are 
low enough to be comparable to levels experienced by the general 
public. The assumption is that this high dose testing protocol predicts 
the types of effects that might take place at much lower levels. And 
because `the dose makes the poison,' the expectation is that by working 
down the dose-response curve, from a level that clearly causes an 
effect to one that doesn't, this process can identify exposures beneath 
which there will be no harm.
    Endocrinology, however, is replete with cases in which hormone 
action at low levels differs dramatically from hormone action at high 
levels. For example, administering newborn mice a high dose (1000 mg/
kg/day) of the estrogenic drug diethylstilbestrol (DES) cause weight 
loss in adult mice. In contrast, a dose of 1 mg/kg/day causes grotesque 
obesity in adulthood.\3\
    Another example with clinical implications comes from the well-
known `tamoxifen flare.' Tamoxifen is useful clinically because at high 
doses (administered daily at 20 to 40 mg daily) it is an anti-estrogen, 
suppressing proliferation of breast cancer cells and producing tumor 
regression.\4\ Early during treatment, however, when tissue levels are 
still rising, tamoxifen administration can cause several estrogenic 
effects including a slight increase in tumor size. Research by Wade 
Welshons at the University of Missouri has explored the molecular 
mechanisms of the tamoxifen flare and finds that at serum 
concentrations 10,000 times beneath the level used to suppress breast 
cancer cell proliferation, tamoxifen acts as an estrogen, actually 
promoting proliferation.\5\ Ironically, his calculations show that if 
one were to use standard risk assessment procedures with the tamoxifen 
dose-response curve--identifying the highest exposure with no 
discernable effect and then applying a series of safety factors that 
take into account various sources of uncertainty--the concentration 
with maximum proliferative effect would be identified as a safe level 
of exposure. (Welshons, pers. comm.).
    In the tamoxifen flare, the dose-response curve showed inhibition 
at high levels and proliferation at low, i.e., completely opposite 
effects. This is a special case of what are called non-monotonic dose-
response curves: dose-response relationships in which the slope of the 
line plotting response as a function of dose changes its sign (positive 
to negative or the reverse) somewhere over the range of doses used.
    Clinicians who treat women and men for hormone-stimulated diseases 
(uterine fibroids, prostate cancer) advise their patients who take a 
hormone (Lupron) that some adverse effects occur during the initial 
phase of treatment. This is due to the fact that as the amount of the 
drug increases after injection, the low doses of Lupron result in the 
ovaries producing estrogen or testes to producing testosterone, and 
only after reaching a high dose is the drug's desired effect, 
inhibition of estrogen or testosterone production, achieved--opposite 
effects occur at low and high doses. This is not just true for 
hormonally active drugs, but is true for all hormones and hormone-
mimicking chemicals used in products.
    As research has progressed in the toxicology of endocrine-
disrupting compounds, non-monotonic curves have been reported 
regularly.\6\ One of the earliest examples involved the response of the 
mouse prostate to exposure to several different estrogenic compounds 
during fetal development.\7\ These experiments examined the adult 
prostate weight following fetal exposure, separately, to estradiol or 
diethylstilbestrol (DES), and analogous non-monotonic findings now 
exist for BPA in human prostate cancer cells.\8\ Each experimental 
series, conducted over an extremely wide range of doses, showed that 
the highest exposures did not differ from the controls, but that 
intermediate doses led to significant increases in prostate weight and 
also to sensitivity to androgen stimulation. The dose-response curve 
took the shape of an inverted `U' (a descriptor now used in the 
literature to describe this type of non-monotonic dose-response curve). 
If the dose range had been extended even higher, the response would 
have fallen significantly beneath the controls as exposure moved into a 
concentration at which the compounds were overtly toxic. This was 
demonstrated at the level of individual genes involved in regulating 
prostate growth.\9\
    Other endocrine-disrupting compounds demonstrating non-monotonic 
patterns include the phthalate DEHP, the pesticides DDE, dieldrin, 
endosulfan and hexachlorobenzene, and arochlor 1242, a PCB (reviewed in 
Myers and Hessler 2007). Some of the reported effects include strong 
exacerbation of allergic reactions following exposures well beneath 
current safety standards.
    Extensive evidence is now available on the molecular and 
physiological mechanisms that are responsible for these findings. At 
very low doses hormones can stimulate the receptors in cells that allow 
the hormone to cause effects in the cells (called ``receptor up 
regulation''), while at higher doses, receptor ``down regulation'' 
occurs and the number of receptors available to mediate the action of 
the hormone is reduced (Medlock et al., 1991). Also, there are myriad 
hormonal feedback mechanisms between the brain, pituitary gland and 
hormone producing organs (thyroid gland, adrenal glands, ovaries, 
testes) that contribute to the presence of non-monotonic dose-response 
curves.
    The chemical risk assessment establishment has been unresponsive to 
the fact that one of their core assumptions has been invalidated. 
Hence, no standard for any contaminant has incorporated these well-
established findings from endocrinology. Instead, standards continue to 
be based upon testing procedures that assume high dose testing can 
adequately predict low dose results.
    The American public depends upon regulatory agencies to set public 
health standards that will avoid harmful exposures. It is time that the 
FDA and EPA move beyond 16th Century dogma and begin using 21st Century 
scientific knowledge to accurately determine the safety of the 
chemicals being used in plastic, toys, food containers, pesticides, 
cosmetics, building materials, clothes--in other words, countless 
products and materials we incorrectly assume are safe. Given the wide 
range of health effects now shown to be caused in animals by exposure 
to these contaminants, modernizing the standards may reap large 
benefits for public health.
    [1] Dr. Myers is Chief Scientist for Environmental Health Sciences, 
609 E High St., Charlottesville, VA 22903.
    [2] Dr. vom Saal is Curators Professor in the Division of 
Biological Sciences, 105 Lefevre Hall, University of Missouri, 
Columbia, MO 65211.
References
    \1\ Medlock, K.L., C.R. Lyttle, N. Kelepouris, E.D. Newman and D.M. 
Sheehan. 1991. Estradiol down-regulation of the rat uterine estrogen 
receptor. Proc. Soc. Exp. Biol. Med. 196:293-300.
    \2\ Vandenberg, L.N., R. Hauser, M. Marcus, N. Olea and W.V. 
Welshons. 2007. Human exposure to bisphenol A (BPA). Reproductive 
Toxicology 24:139-177.
    \3\ Newbold, R.R., E. Padilla-Banks, R.J. Snyder and W.N. 
Jefferson. 2005. Developmental exposure to estrogenic compounds and 
obesity. Birth Defects Research (Part A) 73:478-480.
    \4\ Hortobagyi, G.N. 2001. Endocrine treatment of breast cancer. pp 
2039-2046 in Becker, K.L. (ed), Principles and practices of 
endocrinology and metabolism. 3rd edition. Lippincott Williams and 
Wilkins, Philadelphia.
    \5\ Welshons, W.V., K.A. Thayer, B.M. Judy, J.A. Taylor, E.M. 
Curran and F.S. vom Saal. 2003. Large effects from small exposures. I. 
Mechanisms for endocrine disrupting chemicals with estrogenic activity. 
Environmental Health Perspectives 111:994-1006.
    \6\ Myers, J.P. and W Hessler. Does `dose make the poison.' 
(downloaded from http://www.environmentalhealthnews.org/
sciencebackground/2007/2007-0415nmdrc.html 15 December 2007).
    \7\ vom Saal F.S., B.G. Timms, M.M. Montano, P. Palanza, K.A. 
Thayer, S.C. Nagel, et al., 1997. Prostate enlargement in mice due to 
fetal exposure to low doses of estradiol or diethylstilbestrol and 
opposite effects at high doses. Proc. Natl. Acad. Sci. USA 94:2056-
2061.
    \8\ Wetherill Y.B., C.E. Petra, K.R. Monk, A. Puga and K.E. 
Knudsen. 2002. The xenoestrogen bisphenol A induces inappropriate 
androgen receptor activation and mitogenesis in prostate adenocarcinoma 
cells. Molec. Cancer Therapeut. 7:515-24.
    \9\ Richter, C.A., J.A. Taylor, R.L. Ruhlen, W.V. Welshons and F.S. 
vom Saal. 2007. Estradiol and bisphenol A stimulate androgen receptor 
and estrogen receptor gene expression in fetal mouse prostate 
mesenchyme cells. Environmental Health Perspectives 115: 902-908.
                                 ______
                                 
  Response to Written Question Submitted by Hon. Daniel K. Inouye to 
                          Elizabeth Hitchcock
    Question. Is there any evidence that humans can be exposed to these 
chemicals through the food, specifically seafood, which we eat?
    Answer. In October and November 2007, Environmental Working Group 
surveyed the 5 leading makers of baby formula sold in the U.S. to 
determine whether they use BPA in their packaging. We found:

   The makers of Nestle, Similac, Enfamil and PBM (who make 
        store-brand formulas sold at Wal-Mart, Target, Kroger and 
        dozens of other retailers) all said that they use BPA in the 
        linings of metal cans holding liquid formula.

   BPA is widely used in powdered formula containers as well. 
        Every manufacturer except Nestle said it uses a BPA-based 
        lining on the metal portions of their powdered formula cans. 
        Nestle failed to provide EWG with reliable documentation of 
        their alternative packaging, and thus is not a clear 
        improvement over other types.

   Powdered formulas are a better choice. Our calculations 
        indicate that babies fed reconstituted powdered formula likely 
        receive 8 to 20 times less BPA than those fed liquid formula 
        from a metal can.

    Liquid formula is of greatest concern, and its use could lead to 
high BPA exposures for babies. Recent studies documenting that BPA 
leaches out of plastic baby bottles prompted a run on glass bottles by 
concerned parents. But testing by EWG and by the Food and Drug 
Administration (FDA) indicates that under normal use, liquid formula 
itself could expose an infant to substantially more BPA than a plastic 
bottle. An August 2007 investigation by EWG estimated that at BPA 
levels found in ready-to-eat liquid formula, 1 of every 16 infants fed 
the formula would be exposed to the chemical at doses exceeding those 
that caused harm in laboratory studies.\1\
---------------------------------------------------------------------------
    \1\ Environmental Working Group, EWG's Guide to Infant Formula and 
Baby Bottles, December 2007.
---------------------------------------------------------------------------
                                 ______
                                 
     Response to Written Questions Submitted by Hon. Mark Pryor to 
                          Elizabeth Hitchcock
    Question 1. In 1998, the U.S. PIRG along with other consumer groups 
petitioned CPSC to ban polyvinyl chloride (PVC). In 2003, following a 
review by a Chronic Hazard Advisory Panel, CPSC commissioners voted to 
deny the petition. However, after the ruling some manufacturers have 
moved toward voluntarily removing phthalates from children's products. 
What recommendations does U.S. PIRG have for parents that are concerned 
about phthalates?
    Answer. A few small, easy changes in the products that consumers 
buy and use can help reduce our children's exposure to toxic chemicals.
At the Store
Choose safer toys and teethers
    Look for ``PVC-free'' on the labels of soft plastic toys and 
teethers. Another class of chemicals shown to disrupt the hormone 
system--phthalates--is found in polyvinyl chloride (PVC) plastic. PVC 
plastic is used to make different types of children's products, 
including some teethers and soft plastic toys. Some manufacturers have 
removed PVC from their children's products, especially products 
intended to be put into children's mouths. Unfortunately, no law 
requires or regulates these labels, and few products are labeled as 
such. When parents have a question about the chemicals in a product, 
they should call the manufacturer.
Choose wooden toys
    There are countless manufacturers of high quality wooden toys in 
the market. Everything from baby rattles to kitchen play-sets are now 
made out of wood. Some commonly available brands include Plan Toys, 
Haba, Turner Toys, Selecta, and Holztiger.
Choose Safer Food Packaging and Serving Containers
   Avoid polycarbonate plastic in food containers. Check the 
        bottom/underside of the product. If you see ``PC'' (usually in 
        or near the recycling triangle) signifying polycarbonate 
        plastic, do not purchase it. Often a number ``7'' on the bottom 
        in the recycling triangle, by itself, also means the material 
        is polycarbonate, but not always. To be safe, avoid #7 plastic. 
        Choose plastics labeled #1, #2, or #5 in the recycling 
        triangle, but do not heat beverages or food in plastic 
        containers of any kind.

   Avoid PVC plastic in food containers. Check the bottom/
        underside of the product. If you find the number ``3'' in the 
        recycling triangle, it is made from PVC plastic and should be 
        avoided. Choose plastics labeled #1, #2, or #5 in the recycling 
        triangle, but do not heat beverages or food in plastic 
        containers of any kind.

   Avoid canned foods: Unfortunately, bisphenol A can leach 
        from metal can lining into the foods and liquids contained 
        within. Buy baby food in glass containers, and avoid feeding 
        your child food from cans as much as possible. You can often 
        find popular children's foods, such as tomato sauce, 
        applesauce, and black beans, in glass jars.

   Choose safer containers for sippy cups and water bottles. 
        Look for plastics labeled #1, #2, or #5 in the recycling 
        triangle. As an alternative to hard plastic water bottles (such 
        as the polycarbonate Nalgene bottles), try a lightweight 
        stainless steel bottle instead.

   Choose glass or safer-plastic baby bottles. Almost all 
        plastic baby bottles are made from polycarbonate plastic 
        containing bisphenol A, but they are rarely labeled as such. 
        With as few as 50-100 washings--even before you see wear--
        significant amounts of bisphenol A can leach into your baby's 
        milk. For the best protection, switch to using glass bottles 
        for all or most of baby's use. Contrary to claims by the 
        plastics industry, glass bottles are extremely durable and safe 
        (and wash well in the dishwasher). And after all, they were 
        good enough for you when you were a baby! Evenflo is one of the 
        only glass bottle makers around (some Babies ``R'' Us stores 
        carry them and they are available on-line). A couple of 
        manufacturers make their baby bottles from a safer 
        polypropylene-based plastic (a softer, opaque plastic), which 
        has not been associated with the developmental problems linked 
        to bisphenol A.

   Choose metal feeding utensils and enamel or ceramic plates. 
        While many manufacturers have removed phthalates from products 
        intended to be put into young children's mouths, without a law 
        prohibiting their use, there is no guarantee that these 
        products, such as soft, plastic-coated feeding spoons, are made 
        without phthalates. Look for PVC-free labels or buy stainless 
        steel, enamel, ceramic, or glass. (Note that enamel cannot be 
        put in the microwave, and you should not use old pottery that 
        could have lead-based glazes).

   Avoid foods wrapped in plastic. Almost all commercial grade 
        plastic cling wrap contains PVC plasticized with phthalates, 
        and other plastic food packaging may be made of PVC, as well. 
        Avoid buying foods wrapped in plastic, especially cheeses and 
        meats. Buy deli-sliced cheeses and meats and have them wrapped 
        in paper. If you can't avoid buying plastic-wrapped foods, 
        cutoff a thin layer of the cheese or meat when you get home and 
        store the remainder in glass or less-toxic plastic.
At Home
   Use glass to heat food or liquid in the microwave. You 
        should not heat food in plastic containers or on plastic 
        dishware, or heat liquids in plastic baby bottles. Heating food 
        and liquids in plastic containers can cause chemicals and 
        additives in the plastics to leach out more readily--right into 
        baby's food and milk. While some plastic containers are 
        marketed as ``microwave safe,'' it is safest to avoid them for 
        heating.

   If you do use plastic bottles, containers, or dishware, 
        avoid harsh detergents or hot water when washing them to reduce 
        exposure. Do not put plastic bottles, containers, or dishware 
        in the dishwasher. Also, throw out any plastic bottles, 
        containers, and dishware that start to look scratched or hazy. 
        Do not let milk sit for long periods of time in plastic.

   Avoid letting your child put plastic toys in his/her mouth. 
        Toys designed for older children are more likely to contain 
        phthalates or bisphenol A. It is assumed that young children 
        will not mouth these toys--such as action figures and Barbie 
        dolls. To be safe, keep all plastic toys out of children's 
        mouths. Call the manufacturer if you want to know if a product 
        contains phthalates or bisphenol A.

    Question 2. Since some manufacturers have taken steps to remove 
phthalates from certain children's products, has U.S. PIRG seen 
significant evidence that ``phthalate-free'' toys are better for 
children than those containing phthalates?
    Answer. Some manufacturers have removed PVC from their children's 
products, especially products intended to be put into children's 
mouths. Unfortunately, no law requires or regulates these labels, and 
few products are labeled as such. When parents have a question about 
the chemicals in a product, they should call the manufacturer.
    The U.S. Government, however, does not regulate the ``phthalate-
free'' label or ensure that products labeled ``phthalate-free'' 
actually do not contain phthalates. Since the U.S. Government has not 
established any guidelines for what the label means, or established any 
standards for the phthalate content in children's products, consumers 
can only assume that it means phthalates are not present in the item.
    In 2005, to test the reliability of the ``phthalate-free'' label, 
U.S. PIRG commissioned STAT Analysis Corporation in Chicago, Illinois 
to test eight soft plastic toys labeled as not containing phthalates. 
Of the eight toys tested, six contained detectable levels of 
phthalates.\2\ Based on these results, we asked the Federal Trade 
Commission (FTC) to investigate whether manufacturers' use of the 
``phthalate-free'' label constitutes unfair or deceptive marketing 
practices when the product actually contains phthalates.\3\
---------------------------------------------------------------------------
    \2\ U.S. PIRG Education Fund, Trouble in Toyland: The 20th Annual 
Survey of Toy Safety, November 2005.
    \3\ Letter to The Honorable Deborah Platt Majoras, Chairman, FTC, 
November 21, 2005. On file with the author. Our petition was later 
denied.
---------------------------------------------------------------------------
    With the results of the FTC investigation still pending, we once 
again commissioned STAT Analysis Corporation in the fall of 2006 to 
test 10 soft plastic toys labeled as not containing phthalates.\4\ Of 
the 10 toys tested, just two contained detectable levels of phthalates. 
Some of the items that tested positive for phthalates in the first year 
did not in the second. While this may be good news for consumers, 
nothing in U.S. law has changed to hold manufacturers accountable to 
their ``phthalate-free'' label or require them to stop using 
phthalates. Consumers still have no guarantee that the ``phthalate-
free'' products they purchase truly are phthalate-free, as evidenced by 
our test results.
---------------------------------------------------------------------------
    \4\ Eight of the toys were labeled ``phthalate-free'' on the 
packaging. One item was labeled ``phthalate-free'' on the 
manufacturer's website. For the last item, the manufacturer's website 
claimed not to use phthalates in any of its children's products.

    Question 3. Please explain the significance of low-dose exposures 
to BPA and how it relates to the traditionally held belief of ``the 
dose makes the poison''?
    Answer. Hundreds of studies that explore the effects of low-dose 
exposure to bisphenol A, pesticides and similar toxins have led to a 
shift in the way that many scientists and activists view toxicity. The 
older paradigm focused on acute toxicity, or ``the dose makes the 
poison.'' This theory assumes that higher doses of a toxin will have a 
greater effect on the subject. The newer paradigm recognizes that 
exposure to even very low doses of endocrine disruptors can alter 
development and initiate signaling pathways, rendering the levels of 
toxicity that have been considered ``acceptable'' inaccurate. So, while 
exposure to bisphenol A in one given instance might be low, there is 
reason to believe it can still be very dangerous, and that the near 
constant rate of low-dose exposure is cause for alarm.
    Some animal studies show adverse health affects from exposure of 
only 0.025 micrograms per kilogram of body weight, yet a polycarbonate 
baby bottle with room temperature water can leach 2 micrograms of BPA 
per liter. A 3-month-old baby drinking from a polycarbonate bottle may 
be exposed to as much as 11 micrograms per kilogram of body weight 
daily. The current U.S. Environmental Protection Agency daily upper 
limit for BPA, 50 micrograms per kilogram of body weight, is based on 
industry-sponsored experiments conducted in the 1980s.
    BPA raises particularly troubling health questions because it can 
affect the endocrine system, mimicking the effects of estrogen in the 
body. Experiments in animals and with human cells strongly suggest 
exposures typical in the U.S. population may increase susceptibility to 
breast and prostate cancer, reproductive system abnormalities, and, for 
exposure in the womb and early childhood, a host of developmental 
problems. Concerns about early life exposures also extend to early 
onset of puberty in females, potential prostate problems in males, and 
obesity.

    Question 4. How is the average person exposed to phthalates?
    Answer. Phthalates are used to build cars, homes and offices. They 
are used in cosmetics, toys and medical devices, and they are used to 
package food.\5\ Because of their widespread use, Americans are 
constantly exposed to these chemicals. Phthalates leach out of the 
plastics that contain them making the chemicals available for 
inhalation, ingestion and absorption.\6\ Because of this, we are 
exposed to phthalates when we touch the products that contain them. We 
are also exposed to phthalates because they come out of their original 
sources and into the air that we breathe.\7\
---------------------------------------------------------------------------
    \5\ Phthalate Esters Panel of the American Chemistry Council. 
Essential2Know About Phthalates downloaded on June 19, 2008 at 
www.phthalates.org.
    \6\ J. H. Kin et al., ``DEHP migration behavior from excessively 
plasticized PVC sheets,'' Bulletin of the Korean Chemical Society, 2003 
Volume 24(3) 345-349.
    \7\ Ruthann A. Rudel, David E. Camann, John D. Spengler, Leo R. 
Korn and Julia G. Brody, Silent Spring Institute and Harvard School of 
Public Health, ``Phthalates, Alkylphenols, Pesticides, Polybrominated 
Diphenyl Ethers and Other Endocrine Disrupting Compounds in Indoor Air 
and Dust,'' Environmental Science and Technology 37:4543-4553, 15 
October 2003

    Question 5. What is the best way to reduce exposure to phthalates?
    Answer. The best way to reduce exposure to phthalates is to 
phaseout their use. Both Federal and state governments should act to 
regulate these chemicals, especially in children's products. Congress 
should require that chemical manufacturers demonstrate the safety of 
their products before putting them on the market. The Consumer Product 
Safety Commission should protect consumers from these hazardous 
products. First, the Commission should take a precautionary approach to 
the chemicals in products. Second, the Commission should require 
products to be labeled appropriately.

    Question 6. Please explain the significance of phthalate mixtures.
    Answer. When used in combination with other phthalates, there is an 
additive dose-response relationship. A study by scientists at the EPA 
and the North Carolina State University showed that phthalates with 
similar action mechanisms have a dose additive effect on fetal 
testosterone when administered in combination.\8\ Another study by 
scientists at the University of Surrey in the United Kingdom showed 
that a mixture of phthalates caused a seemingly additive effect of 
serum cholesterol in rats.\9\
---------------------------------------------------------------------------
    \8\ Howdeshell, Kembra L., Vickie S. Wilson, Johnathan Furr, 
Christy R. Lambright, Cynthia V. Rider, Chad R. Blystone, Andrew K. 
Hotchkiss and Leon Earl Gray, Jr. ``A mixture of five phthalate esters 
inhibits fetal testicular testosterone production in the Sprague Dawley 
rat in a cumulative, dose additive manner.'' Toxicological Sciences. 
Accessed June 19, 2008 at http://toxsci.oxfordjournals.org/cgi/content/
abstract/kfn077.
    \9\ Howarth, J. A., Price S. C., Dobrota M., Kentish P. A., Hinton 
R. H. ``Effects on male rats of di-(2-ethylhexyl) phthalate and di-n-
hexylphthalate administered alone or in combination.'' Toxicology 
Letters. 121:1:35-43 8 April 2001

    Question 7. What are endocrine disruptors and how do they affect 
us?
    Answer. Endocrine disruptors are chemicals that mimic or block 
hormones or interfere with hormone production.\10\ Hormones transfer 
signals between cells over long distances using the bloodstream. Once a 
hormone reaches a cell, it fits into a receptor and initiates a cell 
response using the signal transduction pathway. If a different molecule 
is substituted for the hormone in the receptor, then the cell will 
receive alternate instructions.\11\ Hormone blockers prevent hormones 
from delivering signals from one cell to another. Hormone replacers 
replace hormones and send either excessive or insufficient signals to 
cells. The change in the signals received by cells alters the cells 
response and thus how the body functions. Because of these actions, 
endocrine disruptors impede normal functions and cause damage to the 
body. Endocrine disruptors have been linked with abnormalities in the 
reproductive, immune, nervous and endocrine systems.\12\ Endocrine 
disruptors can cause decreased sperm count and testicular cancer. They 
can also interfere with proper immune function causing immunotoxicity. 
They can effect the nervous system by limiting thyroid function and 
thus brain development. They can also cause endometriosis, which leads 
to infertility in women.
---------------------------------------------------------------------------
    \10\ The Natural Institute of Environmental Health Sciences. 
``Endocrine disruptors'' Downloaded on June 19, 2008 at http://
www.niehs.nih.gov/health/topics/agents/endocrine/docs/endocrine-
disruptors.pdf.
    \11\ Sadava, David, H. Craig Heller, Gordon H. Orians, William K. 
Purves, David M. Hillis Life: The Science of Biology 8th edition 
Sinauer Associates, Inc. 2007.
    \12\ World Health Organization. ``Global Assessment of the state-
of-the-science of endocrine disruptors'' WH/PCS/EDC/02.2 (2002)

    Question 8. Is there an established list of known endocrine 
disruptors?
    Answer. In 2007 the Environmental Protection Agency (EPA) compiled 
a draft list of endocrine disruptors that was selected on the basis of 
exposure potential. The EPA is now investigating these chemicals and is 
planning to issue a final list.\13\ Although there is no governmental 
list of known endocrine disruptors, scientists have identified many 
chemicals as such. Paul Geottlich has a list of known endocrine 
disruptors published in Fundamentals of Naturopathic Endocrinology.\14\
---------------------------------------------------------------------------
    \13\ www.epa.gov/endo.
    \14\ Michael, Dr. Friedman. (ed.) Fundamentals of Naturopathic 
Endocrinology. CCNM Press (2005)

    Question 9. Are there already alternatives to BPA and phthalates? 
Are these alternatives safer than what is currently being used? What 
science or studies exists into these alternatives?
    Answer. Several products that are made with phthalates or BPA could 
easily be made with alternatives. Phthalates can be replaced with 
either polymeric or adipate plasticizers.\15\ A study at Cochin 
University of Science and Technology showed the use of polymeric 
plasticizers reduces the leaching of chemicals from PVC.\16\ A study 
performed by the Institute of Food Safety and Nutrition in conjunction 
with the Danish Veterinary and Food Administration found that adipate 
plasticizers did not induce the antiandrogenic effects that phthalates 
induce.\17\ Another alternative to using phthalates is to switch from 
PVC to other plastics such as thermoplastic elastomers, ethylene vinyl 
acetate and polyolefins.\18\ The alternatives are also safer than PVC. 
The alternatives to PVC plastic are only 2 percent plasticizers, while 
the phthalate content in PVC is up to 50 percent. Furthermore the 
alternatives are less likely to leach plasticizers when compared to 
PVC.\19\ Both alternatives pose little safety concern and offer 
flexibility in the production process. Products made with polycarbonate 
plastic containing BPA could instead be made with polyamide, a plastic 
that does not require BPA for production.\20\ The alternatives to BPA 
have not been as heavily tested as the alternatives to phthalates. 
Polyamide plastic is not known to contain harmful plasticizers, and so 
the effects of polyamide on human health is believed to be 
negligible.\21\
---------------------------------------------------------------------------
    \15\ Svoboda, Ronald D. ``Polymeric Plasticizers for Higher 
Performance Flexible PVC'' The C.P. Hall Company. Chicago, IL.
    \16\ Sunny, M.C., P. Ramesh and K.E. George. ``Use of polymeric 
Plasticizers in Polyvinyl Chloride to Reduce Conventional Plasticizer 
Migration for Critical Applications'' Journal of Elastomers and 
Plastics 36:1:19-31 (2004).
    \17\ Dalgaard M. et al. ``Di(2-ethylhexyl) adipate (DEHA) induced 
developmental toxicity but not antiandrogenic effects in pre- and post-
natally exposed Wistar rats'' Reproductive Toxicology. March-April 2003 
17(2):163-170.
    \18\ Tickner, Joel. ``Review of the Availability of Plastic 
Substitutes for Soft PVC in Toys'' Department of Work Environment. 
University of Massachusetts at Lowell, USA.
    \19\ Tickner, Joel. ``Review of the Availability of Plastic 
Substitutes for Soft PVC.
    \20\ McNichols, Jeremiah ``Sippy Cup Showdown: Safer BPA-Free 
Drinkware for Toddlers'' accessed July 19, 2008 at http://
zrecs.blogspot.com/2007/05/sippy-cup-showdown-safer-bpa-free-
sippy.html.
    \21\ Labour Environmental Alliance Society ``Frequently Asked 
Questions'' accessed Jun. 23, 2008 at www.leas.ca/Frequently-Asked-
Questions.htm.

    Question 10. Do infants and children have the same immune and 
endocrine system as adults? Do studies take into account these 
differences?
    Answer. People are born with all of the necessary organs in the 
immune and endocrine system; however these organs are not developed. 
They will grow and develop during infancy and childhood. Because 
infants and children have immune and endocrine systems that are 
developing, they are more susceptible to interaction with and damage 
from dangerous chemicals. Several studies are designed to account for 
this, as well as for the developmental effects of phthalates and BPA on 
the human systems. A study conducted at the Mitsubishi Chemical Safety 
Institute exposed female rats to phthalates during gestation.\22\ The 
study found that exposure to phthalates during development caused 
inhibition in weight gain of offspring as well as abnormal reproductive 
development among male and female rats in the first and second 
generations.
---------------------------------------------------------------------------
    \22\ Hoshino N. et al., ``A two-generation reproductive toxicity 
study of dicyclohexyl phthalate in rats.'' Journal of Toxicological 
Science. Dec. 2005 30 Spec No. 79-96.

    Question 11. Have we seen many human studies on these chemicals? Is 
it even possible or ethical to conduct human studies?
    Answer. Epidemiologic studies are often conducted in place of 
clinical trials, because they do not present the same ethical issues. 
Several epidemiologic studies have been conducted regarding phthalates, 
BPA and their effects on humans. Three studies, one at Fudan 
University's School of Public Health in Shanghai and two at the Harvard 
School of Public Health, showed an association between phthalate 
exposure and reduced semen quality in adult males.\23\
---------------------------------------------------------------------------
    \23\ Zhang Y.H. et al., ``Phthalates exposure and semen quality in 
Shanghai: a cross-sectional study'' Biomedical Environmental Science 
June 2006 19(3):205-209; Duty S.M. et al., ``Phthalate Exposure and 
human semen parameters'' Epidemiology. May 2003 14(3):269-277; Hauser 
R. et al., ``Altered semen quality in relation to urinary concentration 
of phthalate monoester and oxidative metabolites'' Epidemiology Nov. 
2006 17(6):682-691.

    Question 12. Usually chemicals are tested one at a time. However, 
we come into contact with numerous chemicals every day. Do these 
studies simulate real world exposures and what is the best way to test 
chemicals?
    Answer. Chemicals are tested individually or in carefully 
controlled groups because it eliminates possible sources of error and 
confounding in the study. When only a single chemical is administered, 
the effect on the subject can be linked strongly to the chemical. 
Furthermore if two chemicals are administered together, then the 
possibility of interaction between these chemicals must be considered, 
multiplying the possibilities of what causes the result.
    Studies that test chemicals individually simulate individual 
pathways of exposure focusing on the elements of exposure that are most 
easily reduced. The studies have focused on the presence of phthalates 
and BPA in children's products for several reasons. First, phthalates 
and BPA pose special hazards to infants and children. Second, the 
elimination of phthalates and BPA in toys is more easily achieved, 
since toys and childcare products do not exist as long in the market as 
cars and carpets. Third, the exposure of children to phthalates and BPA 
in childcare products can be more easily controlled in an experimental 
setting.

    Question 13. What about workers who are in the plants that 
manufacture phthalates and BPA. Are protections in place to make sure 
that they aren't unnecessarily exposed?
    Answer. In addition to basic safety measures taken when chemicals 
are used in production, the Occupational Safety and Health 
Administration has established limits on the amount of certain 
phthalates and BPA to which workers may be exposed.\24\ In air, 
concentrations can not exceed 0.5 mg/m\3\ for DEHP, 5 mg/m\3\ for DEP. 
Bisphenol-A should not exceed 860 mg/m\3\ in air concentration.
---------------------------------------------------------------------------
    \24\ The Occupational Safety and Hazard Administration Regulations 
(Standards--29C FR) Air Contaminants 1915.1000.
---------------------------------------------------------------------------
                                 ______
                                 
   Response to Written Questions Submitted by Hon. John F. Kerry to 
                          Elizabeth Hitchcock
    Question 1. Why are there such dramatically different results on 
the low-dose effects of BPA between the results of studies sponsored by 
the chemical industry and studies conducted by academics or government 
entities?
    Answer. A recently-published review of scientific studies shows 
that, in the last 7 years (through November 2005), 151 studies on the 
low-dose effects of BPA have been published.\25\ None of the 12 studies 
funded by the chemical industry reported adverse effects at low levels, 
whereas 128 of 139 government-funded studies found effects. These many 
studies were conducted in academic laboratories in the U.S. and abroad.
---------------------------------------------------------------------------
    \25\ vom Saal, F. and C. Hughes, An Extensive New Literature 
Concerning Low-Dose Effects of Bisphenol A Shows the Need for a New 
Risk Assessment. Environmental Health Perspectives 113:926-933 (2005).
---------------------------------------------------------------------------
    Even the 12 industry-funded studies have flaws, however. Of the 
industry studies, two had its positive control fail--an indication that 
the entire experiment had failed, not that BPA had not caused an 
effect. Another industry study concluded BPA caused no effect, but an 
independent analysis of the experiment's data by scientists convened by 
the National Toxicology Program of the U.S. Department of Health & 
Human Services concluded that in fact there was an effect. Industry 
scientists had misreported their own results.
    The chemical industry relies on an incomplete review of scientific 
studies by an effort funded by the American Plastics Council at the 
Harvard Center for Risk Analysis. The panel funded by the American 
Plastics Council only considered 19 studies in concluding in 2004 that 
the weight of the evidence for low-dose effects of BPA was weak.\26\ As 
of November 2005, there were 151 published studies on the low-dose 
effects of BPA.
---------------------------------------------------------------------------
    \26\ vom Saal, F. and C. Hughes, An Extensive New Literature 
Concerning Low-Dose Effects of Bisphenol A Shows the Need for a New 
Risk Assessment. Environmental Health Perspectives 113:926-933 (2005) 
(``The charge to the HCRA panel, which was to perform a weight-of-the 
evidence evaluation of available data on the developmental and 
reproductive effects of exposure to BPA in laboratory animals, led to 
an analysis of only 19 of 47 available published studies on low-dose 
effects of BPA. The deliberations of the HCRA were in 2001-2002, and 
accordingly, a cut-off date of April 2002 was selected for 
consideration of the published literature. It is regrettable that the 
relevance of the analysis was further undermined by a delay of 2.5 
years in publication of the report. During the intervening time, 
between April 2002 and the end of 2004, a large number of additional 
articles reporting low-dose effects of BPA in experimental animals have 
been published. The result is that by the end of 2004, a PubMed 
(National Library of Medicine, Bethesda, MD) search identified 115 
published studies concerning effects of low doses of BPA in 
experimental animals.'').

    Question 2. In light of dozens of advanced studies over the past 
several years, in conjunction with the recent assessment from the 
National Toxicology Program, do you believe that the Federal Government 
should control exposure to BPA and phthalates?
    Answer. The Federal Government has an obligation to protect 
consumers from dangerous products. The CPSC should first label products 
containing Bisphenol A and phthalates with the names of the chemicals 
they contain to allow parents to choose less toxic products. Second, 
the CPSC should take the precautionary approach and require 
manufacturers to remove chemicals that may pose a particular threat to 
fetuses, infants and children, particularly when the chemical is not 
necessary for the product to function according to design. In addition, 
CPSC and the Federal Trade Commission should look into manufacturers' 
use of the ``phthalate-free'' label and take action against 
manufacturers that may be misleading consumers.
    Congress has the opportunity to take action on these two chemicals 
now. The final version of CPSC reform legislation now in conference 
should include the Feinstein amendment banning phthalates in children's 
products (incorporated as Section 40 of H.R. 4040 as passed by the 
Senate). The amendment will:

   Prohibit the use of phthalates (any combination of certain 
        listed chemicals in concentrations exceeding 0.1 percent) in 
        any children's product or child care article.

   Require manufacturers to use the least toxic alternative to 
        phthalates.

   Prohibit the use of certain harmful alternatives--including 
        substances known to be, likely to be, or suggestive of being 
        carcinogens; and reproductive toxicants identified as causing 
        either birth defects, reproductive harm, or developmental harm.

   The amendment also includes an important ``savings clause'' 
        that would prevent Federal preemption of stronger state laws 
        regulating phthalates in toys or other product categories.

    In addition, U.S. PIRG supports legislation introduced by Senator 
Schumer (NY) and Rep. Markey (MA) that would ban bisphenol A in 
children's products or in food containers.

    Question 3. Can consumers trust products that are currently labeled 
as ``BPA-free'' or ``phthalate-free''?
    Answer. Some manufacturers label their baby products and toys as 
``phthalate-free,'' which should provide parents the information they 
need to make educated purchasing decisions. The U.S. Government, 
however, does not regulate the ``phthalate-free'' label or ensure that 
products labeled ``phthalate-free'' actually do not contain phthalates. 
Since the U.S. Government has not established any guidelines for what 
the label means, or established any standards for the phthalate content 
in children's products, consumers can only assume that it means 
phthalates are not present in the item.
    In 2005, to test the reliability of the ``phthalate-free'' label, 
U.S. PIRG commissioned STAT Analysis Corporation in Chicago, Illinois 
to test eight soft plastic toys labeled as not containing phthalates. 
Of the eight toys tested, six contained detectable levels of 
phthalates.\27\ Based on these results, we asked the Federal Trade 
Commission (FTC) to investigate whether manufacturers' use of the 
``phthalate-free'' label constitutes unfair or deceptive marketing 
practices when the product actually contains phthalates.\28\
---------------------------------------------------------------------------
    \27\ U.S. PIRG Education Fund, Trouble in Toyland: The 20th Annual 
Survey of Toy Safety, November 2005.
    \28\ Letter to The Honorable Deborah Platt Majoras, Chairman, FTC, 
November 21, 2005. On file with the author. Our petition was later 
denied.
---------------------------------------------------------------------------
    With the results of the FTC investigation still pending, we once 
again commissioned STAT Analysis Corporation in the fall of 2006 to 
test 10 soft plastic toys labeled as not containing phthalates.\29\ Of 
the 10 toys tested, just two contained detectable levels of phthalates. 
Some of the items that tested positive for phthalates in the first year 
did not in the second. While this may be good news for consumers, 
nothing in U.S. law has changed to hold manufacturers accountable to 
their ``phthalate-free'' label or require them to stop using 
phthalates. Consumers still have no guarantee that the ``phthalate-
free'' products they purchase truly are phthalate-free, as evidenced by 
our test results.
---------------------------------------------------------------------------
    \29\ Eight of the toys were labeled ``phthalate-free'' on the 
packaging. One item was labeled ``phthalate-free'' on the 
manufacturer's website. For the last item, the manufacturer's website 
claimed not to use phthalates in any of its children's products.

    Question 4. Why are low-dose effects of endocrine-disrupting 
chemicals like BPA and phthalates more dangerous than those of other 
compounds?
    Answer. See answer above to Senator Pryor's similar question.
                                 ______
                                 
     Response to Written Questions Submitted by Hon. Mark Pryor to 
                        Steven G. Hentges, Ph.D.
    Question 1. The ``low-dose hypothesis'' claims that exposure to 
extremely low levels of certain substances could cause adverse health 
effects in humans. Some have criticized existing studies and reviews 
for looking at only high dosage exposure. How would you respond to 
those that claim either lack of evidence supporting the use of these 
chemicals or that low dose evidence demonstrates a concerned risk?
    Answer. Many hundreds of studies on bisphenol A have been conducted 
in the last 10 years and a substantial percentage of these studies were 
aimed at addressing the question whether bisphenol A could cause 
adverse health effects at very low doses. These studies are not all 
equivalent, and in general, they vary vastly in size, scope, quality 
and relevance to human health. The most comprehensive studies cover 
multiple generations of laboratory animals, are large in scale and 
statistically powerful, include a wide range of doses from very low to 
very high, and dose animals by the most relevant oral route of 
exposure. Other studies are small in size and scope, may be poorly 
conducted or reported, and dose animals by routes that are of little or 
no relevance to humans (e.g., subcutaneous injection, direct injection 
into the brain). A further complication is that the results of these 
many studies are not consistent and often are conflicting.
    When faced with a large and diverse body of data, as is the case 
for bisphenol A, scientists systematically evaluate the weight of 
scientific evidence to draw conclusions based on all of the available 
evidence. In recent years, numerous weight of evidence evaluations of 
bisphenol A have been conducted by independent scientific and 
government bodies worldwide. These evaluations consistently support the 
conclusion that bisphenol A is not a significant risk to human health, 
in particular at the very low levels to which people could be exposed 
through use of consumer products.
    In addition to evaluating each available study on its own merits, a 
weight of evidence evaluation also assesses whether the findings of 
studies have been replicated or corroborated in independent 
laboratories, whether they are consistent within and across studies, 
and whether they are coherent when considered together. Repeatability 
is a fundamental principle of the scientific process; findings that 
cannot be replicated in robust studies cannot be accepted as valid.
    Since much of the recent research on bisphenol A is aimed 
specifically at assessing the potential for bisphenol A to cause health 
effects at low doses, the many recent weight of evidence evaluations 
are focused almost entirely on this question. None of these evaluations 
are focused only at high dose exposures. The conclusions of these 
evaluations are based on the full weight of scientific evidence, 
including all relevant studies that report effects at low doses and 
studies that do not report low dose effects.

    Question 2. There seems to be a marked difference between studies 
funded by the chemical industry, those funded by governments, and those 
conducted by academic institutions. How have these studies differed to 
produce such opposite results?
    Answer. We understand this question to be directed to the body of 
scientific literature on bisphenol A and not generally with respect to 
the entire chemical industry, so we answer it here.
    Scientific studies can only answer questions they are designed to 
answer. Studies sponsored by industry are typically, but not always, 
aimed at answering the critical question of whether a product is safe 
for use. These studies are generally designed to meet the requirements 
of internationally accepted test guidelines that were developed for 
this purpose. The studies are typically large in scale to be sure the 
studies have adequate statistical power and examine appropriate 
endpoints to address the question that the study is intended to answer. 
The studies are also typically conducted in highly qualified test 
laboratories under Good Laboratory Practices, which provides further 
assurance of the integrity of the study results.
    Other studies, which can also include industry sponsored studies, 
are often aimed at other scientific questions that may or may not be 
directly relevant to assessing human health concerns. These studies may 
be limited in scope and examine endpoints that are difficult to 
interpret with respect to the safety of the substance being tested. 
Some studies, although scientifically well conducted, may have limited 
or no relevance for assessing human health concerns.
    For bisphenol A, a very wide diversity of studies have been 
conducted and it is a gross oversimplification to say that studies 
sponsored by the chemical industry have opposite results to studies 
conducted by academic institutions. Very often, studies cannot be 
directly compared because they are so different.
    As described in the answer to the question above, all relevant 
studies on bisphenol A have been systematically assessed in numerous 
weight of evidence evaluations. When all of the relevant data from 
these many studies are compared, in particular to determine whether the 
findings are repeatable or corroborated in independent laboratories, 
the most consistent result is that no effects from exposure to low 
doses of bisphenol A are reliably found. This conclusion is true even 
if the analysis is limited to non-industry studies. In that regard, 
studies sponsored by industry are consistent with the broader database 
and validate the overall conclusion that low doses of bisphenol A have 
not been reliably shown to cause adverse health effects.

    Question 3. Please explain the significance of low-dose exposures 
to bisphenol A and how it relates to the traditionally held belief of 
``the dose makes the poison''?
    Answer. The so-called ``low-dose hypothesis'' asserts that very low 
doses of endocrine-active substances may cause adverse health effects 
at very low doses. In particular, such low-dose health effects are 
postulated to occur with a non-monotonic dose-response, which means 
that health effects observed at very low doses would not be observed at 
higher doses. This hypothesis has not been scientifically proven and 
there is at best limited evidence that it could be valid.
    A fundamental principle of toxicology is commonly expressed as 
``the dose makes the poison,'' which means that health effects observed 
at a particular dose will uniformly increase in intensity or severity 
as the dose is increased. Conversely, as the dose is decreased, a dose 
causing no effect can be found (a no-effect level) and any lower dose 
will also cause no effect. This is referred to as a monotonic dose-
response (sometimes called a linear dose-response).
    Toxicology studies are often designed to identify a dose at which 
no adverse effects occur, which is referred to as a No-Observed-
Adverse-Effect-Level (NOAEL). Doses below the NOAEL may not be tested 
experimentally since no adverse effects are expected. If the low-dose 
hypothesis is valid, health effects below the NOAEL might occur but not 
be found.
    In response to the low-dose hypothesis, there are now a large 
number of studies on bisphenol A that examined low doses well below the 
accepted NOAEL. Most of these studies did not examine a sufficient 
number or range of doses to determine whether any dose-response is 
monotonic or non-monotonic and are thus not capable of validating the 
low-dose hypothesis.
    It is important to note that the accepted NOAEL for bisphenol A is 
based on the most comprehensive studies, which were conducted over 
multiple generations of laboratory animals and included a wide range of 
doses from very low doses up to a very high dose above the NOAEL that 
induces toxicity. These studies do not validate claims that bisphenol A 
causes adverse effects at low doses, regardless of the dose-response, 
and only monotonic dose-responses were observed. These studies provide 
the most powerful evidence that the low-dose hypothesis, at least for 
bisphenol A, is not valid.
    Beyond bisphenol A, the biological plausibility of the low-dose 
hypothesis is not supported by research on other endocrine-active 
substances. For example, two very robust and comprehensive studies have 
recently been published on estradiol and ethinylestradiol, the first 
being the prototypical naturally occurring estrogen and the second 
being the estrogenic substance commonly used in birth control pills. 
Both studies covered a wide dose range and neither study found non-
monotonic dose-response for any observed effect. In comparison to these 
two substances, bisphenol A is a very weak estrogen that is 10,000-
100,000 times less potent. No plausible explanation has been advanced 
to explain why bisphenol A would cause adverse effects at low doses 
with non-monotonic dose-response while more potent estrogens would not 
do so.
    There is at best very limited evidence to support the validity of 
the low-dose hypothesis and very strong evidence that indicates the 
hypothesis is not valid. Lacking reliable evidence and biological 
plausibility, the low-dose hypothesis is just that--a hypothesis that 
has not been proven.

    Question 4. Have or haven't we seen many human studies on bisphenol 
A? Is it even possible or ethical to conduct human studies?
    Answer. In our general answers, we note that there are different 
types of studies that could involve humans, some of which are 
considered ethical and some of which are not. Here we address the 
question with specific reference to bisphenol A.
    Several human studies have been conducted to understand how 
bisphenol A is processed in the body. In these studies, human 
volunteers are treated with a small dose of bisphenol A that is well 
below a dose that could cause toxicity as determined from reliable 
studies on laboratory animals. The objective of these studies is to 
determine whether bisphenol A is absorbed, where it is distributed in 
the body, whether it is metabolized and to what metabolites, and how 
quickly and where it is excreted.
    These studies confirm that people efficiently convert bisphenol A, 
as it is absorbed, to a metabolite that has no known biological 
activity, and then quickly excrete that metabolite with a half-life of 
about 5 hours. This means that bisphenol A is eliminated from the body 
into urine within the day of exposure and does not accumulate in the 
body. Of equal importance is that these studies also identified a 
critical difference between how rodents and humans process bisphenol A. 
The amount of time that bisphenol A remains in the body is 
substantially shorter for humans compared to rodents, which indicates 
that people are likely to be less sensitive to any potential health 
effects from exposure to bisphenol A. This is significant since most 
laboratory animal studies on bisphenol A have been conducted on rodents 
(e.g., mice, rats), which could overestimate human health concerns.
    A second type of study on humans that has been performed with 
respect to bisphenol A is biomonitoring to measure the presence of 
trace levels of chemicals in the body. Biomonitoring data provides a 
direct measure of exposure, which is necessary to assess whether 
bisphenol A poses a risk to humans. Since bisphenol A is entirely and 
quickly excreted into urine in the form of a metabolite, most 
biomonitoring studies measure the amount of that metabolite in urine 
samples. The largest set of biomonitoring data on bisphenol A is from 
the CDC National Health and Nutrition Examination Survey (NHANES), 
which is an ongoing population-scale program. That data was recently 
published and is generally consistent with the results of many smaller 
scale studies conducted around the world. Collectively these studies 
demonstrate that human exposure to bisphenol A is extremely low, which 
confirms what is expected in light of the use patterns of bisphenol A. 
Almost all bisphenol A is chemically reacted to form plastics and 
resins, meaning that there are no consumer products that contain any 
more than trace residual levels of bisphenol A. The typical level of 
bisphenol A found in human urine corresponds to an exposure level that 
is approximately 500-1,000 times below the science-based safety 
standard recently established in Europe based on an up-to-date review 
of the science.
    A small number of small-scale epidemiology studies, which attempt 
to associate human exposure to bisphenol A with specific health 
effects, have also been conducted. Biomonitoring measurements have been 
used in all of the available studies to quantify human exposure. The 
earliest such studies used an analytical method that was subsequently 
found to be invalid and are thus fatally flawed. More recent studies 
have used analytical methods that are likely to be valid, including 
several studies in which the measurements were conducted by CDC 
researchers. Although these studies have found no associations between 
exposure to bisphenol A and the examined health effects (e.g., birth 
weight and related parameters, earlier age of puberty in girls, 
endometriosis in adult women), the studies are limited and do not 
provide definitive results, which would require longer term and larger 
scale studies.

    Question 5. Are there already alternatives to BPA? Are these 
alternatives safer than what is currently being used? What science or 
studies exists into these alternatives?
    Answer. Bisphenol A is primarily used to make polycarbonate plastic 
and epoxy resins. Since neither of these materials would exist without 
bisphenol A, alternatives to bisphenol A effectively means alternatives 
to these materials.
    Both of these materials are used in a wide array of consumer and 
industrial products. As a general matter, they are used in these 
products because their key properties provide a necessary function and 
they are often the material of choice to provide that function. In 
short, they are used because they work.
    Polycarbonate plastic is a lightweight, clear and highly shatter-
resistant material that makes it useful in products such as sports 
safety equipment (e.g., bicycle and football helmets), CDs and DVDs, 
housings on electrical and electronic equipment (e.g., computers, cell 
phones, appliances), eyeglass lenses and components of medical devices, 
and automotive components, as well as baby bottles, water bottles and 
food storage containers.
    Epoxy resins are durable and chemically resistant materials that 
function well as protective coatings on metal products and as laminates 
in electronic circuit boards. Along with coatings on structural steel 
and pipes and fittings, epoxy resins are widely used as the protective 
coating on most food and beverage cans where they protect the safety 
and integrity of the contents. Without a coating, foods and beverages 
can corrode the metal can, resulting in contamination of food with 
metals and potentially with harmful bacteria if the integrity of the 
can is breached.
    To our knowledge, there are no alternatives that could easily 
substitute for all applications of these materials. In each case, a 
variety of factors must be considered to identify suitable 
alternatives, and the critical requirements for each application vary 
considerably. For any alternative, two immediate hurdles are 
functionality (i.e., the alternative must provide the function needed 
for that application) and safety (i.e., the alternative must be safe 
for the application).
    Compared to bisphenol A, no alternative has been so well tested or 
vetted so thoroughly by government agencies. Consequently, it is not 
likely that scientific data exists to support a claim that any 
alternative is safer than bisphenol A.

    Question 6. What about workers who are in the plants that 
manufacture BPA. Are protections in place to make sure that they aren't 
unnecessarily exposed?
    Answer. Bisphenol A is manufactured in a closed process that offers 
little opportunity for human exposure. Since bisphenol A is a high 
melting solid with very low volatility, the primary opportunity for 
occupational exposure in plants that manufacture bisphenol A involves 
contact with dust, in particular skin contact. Studies have shown that 
transfer of bisphenol A through skin into the body is limited and the 
primary health concern is for skin irritation or sensitization. 
Personal protection equipment is used to limit worker exposure to 
bisphenol A in circumstances where there is the potential for contact 
with bisphenol A.

    Question 7. How is the average person exposed to phthalates? What 
is the best way to reduce exposure to phthalates?
    Answer. Exposure to phthalates comes from many sources. These are a 
very valuable class of chemicals; different phthalates are used in 
personal care products, inks, caulks, sealants and vinyl products. A 
review of the scientific literature suggests that the greatest exposure 
to phthalates is through ingestion of food. Data from the U.S. Center 
for Disease Control indicates that total exposures to the general U.S. 
population from phthalate esters from all sources are well within EPA 
reference doses.

    Question 8. Please explain the significance of phthalate mixtures.
    Answer. There are about 13 phthalates commonly used today, so there 
can be exposure to multiple phthalates. Data from recent U.S. Centers 
for Disease Control (CDC) biomonitoring data indicates that humans are 
exposed to extremely low levels of several phthalates simultaneously. 
The CDC data indicates that the general population's exposure for each 
phthalate measured is below its EPA reference dose. A reference dose is 
an exposure level defined by the Environmental Protection Agency as ``a 
numerical estimate of a daily oral exposure to the human population, 
including sensitive subgroups such as children, that is not likely to 
cause harmful effects during a lifetime.''
    Some have suggested that while exposures to one phthalate ester are 
below the reference dose, scientists should also study whether more 
than one phthalate could interact. The evidence indicates that for the 
few chemicals that we know do interact, most do so by a process called 
``additivity,'' in which the effects of these chemicals are added 
together. But in order to be ``additive,'' chemicals must produce their 
effects not only on the same organ systems, but in the same way. In a 
toxicologist's terms, their ``mechanism of action'' in the body has to 
be the same for the effects to be additive. Another important point 
relates to the exposure levels. To produce meaningful interactions, 
exposures must be at levels at which the respective chemicals produce 
effects. If the exposures are below a critical threshold, an 
``additive'' effect would not generally be expected. This is an 
emerging field of study.
    Importantly, it is seen from the CDC data that maximum exposure in 
the most sensitive human subpopulations are still orders of magnitude 
less than doses with which additivity has been demonstrated in 
rodents.\1\ Since the current reference dose for DBP (EPA IRIS) is 0.3 
mg/kg/day, the estimated theoretical toxicity threshold for combined 
exposure to the phthalates DEHP, DBP, DIBP, and BBP would also be 
orders of magnitude higher than the EPA reference dose for DBP based on 
the simple dose addition model.
---------------------------------------------------------------------------
    \1\ Maximum estimated human daily exposure to one of the most 
commonly used phthalates, DEHP, was calculated from measurements in 
children aged 3-14 (0.0031 mg/kg/d.).

    Question 9. Have or haven't we seen many human studies on 
phthalates? Is it even possible or ethical to conduct human studies?
    Answer. In our general answers, we note that there different types 
of studies that could involve humans, some of which are considered 
ethical and some of which are not.
    Several human studies have been conducted to understand how 
phthalate esters are processed in the body. In these studies, human 
volunteers are treated with a small dose of phthalate esters that are 
well below a dose that could cause toxicity as determined from reliable 
studies on laboratory animals. The objective of these studies is to 
determine whether phthalate esters are absorbed, where they are 
distributed in the body, whether they are metabolized and to what 
metabolites, and how quickly and where they are excreted.
    These studies confirm that people efficiently convert phthalate 
esters to metabolites, which are then quickly excreted through urine in 
about twenty-four hours of exposure and not accumulated in the body.
    A second type of study on humans that has been performed with 
respect to phthalate esters is biomonitoring to measure the presence of 
trace levels of chemicals in the body. Biomonitoring data provides a 
direct measure of exposure, and understanding exposure is necessary to 
assess whether phthalate esters pose a risk to humans. Since phthalate 
esters are excreted into urine in the form of metabolites, most 
biomonitoring studies measure the amount of the metabolites in urine 
samples. The largest set of biomonitoring data on phthalate esters is 
from the CDC National Health and Nutrition Examination Survey (NHANES), 
which is an ongoing population-scale program. The CDC data demonstrate 
that human exposure to phthalate esters is extremely low, and below EPA 
reference doses for those compounds.
    A small number of small-scale epidemiology studies, which attempt 
to associate human exposure to phthalate esters with specific health 
effects, have also been conducted. Biomonitoring measurements have been 
used in all of the available studies to quantify human exposure. To 
date, the studies are limited and do not provide definitive results, 
which would require longer term and larger scale studies. EPA has 
declined to rely on data from these early studies due to their 
limitations.

    Question 10. Are there already alternatives to phthalates? Are 
these alternatives safer than what is currently being used? What 
science or studies exists into these alternatives?
    Answer. Phthalates have been used to make vinyl soft and flexible 
for many years since their chemical properties make them the most 
suitable softeners for a wide range of consumer and industrial 
products. Several non-phthalate plasticizers are commercially 
available; however, each one's suitability for use as a phthalate 
alternative depends on the technical requirements for the particular 
application (i.e., will the finished product perform satisfactorily). 
By way of example, many important medical applications depend on the 
performance of flexible vinyl tubing. Soft tubing adds patient comfort 
when patients are intubated; in addition, plasticized tubing resists 
kinking and holds its shape, helping in the administration of the 
correct dosage of drugs and treatments. One can easily see that in 
evaluating whether there might be an alternative to phthalates in such 
an application, doctors could insist that any alternative perform 
equally as well or better in the delivery of key medical services. And 
one can also easily see how a hospital administrator, charged with 
keeping costs down, might likewise insist on cost equivalence before 
moving to an alternative plasticizer.
    The recently published report on alternatives to DEHP in medical 
devices by the European Scientific Committee on Emerging and New-
Identified Health Risks (SCENIHR) provides the most up to date summary 
of data available on the most common alternative plasticizers. The 
report shows that some products have been as broadly studied as 
phthalates but that several have not. A few of the alternatives also 
have been reviewed in recent safety assessments.\2\
---------------------------------------------------------------------------
    \2\ Scientific Committee on Emerging and Newly Identified Health 
Risks (SCENIHR). 2008. ``Opinion on the Safety of Medical Devices 
Containing DEHP-Plasticized PVC or Other Plasticizers on Neonates and 
Other Groups Possibly at Risk.'' This report is available online at 
http://ec.europa.eu/health/ph_risk/committees/04_scenihr/docs/
scenihr_o_008.pdf.
---------------------------------------------------------------------------
    The most commonly used phthalates perform well, are economical, and 
have a rich toxicological database; more important, government safety 
assessments have consistently concluded that they may continue to be 
used safely in many applications, despite some concerns for a few 
applications where high exposures may be possible.

    Question 11. What about workers who are in the plants that 
manufacture phthalates. Are protections in place to make sure that they 
aren't unnecessarily exposed?
    Answer. Typically phthalates are manufactured in closed systems and 
the operator controls the reaction remotely on a computer terminal so 
worker exposure in manufacturing facilities is very low.

    Question 12. What are endocrine disruptors and how do they affect 
us?
    Answer. The term ``endocrine disruptor'' (ED) was invented in 1991 
at a World Wildlife fund-sponsored conference held at the Wingspread 
retreat in Racine, Wisconsin (Colborn and Clement 1992). The 
participants cited environmental and experimental findings in fish and 
wildlife, in vitro study results, and clinical findings in humans 
exposed to high levels of the clinically prescribed pharmaceutical 
diethylstilbestrol (DES) as the basis for the ED hypothesis. Under the 
ED hypothesis, the most relevant question is not whether highly potent 
pharmaceutical agents can cause effects, but rather are the exposures 
to trace ambient environmental levels of substances of sufficient 
magnitude and duration to exert adverse effects on the general 
population?
    Various organizations have held numerous conferences on the ED 
issue, and several have wrestled with the term ED. The term ED remains 
somewhat controversial because of the imprecise and inconsistent manner 
in which it is applied. Many use the term very broadly, such that many 
substances have been implied by some to be EDs, despite no evidence of 
harm. One of the clearer and most useful definitions of ED (and 
potential ED) was published by the ``European Workshop on the Impact of 
Endocrine Disrupters on Human Health and Wildlife'' held in Weybridge, 
UK (1996):

   ``An endocrine disrupter is an exogenous substance that 
        causes adverse health effects in an intact organism, or its 
        progeny, secondary to changes in endocrine function.''

   ``A potential endocrine disrupter is a substance that 
        possesses properties that might be expected to lead to 
        endocrine disruption in an intact organism.''

    Scientists have agreed that the definition requires that an ED have 
a link between the endocrine activity and some adverse health effect; 
otherwise the endocrine effect is not toxicologically significant. 
While some groups have lobbied for a broader and less rigorous 
definition, scientists have, across a variety of conferences and 
venues, consistently agreed with a definition identical to or very 
similar to the Weybridge definition.
    A number of excellent and comprehensive reviews of endocrine 
disruption studies have been published. Collectively, these reviews 
represent a significant body of scientific work compiled and or 
reviewed by more than 500 scientists across the world, resulting in 
extensive volumes covering human and wildlife toxicology, mechanisms of 
action, risk assessment, testing, test method development and 
validation, and other science policy concerns (NRC 1999; U.S. EPA 1998; 
EU 1999; SETAC 1998, 1999; IUPAC 2003; IPCS 2002; Environment Canada, 
1999). The consensus of the research is clear, that there is no 
evidence that humans have been adversely affected by ambient, 
environmental exposures to endocrine active substances and there is not 
convincing evidence of a growing human health issue. (Breithaupt 2004). 
In addition, the evidence in wildlife studies shows that some specific 
populations have been affected in areas of high contamination and 
exposure. As stated in the review of the International Union of Pure 
and Applied Chemistry (IUPAC), ``. . . it is somewhat reassuring that 
after substantial research in the past decade, there have been no 
conclusive findings of low level environmental exposures to EAS causing 
human disease'' (http://www.icsu-scope.org/projects/complete/endocrine
execsum.htm).

    Question 13. Is there an established list of known endocrine 
disruptors?
    Answer. No. In the U.S., under the Food Quality Protection Act 
(FQPA) of 1996, Congress required EPA to develop and implement a 
screening program--using validated test methods--to determine whether 
certain chemicals have estrogenic or other endocrine effects. Since 
then, EPA solicited advice from an advisory panel on what screens and 
what tests should be validated to determine whether chemicals have 
endocrine effects and then EPA began validating these tests. The issue 
which Congress put before EPA relative to testing for endocrine effects 
is much more complex than Congress appreciated in 1996, so the 
validation exercise has taken longer than anticipated. The mandate of 
the FQPA was on pesticide chemicals, so EPA has published a candidate 
list of pesticide chemicals for screening and testing in its Phase 1 of 
the Endocrine Disruptor Screening Program--but these are simply 
candidates for testing, not endocrine disruptors. EPA plans to begin 
ordering pesticide registrants and manufacturers to begin testing these 
chemicals for endocrine effects starting in August of 2008. Since these 
validated tests have not been applied yet, however, there is no 
established list of known endocrine disruptors in the U.S.

    Question 14. Do infants and children have the same immune and 
endocrine system as adults? Do studies take into account these 
differences?
    Answer, Do infants and children have the same immune and endocrine 
system as adults: Although the endocrine and immune systems of infants 
and children are composed of the same components as adults, these 
systems function in a manner that is somewhat different from adults. In 
all mammals, including humans, all organ systems develop, 
differentiate, grow and mature during development in the womb, during 
postnatal growth and throughout all life stages. Thus, the endocrine 
and immune systems differentiate during fetal development and grow and 
mature throughout childhood and adolescence. During puberty, the 
functions of the endocrine system change, becoming those of an adult. 
Similarly, the immune system grows and matures during childhood.
    Studies of the potential toxicity of chemical substances 
specifically examine effects on the endocrine and immune systems to 
address questions of potential vulnerability during growth and 
development in utero and growth and development postnatally up to and 
including attainment of sexual maturation (and these include evaluation 
of reproductive function after puberty. Typical developmental toxicity 
tests evaluate the effects of exposures during organogenesis and 
histogenesis, those periods during which organ systems are 
differentiating, forming and growing in utero. In developmental tests, 
pregnant animals are treated with the test agent (thus exposing the 
offspring in utero) and then fetuses are evaluated just before 
parturition for effects on the skeletal and organ systems. The period 
that is covered by the developmental toxicity study is sensitive to 
induction of structural malformations (birth defects). Reproductive 
tests can include one, two or more generations. The purpose of these 
studies is to examine successive generations to identify possible 
increased sensitivity to a chemical, effects on the fertility of male 
and female animals, prenatal, perinatal, and postnatal effects on the 
ovum, fetus and offspring, including teratogenic effects, as well as 
perinatal and postnatal effects on the mother. In such tests, the males 
and females of the parental generation are exposed to the test 
substance prior to mating. Exposure of the parental generation (males 
and females) continues throughout the gestation and weaning periods 
(offspring continue to be exposed via their mother through lactation 
for test agents that are transferred into milk). After weaning, the 
offspring are placed on a direct exposure regimen. Exposure is 
continued through the stages of adolescent growth and development, and 
at the stage of sexual maturation, in multigeneration studies, the 
exposed animals are mated and the effects on reproduction are 
evaluated.
    Scientists have long recognized that the endocrine systems and 
immune systems differ in younger mammals compared to adults. Such 
differences or ``windows of vulnerability during fetal development and 
sexual maturation'' are not a new concept, as these have been 
incorporated into research, testing and safety assessments for more 
than 40 years.\3\ Reproductive toxicity testing is generally focused on 
determination of the potential of a chemical to affect the ability of 
an organism to reproduce, while developmental toxicity testing focuses 
on the potential of a chemical to affect the viability or normal 
development of offspring of an organism during gestation. There are a 
number of standardized test methods that can be used to evaluate the 
effects of substances on development and reproduction.\4\ \5\ 
Reproductive tests can include one, two or more generations. The 
purpose of these studies is to examine successive generations to 
identify possible increased sensitivity to a chemical, effects on the 
fertility of male and female animals, prenatal, perinatal, and 
postnatal effects on the ovum, fetus and offspring, including 
teratogenic effects, as well as perinatal and postnatal effects on the 
mother. These studies require evaluations of all organ systems for 
abnormalities, including the endocrine and immune systems (specifically 
thymus and spleen).
---------------------------------------------------------------------------
    \3\ Wilson J.G. Teratology Principles and Techniques. Chicago, 
University of Chicago Press; 1965.
    \4\ USEPA (U.S. Environmental Protection Agency). OPPTS Harmonized 
Test Guidelines Series 870 Health Effects Test Guidelines--Final 
Guidelines. 2007. Available from: http://www.
USEPA.gov/docs/OPPTS_Harmonized/870_Health_Effects_Test_Guidelines/
Series/.
    \5\ USFDA (U.S. Food and Drug Administration). Toxicological 
Principles for the Safety Assessment of Food Ingredients, Redbook. 
2000. Available from: http://www.cfsan.fda.gov/redbook/red-toca.html)
---------------------------------------------------------------------------
    With respect to endocrine disruption, within EPA's Endocrine 
Disruptor Screening Program (EDSP), the 2-generation mammalian 
reproduction toxicity test is the scientifically valid, definitive 
laboratory toxicity test for use in human health risk assessment of 
such substances. EPA accepts this test method as ``valid for the 
identification and characterization of reproductive and developmental 
effects, including those due to endocrine disruption (ED) . . .'' 
Therefore, for evaluating endocrine disruption, the chemicals that have 
completed such 2-generation mammalian reproduction toxicity test tests 
are viewed as having fully satisfied the needs for human health risk 
assessment purposes. In the EDSP, the 2-generation mammalian 
reproduction toxicity is often referred to as the definitive Tier 2 
test for use in human health risk assessment. In EPA's EDSP, the Agency 
has clearly described the purpose and policy of such a Tier 2 Test:

        Federal Register/Vol. 63, No. 248/December 28, 1998/71554-71555 
        (emphasis added).

        The purpose of Tier 2 testing is to characterize the 
        likelihood, nature, and dose-response relationship of the 
        endocrine disruption of EAT in humans, fish, and wildlife. To 
        fulfill this purpose, the tests are longer-term studies 
        designed to encompass critical life stages and processes, a 
        broad range of doses, and administration of the chemical 
        substance by a relevant route of exposure, to identify a more 
        comprehensive profile of biological consequences of chemical 
        exposure and relate such results to the dose or exposure which 
        caused them.

        The outcome of Tier 2 is designed to be conclusive in relation 
        to the outcome of Tier 1 and any other prior information. Thus, 
        a negative outcome in Tier 2 will supersede a positive outcome 
        in Tier 1. Furthermore, each full test in Tier 2 has been 
        designed to include those endpoints that will allow a 
        definitive conclusion as to whether or not the tested chemical 
        substance or mixture is or is not an endocrine disruptor for 
        EAT [estrogen, androgen and thyroid] in that species/taxa.

    Toxicological studies designed to explore potential reproductive 
and developmental effects are often designed to be multi-generational, 
which means they explore effects on an exposed rodent and one or more 
generations of its offspring.

    Question 15. Have or haven't we seen many human studies on these 
chemicals? Is it even possible or ethical to conduct human studies?
    Answer. With respect to human studies generally, all human subjects 
research that is considered by EPA--whether conducted or sponsored by 
the Federal Government or other entities--must follow the high 
standards embodied in consensus standards such as the Federal Policy 
for the Protection of Human Subjects, referred to as the Common Rule; 
the Guideline for Good Clinical Practice; the Declaration of Helsinki; 
and the Nuremburg Code. For obvious ethical reasons, humans are not 
typically dosed with compounds to determine effects. Most data 
regarding chemical effects is drawn from traditional toxicological 
testing (the proverbial ``lab rat''). This data is sometimes augmented 
with human studies in the form of epidemiological data. Epidemiology is 
the study of the incidence and prevalence of disease in large 
populations and detection of the source and cause of epidemics of 
infectious disease.

    Question 16. Usually chemicals are tested one at a time. However, 
we come into contact with numerous chemicals every day. Do these 
studies simulate real world exposures and what is the best way to test 
chemicals?
    Answer. The question of exposures to mixtures of substances 
requires an understanding that humans encounter an ever-changing 
combination of natural and man-made chemicals at low levels, in normal, 
every day activities. We are exposed to a number of natural and man-
made chemicals simultaneously and continuously every day. It is no 
surprise that they can be detected, and this should not lead to undue 
concern. Whether we are breathing air, which is composed of chemicals, 
or ingesting food, which is a complex mixture of chemicals, our bodies 
are absorbing a variety of chemicals every day. Scientists, physicians 
and others in related professions have long understood that the actions 
of life are chemical by their very nature. As we interact with our 
environment, we are exposed to many thousands of chemicals, both 
natural and synthetic. The specific chemicals vary from day to day 
depending on our environment and activity. Generally, if a chemical is 
taken in by the body, it is either used or changed into a new chemical 
that can be used (nutrient) or it is altered by systems in the body and 
sequestered or excreted as waste. The increased sensitivity of 
analytical methods allows us to measure simultaneously more chemicals 
at lower concentrations in human tissues. This has led some to assert 
that the mere presence of chemicals in the body, or detection of 
mixtures of chemicals in the body, is harmful without regard for the 
amount of chemicals being referred to or the frequency or duration of 
presence in the body.
    The presence of a substance that has adverse effects at some level 
does not imply that the presence of that chemical will lead to adverse 
effects at all levels. Potential toxicity must be considered in the 
context of the amount, route, duration and timing of exposure. For 
human health risks for chemical induced toxicity, evidence-based 
medicine and toxicology principles--the true scientific consensus--tell 
us that effects at high doses will not be realized at lower doses if 
the concentration falls below the target site threshold level. This 
principle applies just as much to ``windows of susceptibility'' during 
development as it does more broadly to all life stages. And it applies 
to mixtures as well as to a single chemical.
    Our scientific understanding of how the body functions when exposed 
to environmental chemicals, and our knowledge based on current 
scientific methods for assessing harm posed by chemicals, indicates a 
large difference between low levels of exposure to chemicals and harm 
or disease resulting from exposure. Potential harm must be considered 
in the context of exposure and inherent toxicity of the chemical(s)--
the amount, route, duration and timing of exposure and toxicity. Both 
naturally occurring and environmental chemicals--can be toxic at some 
dose. Indeed, many ``naturally occurring'' chemicals are potent toxins. 
The quantity of exposure--the dose--is of utmost importance in 
determining potential risk.
    For example, one aspirin can be an effective therapeutic agent for 
a headache. Ingesting a full bottle of aspirin tablets will lead to 
toxicity. And taking an aspirin tablet and dividing into a hundred or a 
thousand equal parts, and then ingesting one of these small doses will 
not produce any effect whatsoever. This is a fundamental principle of 
biology and medicine and it applies to low level exposures to 
environmental chemicals, just as it applies to therapeutic agents and 
natural substances. The dose-response relationship for a specific 
chemical substance describes the association between exposure and the 
observed response (health effect). In other words, it estimates how 
different levels of exposure change the likelihood and magnitude of 
health effects. For many chemicals, there is a threshold below which an 
internal dose will not elicit a response. As the internal dose 
increases and exceeds the threshold, biochemical changes occur that may 
lead to adverse effects. There are clearly thresholds of exposures--
doses that are so low as to cause no harm. Such doses below the 
threshold would not create any untoward risk whatsoever. For mixtures, 
this principle applies as well.
    The human body is well equipped to manage low levels of chemicals. 
At low levels of many environmental chemicals, cells can act to break 
down and excrete these substances as wastes. However, when any chemical 
is present or accumulates to a toxic level, harm can occur. The same 
would apply for mixtures of chemicals. The question is not simply one 
of whether chemicals, natural or man-made are present in the body (a 
question of exposure), or whether the chemical can cause harm (a 
question of the chemical's inherent toxicity). Rather, it is the amount 
of those chemicals in the body relative to the amount that actually 
causes harm. In other words, the question is one of both exposure and 
toxicity. Therefore, it is the level and not the mere presence of any 
of the hundreds or thousands of chemicals in the body--regardless of 
their origin--that is important. This potential for harm relates to the 
concentrations of the chemicals in the body and their specific 
toxicity.
    The standard battery of toxicity tests employed by the chemical 
industry includes specific tests on animals designed to address 
endpoints of concern to the health of humans, including children. This 
toxicity testing battery for industrial chemicals includes tests that 
have been specifically designed to evaluate endpoints that cover acute 
toxicity, hazards to development in the womb and to growth and 
reproduction, damage to cell components that could possibly trigger 
transformation into cancer later in life, and the potential of 
substances to produce adverse effects on all major organ systems, 
including the nervous system. This test battery specifically includes 
study designs to evaluate potential toxicity during the critical phases 
of development in utero and thus addresses concerns for any 
differential sensitivity of the developing organism during windows of 
development (these types of studies have been conducted routinely since 
the 1960s).
    Animal model systems employed in standard toxicity testing 
routinely employ dose levels that are, 100-, 1,000- or even 10,000-fold 
higher than humans would be expected to experience. In fact, in order 
to provide assurance that potential toxicity will not be missed, the 
standard toxicity testing protocols for reproductive and developmental 
toxicity testing all require that the highest dose tested be chosen 
with the aim to induce some developmental and/or maternal toxicity but 
not death or severe suffering (http://www.epa.gov/opptsfrs/
publications/OPPTS_Harmonized/870_
Health_Effects_Test_Guidelines/Series/870-3800.pdf). While this 
approach is precautionary toxicology, because it ensures that there is 
little chance of ``missing'' a potential adverse effect, it also has 
the consequence of complicating communication efforts and precludes use 
of simple descriptors. Adverse reproductive or developmental effects 
observed at dose levels that produce parental toxicity may be secondary 
effects. If studies are conducted under conditions of overt toxicity, 
such effects may not be indicative of unique or selective developmental 
or reproductive toxicity. As a result, the only way to adequately 
communicate potential hazards of exposures is in a risk context. This 
means that the evaluative process must compare the dose-response data 
generated in the toxicity studies to estimated levels of human exposure 
to derive a margin of exposure (MOE). The MOE expresses the magnitude 
of the difference between a level of anticipated human exposure and the 
highest level at which there is no significant increase in the 
frequency of an adverse effect. This is critical information not only 
for assessing risk and considering risk management options when 
warranted, but also for communicating potential risks to the public.
    Risk assessment methods have been developed, and continue to be 
researched and refined, to account for aggregate exposure (exposure to 
the same agent from multiple sources/routes) and cumulative risk (risk 
estimated for concurrent exposures to substances which act via the same 
mechanism).
    Some specific risk assessment methods used and relied upon by U.S. 
EPA have been specifically designed for evaluating mixtures include:
    Risk assessment methods for U.S. drinking water regulatory actions 
routinely account for exposures to a specific agent that may occur not 
only from drinking water, but also from other pathways outside of 
drinking water, thus affording adequate protection for all potential 
exposures. http://www.epa.gov/waterscience/humanhealth/method/
chapter4.pdf.

        ``The drinking water program usually takes a conservative 
        approach to public health by applying an [relative source 
        contribution] RSC factor of 20 percent to the RfD when adequate 
        exposure data do not exist, assuming that the major portion (80 
        percent) of the total exposure comes from other sources, such 
        as diet.'' http://www.epa.gov/fedrgstr/EPA-WATER/2000/November/
        Day-03/w
        27924.htm.

    For over 15 years, risk assessment methods for hazardous waste site 
cleanup evaluations have routinely, included aggregate and cumulative 
quantitative calculations to account for both exposures to a single 
chemical from multiple pathways and concurrent exposures to multiple 
substances from the same or multiple routes.

        ``To assess the overall potential for cancer and noncancer 
        effects posed by multiple chemicals, EPA has developed 
        Guidelines for the Health Risk Assessment of Chemical Mixtures 
        that can also be applied to the case of simultaneous exposures 
        to several chemicals from a variety of sources by more than one 
        exposure pathway. Although the calculation procedures differ 
        for carcinogenic and noncarcinogenic effects, both sets of 
        procedures assume dose additivity in the absence of information 
        on specific mixtures.''

        Chapter 8, Risk Assessment Guidance for Superfund (RAGS), 
        Volume 1, Human Health Evaluation Manual, Part A (1989) http://
        www.epa.gov/superfund/programs/risk/ragsa/index.htm''

    With respect to experimental studies of chemical mixtures, many 
published interaction studies in toxicology are not interpretable for 
human health because they used faulty experimental designs, inadequate 
statistical methods or inappropriate biological model systems. Numerous 
interaction studies are not reliable for risk assessment due to a 
number of common problems: failure to characterize the individual dose-
response characteristics of chemicals in a mixture; failure to test a 
no-interaction hypothesis; and failure to apply an appropriate 
statistical test to the data. For example, most individual chemical 
dose response curves are not linear. When testing a mixture of 
chemicals, an additive response can easily be mistaken for a 
synergistic response due to this non-linearity. The response predicted 
under the assumption of additivity must first be determined, followed 
by statistical comparison of observed vs. actual responses. (Borgert 
C.J. et al., ``Evaluating interaction studies for mixture risk 
assessment.'' Human and Ecological Risk Assessment, vol. 7, pages 259-
306, 2001.)
    A Society of Toxicology panel has concluded that if toxicological 
data on chemical mixtures are to be relevant and useful for assessing 
risks to humans, it should be conducted at doses relevant to 
environmental exposures, including doses below the toxic threshold for 
individual chemicals. The scientific community has an obligation to 
demonstrate the clinical relevance of toxicological interactions of 
chemical mixtures to avoid the accumulation of ``interactions'' of 
doubtful relevance. (Teuschler L. et al. ``Support of science-based 
decisions concerning the evaluation of the toxicology of mixtures: A 
new beginning.'' Regulatory Toxicology and Pharmacology, vol. 36, No. 
1, pages 34-39, 2002.)
                                 ______
                                 
   Response to Written Questions Submitted by Hon. John F. Kerry to 
                        Steven G. Hentges, Ph.D.
    Question 1. Why are there such dramatically different results on 
the low-dose effects of BPA between the results of studies sponsored by 
the chemical industry and studies conducted by academics or government 
entities?
    Answer. Scientific studies can only answer questions they are 
designed to answer. Studies sponsored by industry are typically, but 
not always, aimed at answering the critical question of whether a 
product is safe for use. These studies are generally designed to meet 
the requirements of internationally accepted test guidelines that were 
developed for this purpose. The studies are typically large in scale to 
be sure the studies have adequate statistical power and examine 
appropriate endpoints to address the question that the study is 
intended to answer. The studies are also typically conducted in highly 
qualified test laboratories under Good Laboratory Practices, which 
provides further assurance of the integrity of the study results.
    Other studies, which can also include industry sponsored studies, 
are often aimed at other scientific questions that may or may not be 
directly relevant to assessing human health concerns. These studies may 
be limited in scope and examine endpoints that are difficult to 
interpret with respect to the safety of the substance being tested. 
Some studies, although scientifically well conducted, may have limited 
or no relevance for assessing human health concerns.
    For bisphenol A, a very wide diversity of studies have been 
conducted and it is a gross oversimplification to say that studies 
sponsored by the chemical industry have opposite results to studies 
conducted by academic institutions. Very often, studies cannot be 
directly compared because they are so different.
    As described in the answer to the question below, all relevant 
studies on bisphenol A have been systematically assessed in numerous 
weight of evidence evaluations. When all of the relevant data from 
these many studies are compared, in particular to determine whether the 
findings are repeatable or corroborated in independent laboratories, 
the most consistent result is that no effects from exposure to low 
doses of bisphenol A are reliably found. This conclusion is true even 
if the analysis is limited to non-industry studies. In that regard, 
studies sponsored by industry are consistent with the broader database 
and validate the overall conclusion that low doses of bisphenol A have 
not been reliably shown to cause adverse health effects.

    Question 2. In light of dozens of advanced studies over the past 
several years, in conjunction with the recent assessment from the 
National Toxicology Program, do you believe that the Federal Government 
should control exposure to BPA?
    Answer. Many hundreds of studies on bisphenol A have been conducted 
in the last 10 years and a substantial percentage of these studies were 
aimed at addressing the question whether bisphenol A could cause 
adverse health effects at very low doses. These studies are not all 
equivalent and, in general, they vary vastly in size, scope, quality 
and relevance to human health. The most comprehensive studies cover 
multiple generations of laboratory animals, are large in scale and 
statistically powerful, include a wide range of doses from very low to 
very high, and dose animals by the most relevant oral route of 
exposure. Other studies are small in size and scope, may be poorly 
conducted or reported, and dose animals by routes that are of little or 
no relevance to humans (e.g., subcutaneous injection, direct injection 
into the brain). A further complication is that the results of these 
many studies are not consistent and show conflicting results.
    When faced with a large and diverse body of data, as is the case 
for bisphenol A, scientists systematically evaluate the weight of 
scientific evidence to draw conclusions based on all of the available 
evidence. In recent years, numerous weight of evidence evaluations of 
bisphenol A have been conducted by independent scientific and 
government bodies worldwide. These evaluations consistently support the 
conclusion that bisphenol A is not a significant risk to human health, 
in particular at the very low levels to which people could be exposed 
through use of consumer products.
    In addition to evaluating each available study on its own merits, a 
weight of evidence evaluation also assesses whether the findings of 
studies have been replicated or corroborated in independent 
laboratories, whether they are consistent within and across studies, 
and whether they are coherent when considered together. Repeatability 
is a fundamental principle of the scientific process; findings that 
cannot be replicated in robust studies cannot be accepted as valid.
    Specifically in regard to the National Toxicology Program 
assessment, no serious or high level concerns were identified. Several 
possible health effects were identified as ``some concern,'' which 
indicated that only limited and inconclusive evidence was available 
from laboratory animal studies and additional research is needed to 
determine whether the limited evidence is of any relevance for human 
health.
    Based on the many evaluations that support the conclusion that 
bisphenol A is not a significant health risk, there is no apparent need 
based in science for action by the Federal Government regarding 
bisphenol A.

    Question 3. Can consumers trust products that are currently labeled 
as ``BPA-free''?
    Answer. Bisphenol A is primarily used to make polycarbonate plastic 
and epoxy resins. Since neither of these materials would exist without 
bisphenol A, alternatives to bisphenol A effectively means alternatives 
to these materials. Presumably products labeled as ``BPA-free'' are 
made from alternative materials that are not made from bisphenol A.
    To our knowledge, there are no alternatives that could easily 
substitute for all applications of these materials. In each case, a 
variety of factors must be considered to identify suitable alternatives 
and the critical requirements for each application vary considerably. 
For any alternative, two immediate hurdles are functionality (i.e., the 
alternative must provide the function needed for that application) and 
safety (i.e., the alternative must be safe for the application).
    Compared to bisphenol A, no alternative has been so well tested or 
vetted so thoroughly by government agencies. Consequently, it is not 
likely that scientific data exists to support a claim that any 
alternative is safer than bisphenol A.
    Whether consumers should trust products labeled as ``BPA-free'' 
must consider several factors including the veracity of the claim, the 
performance of the product, and the safety of the product. We do not 
have sufficient information on any of these factors to know whether 
consumers should trust these products.

    Question 4. Why are low-dose effects of endocrine-disrupting 
chemicals like BPA more dangerous than those of other compounds?
    Answer. The so-called ``low-dose hypothesis'' asserts that very low 
doses of endocrine-active substances may cause adverse health effects 
at very low doses. In particular, such low-dose health effects are 
postulated to occur with a non-monotonic dose-response, which means 
that health effects observed at very low doses would not be observed at 
higher doses. This hypothesis has not been scientifically proven and 
there is at best limited evidence that it could be valid.
    A fundamental principle of toxicology is commonly expressed as 
``the dose makes the poison,'' which means that health effects observed 
at a particular dose will uniformly increase in intensity or severity 
as the dose is increased. Conversely, as the dose is decreased, a dose 
causing no effect can be found (a no-effect level) and any lower dose 
will also cause no effect. This is referred to as a monotonic dose-
response (sometimes called a linear dose-response).
    Toxicology studies are often designed to identify a dose at which 
no adverse effects. occur, which is referred to as a No-Observed-
Adverse-Effect-Level (NOAEL). Doses below the NOAEL may not be tested 
since no adverse effects are expected. If the low-dose hypothesis is 
valid, health effects below the NOAEL might occur but not be found.
    In response to the low-dose hypothesis, there are now a large 
number of studies on bisphenol A that examined low doses well below the 
accepted NOAEL. Most of these studies did not examine a sufficient 
number or range of doses to determine whether any dose-response is 
monotonic or non-monotonic and are thus not capable of validating the 
low-dose hypothesis.
    It is important to note that the accepted NOAEL for bisphenol A is 
based on the most comprehensive studies, which were conducted over 
multiple generations of laboratory animals and included a wide range of 
doses from very low doses up to a very high dose above the NOAEL that 
induces toxicity. These studies do not validate claims that bisphenol A 
causes adverse effects at low doses and only monotonic dose-responses 
were observed. These studies provide the most powerful evidence that 
the low-dose hypothesis, at least for bisphenol A, is not valid.
    Beyond bisphenol A, the biological plausibility of the low-dose 
hypothesis is not supported by research on other endocrine-active 
substances. For example, two very robust and comprehensive studies have 
recently been published on estradiol and ethinylestradiol, the first 
being the prototypical naturally occurring estrogen and the second 
being the estrogenic substance commonly used in birth control pills. 
Both studies covered a wide dose range and neither study found non-
monotonic dose-response for any observed effect. In comparison to these 
two substances, bisphenol A is a very weak estrogen that is 10,000-
100,000 times less potent. No plausible explanation has been advanced 
to explain why bisphenol A would cause adverse effects at low doses 
with non-monotonic dose-response while more potent estrogens would not 
do so.
    There is at best very limited evidence to support the validity of 
the low-dose hypothesis and very strong evidence that indicates the 
hypothesis is not valid. Lacking reliable evidence and biological 
plausibility, the low-dose hypothesis is just that--a hypothesis that 
has not been proven.

    Question 5. In light of dozens of advanced studies over the past 
several years, in conjunction with the recent assessment from the 
National Toxicology Program, do you believe that the Federal Government 
should control exposure to phthalates?
    Answer. Numerous U.S. Federal agencies charged with reviewing 
phthalate esters have done so thoroughly, and after taking exposures 
into consideration. Phthalates have been assessed by the Consumer 
Product Safety Commission (CPSC), the Food and Drug Administration 
(FDA), the Centers for Disease Control, the National Toxicology Program 
(NTP), the Cosmetic Ingredient Review (CIR), the European Union, and 
Health Canada, as well as other countries. Most notably, the CPSC 
assessed the safety of phthalates used in children's toys, using the 
primary phthalate (DINP) for that application as the focal point for 
review, and concluded that there is ``no demonstrated health risk'' to 
young children. The CPSC's review included consideration of exposure 
data drawn from studies of children's mouthing behavior. The FDA 
conducted a risk assessment of the main phthalate used in medical 
devices (DEHP) and concluded ``the risk of not doing a needed procedure 
is far greater than the risk associated with exposure to DEHP.''
    Specifically in regard to the National Toxicology Program 
assessment, the NTP reviewed seven phthalates and concluded there was 
negligible to minimal concern for exposures to all the phthalate esters 
reviewed, except with respect to DEHP in certain situations. In 
particular, the only serious concern expressed was when used in medical 
treatment for critically ill male neonates. FDA responded to the NTP's 
review by cautioning that the benefits of medical treatment 
nevertheless outweighed the risks.
    Based on the many evaluations that support the continued safe use 
of phthalate esters, there is no apparent need based in science for 
additional action by the Federal Government at this time regarding 
phthalate esters.

    Question 6. What has been the experience of the European Union in 
phasing out phthalates in toys and childcare products? Has this been a 
significant logistical and manufacturing challenge for regulators and 
industry?
    Answer. The European Chemicals Bureau, which managed the risk 
assessments performed by the EU member states, provided a draft 
conclusion of the exhaustive safety reviews of the principal phthalate 
(DINP) used in toys. It stated it was ``unlikely to pose a risk'' even 
for newborns. Regrettably, despite the vote of confidence by the 
Bureau, the European Parliament had already moved forward with banning 
phthalates from some children's products. It was a decision based on 
politics, not science. Currently an array of other plasticizers are 
used in Europe.

    Question 7. Why are low-dose effects of endocrine-disrupting 
chemicals like phthalates more dangerous than those of other compounds?
    Answer. Low dose effects have not been claimed to be observed in 
testing of phthalate esters.
                                 ______
                                 

 EA-Free Plastics: The Only Alternative for Safe Plastics *
---------------------------------------------------------------------------

    \*\ Summary only the entire document is retained in Committee 
files.
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By George D. Bittner, Ph.D., Professor of Neurobiology, The University 
                          of Texas at Austin 
             and CEO, CertiChem, PlastiPure, Austin, Texas

Non-Technical Summary
The Problem
    Almost all plastics sold today release chemicals that have 
estrogenic activity (EA). While estrogens (the female sex hormones) 
occur naturally in the body, many scientific studies have shown that 
significant health problems can occur when chemicals are ingested that 
mimic or block the actions of these female sex hormones; the fetus, 
newborn, or young child is especially vulnerable. These health-related 
problems include early puberty in females, reduced sperm counts in 
males, altered functions of reproductive organs, obesity, altered 
behaviors, and increased rates of some breast, ovarian, testicular, and 
prostate cancers.
The Billion Dollar Marketing Band-Aid
    Bisphenol A (BPA) and phthalates are two of thousands of chemicals 
that have EA that are in, and released from, almost all plastics sold 
today. The current commercial approach is to solve this health-related 
problem by producing BPA-free and/or phthalate-free plastic products. 
Unfortunately this incremental ``marketing'' solution to replace an 
individual chemical would not quickly (if ever) provide an EA-free 
health-related solution. Furthermore, chemicals or products substituted 
for BPA or phthalate-containing products often leach other chemicals 
having more total EA than the EA released by the original products.
Legislation to Date
    The call to ban BPA and phthalates is growing rapidly. California 
has passed legislation banning phthalates and legislation to ban BPA is 
pending; similar bills are pending in Connecticut, New York, 
Pennsylvania, Maryland, Maine and Minnesota. The U.S. Senate is 
considering an amendment to the Consumer Product Safety Commission 
Reform Act that would ban phthalates. The European Union and Canada 
have already passed this legislation. However, all current legislation 
attempts to solve this EA problem by banning chemicals having EA one at 
a time. This approach is not an appropriate long-term solution because 
thousands of chemicals used in plastics exhibit EA, not just BPA and 
phthalates.
The Health-Related Solution
    The most appropriate solution is to legislate that all plastics be 
EA-free, rather than ban specific EA-causing ingredients one at a time. 
This is not a pie-in-the-sky solution, as the technology already exists 
to produce EA-free plastics that also have the same advantageous 
physical properties as do almost all existing EA-releasing plastics. 
Some of these advanced-technology plastics are already in the 
marketplace.
Legislation to Date
   NY HB 11277: Bill introduced to the NY House of 
        Representatives on May 27, 2008 that ``Prohibits the 
        manufacture, distribution and sale of toys and child care 
        products containing bisphenol-A''

   Canada has announced plans to restrict the use of BPA, a 
        chemical used to make hardened plastics. The government would 
        prohibit the sale of baby bottles made with BPA. (The ban will 
        take effect mid-June.)

   In April, the U.S. National Toxicology Program, which 
        assesses the health effects of chemicals, also raised concerns 
        about the potential ``neural and behavioral'' effects of BPA on 
        all humans, but especially on fetuses, infants and young 
        children. The program also warned against heating or 
        microwaving food containers made with BPA, since some studies 
        suggest that BPA may break down faster at higher temperatures.

   There will be a public telephone call-in line for the June 
        11-12, 2008 meeting of the NTP Board of Scientific Counselors. 
        The meeting will be held at the Radisson Hotel Research 
        Triangle Park, 150 Park Drive, Research Triangle Park, NC 27709 
        and videocast through the Internet at http://
        www.niehs.nih.gov.libproxy.txstate.edu/news/video/live.

   Senator Charles Schumer of New York and several of his 
        fellow Democrats have proposed a ban on BPA in all children's 
        products, and Representative John Dingell of Michigan is 
        investigating whether the industry-backed studies that are used 
        as the basis of the FDA's advice to consumers are really 
        sufficient to warrant an all-clear for BPA.

   As part of his investigation, Rep. John D. Dingell (D-
        Mich.), Chairman of the House Energy and Commerce Committee, 
        wants to examine the role played by the Weinberg Group, a 
        Washington firm that employs scientists, lawyers and public 
        relations specialists to defend products from legal and 
        regulatory action. The firm has worked on Agent Orange, tobacco 
        and Teflon, among other products linked to health hazards, and 
        Congressional investigators say it was hired by Sunoco, a BPA 
        manufacturer. Dingell has asked the Weinberg Group for all 
        records related to its work in connection with BPA, including 
        studies it has funded and payments made to experts. He cited a 
        letter written by a company vice president in 2003 as Weinberg 
        managed opposition in a long-running regulatory battle over a 
        compound in Teflon. The letter said this strategy would be to 
        discourage ``governmental agencies, the plaintiffs' bar and 
        misguided environmental groups from pursuing this matter any 
        further.''

   Last year, NIH convened two panels to help it analyze BPA 
        risks. One panel, led by Fred vom Saal, Ph.D., Professor of 
        Biology, University of Missouri (Columbia), consisted of 38 
        international experts on BPA who work for universities or 
        governments. Last August, it found a strong cause for health 
        concerns, including cancer and early puberty.

   In July of 2005, the European Union banned six different 
        phthalates from use in toys and childcare items. The EU had 
        already had temporary, renewable restrictions of these 
        phthalates in place since 1999.

   In October 2007, California passed a law that would ban the 
        sale or manufacture of toys containing phthalates, starting in 
        January 2009.

   Japan, Mexico and Argentina, have also outlawed phthalates.

   China, which makes 85 percent of the world's toys, has 
        developed two manufacturing lines, one for the European market 
        and the other like-minded nations that ban phthalates, and 
        another one for the United States and dozens of, mostly 
        developing and Third World, countries that don't restrict them.

   In early March, Washington State passed a strict ban on 
        phthalates in toys.

   The other states considering laws to ban phthalates include:


    Connecticut

    Hawaii

    Illinois

    Maryland

    Massachusetts

    New Jersey

    New York

    Rhode Island

    Vermont

    West Virginia

   In early March, the Senate passed a bill to reform the 
        Consumer Product Safety Commission, that includes a ban on 
        phthalates in children's toys. Lawmakers are working to 
        reconcile the Senate measure with a slightly different version 
        approved by the House of Representatives, which doesn't include 
        the phthalate ban.
Technical Summary
    Plastics are made by polymerizing a specific monomer in the 
presence of catalysts into a high molecular weight chain known as a 
polymer. The resulting polymer (usually in powder form) is mixed with 
much smaller, very specific, quantities of various additives 
(antioxidants, plasticizers, clarifiers, colorants, etc.) called a 
plastic formulation (usually proprietary) and then heated to form 
pellets. Plastic products are then made using processes (blow molding, 
extrusion, injection molding, thermoforming, etc.) that subject these 
pellets with more additives to various combinations of heat and 
pressure.
    PlastiPure, and its sister corporation CertiChem, have extensive 
data showing that almost all existing commercially available plastics 
release chemicals that exhibit endocrine disruptor (ED) activity, 
especially estrogenic activity (EA) at concentrations (micromolar 
(ppm) to nanomolar (ppt) or even picomolar) that have many adverse 
biological effects, especially on fetal and newborn mammals, including 
humans. Endocrine disrupting chemicals (EDCs) having EA can have 
significant deleterious effects at very low (micromolar to picomolar) 
concentrations, especially on fetal or developing mammals (NIEHS, 2006; 
EDSTAC, 1998; NRC, 1999; NTP, 2000; Welshons et al., 2003; Kabuto et 
al., 2004; vom Saal and Hughes, 2005; Swan et al., 2005; Rubin et al., 
2006; vom Saal, 2006). This raises significant concern for human 
exposure because some plastic products, including baby toys, leach EDCs 
having EA at concentrations greater than this nanomolar to picomolar 
range (Takao et al., 1999; Howdeshell et al., 1999; Yang and Bittner, 
2007).
    Other than its products, PlastiPure has not yet identified any 
other commercially available plastic product which has been tested to 
be reliably EA-free [having no detectable EA according to the most 
sensitive available assays]. PlastiPure has not identified any other 
firm that is currently advertising EA-free plastics, although there are 
some firms which are marketing ``Bisphenol A-free'' or ``phthalate-
free'' products (USA Today, 2007). However, although they may not 
contain BPA or phthalates, PlastiPure's and CertiChem's data show that 
in normal use these products do release other additives (or monomers) 
that exhibit EA. In fact, these data show that products advertised as 
BPA-free or phthalate-free plastics often release chemicals that have 
more total EA than the total EA released by products containing BPA or 
phthalates.
    PlastiPure has developed an extensive line of technologically-
advanced formulations and procedures for making safer plastics, food 
additives, and other products that do not release chemicals having EA. 
PlastiPure's unique formulations derived from its intellectual 
property, including one patent already granted (U.S. Patent # 6,894,093 
B2) for some EA-free plastic formulations, and two pending patents. One 
of these pending patents is very broad and identifies many hundreds of 
plastic formulations to make many useful plastic products that in 
normal use would not release any chemicals having EA. This patent 
covers not only almost all monomers and all additives used in plastic 
formulations, but also most chemicals used in the manufacturing process 
to produce plastics that in normal use will not release detectable 
amounts of EA.
    CertiChem has spent over 8 years and $5 million to develop the most 
sensitive and accurate assays available today to detect EA. PlastiPure 
has spent over $1.5 million in the last 8 years to develop plastics 
that do not leach any of thousands of chemicals having detectable EA, 
as measured by CertiChem's most sensitive assays. All PlastiPure 
plastics have also been developed to retain other useful properties of 
other plastics that do release chemicals having EA: flexibility, 
hardness, clarity, heat resistance, cold tolerance, UV tolerance, 
microwavable, etc. PlastiPure's advanced technologies use patent-
protected state-of-the art advances in cell/molecular biology, 
endocrine physiology, polymer chemistry and polymer engineering.
    That is, PlastiPure and CertiChem have used a set of advanced 
technologies to solve a health-related problem found in almost all 
currently marketed plastic items: they release one or more chemicals 
having detectable EA. Other firms have spent many millions to develop 
plastics that do not contain one or two of the thousands of chemicals 
known to have EA. Other firms are now spending many millions to 
billions to market those plastics that still release one or more of the 
thousands of other chemicals having EA. In contrast, PlastiPure has 
used advanced technologies to develop very broad health-related 
solutions to the problem of plastics releasing chemicals with EA, 
rather than market-related solutions that develop plastics that do not 
release specific chemicals having EA, but still release other chemicals 
having EA.

                                  
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