United States
Environmental Protection Agency
REGION/ORD WORKSHOP ON
EMERGING POLLUTANTS
SUMMARY REPORT
August 11-14, 2003
Chicago, IL
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TABLE OF CONTENTS
FOREWORD ix
EXECUTIVE SUMMARY xi
WORKSHOP SESSION SUMMARIES 1
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TABLE OF CONTENTS
Monday, August 11, 2003 1
WELCOME AND INTRODUCTORY REMARKS 1
Bharat Mathur, Deputy Regional Administrator
U.S. EPA Region 5 1
Paul Oilman, Assistant Administrator, Office of Research and Development (ORD),
U.S. EPA Agency Science Advisor 1
David Macarus, U.S. EPA Region 5, Regional Science Liaison to ORD,
Chair, Workshop Planning Group 2
Case Study - Triclosan: One Example of How Emerging Pollutants Come to Our
AttentionEmerging Pollutants Come to Our Attention
Steve Reimer, U.S. EPA Region 10 2
PERFLUORO OCTANE COMPOUNDS IN THE ENVIRONMENT 3
PFOS Toxicity Studies
Christopher Lau, U.S. EPA/ORD/National Health and Environmental Effects
Research Laboratory (NHEERL)/Research Triangle Park (RTP) 3
Studies of Human and Animal Toxicity
John Cicmanec, U.S. EPA/ORD/National Risk Management Research
Laboratory (NRMRL)/Cincinnati 6
Risk Information UpdateRisk Information Update: Overview of Assessment and
Activities of PFOS and PFOA
Jennifer Seed, U.S. EPA/Office of Prevention, Pesticides and Toxic
Substances (OPPTS)/Office of Pollution Prevention and Toxics (OPPT) 7
PFOS and PFOA Program Office Update Program Office Update
MaryF. Dominiak, U.S. EPA/OPPTS/OPPT 8
TOXIC CHEMICALS RESULTING FROM THE DISPOSAL OF ELECTRONIC
EQUIPMENT 10
Examining the Pollution Potential of Discarded Electronic Equipment Disposal
Timothy Townsend, University of Florida 10
Emissions from the Incineration of Electronics Industry Waste Combustion Issues
Eric Stewart, ORD/NRMRL/RTP 11
Toxic Chemicals Resulting From the Disposal of Electronic Equipment
Jason Swift, U.S. EPA Region 5 RCRA Program 12
Tuesday August 12, 2003 15
BROMINATED FLAME RETARD ANTS 15
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Ted Smith, U.S. EPA/Great Lakes National Program Office (GLNPO) 15
Overview of Brominated Flame Retardants
Leif Magnuson, U.S. EPA, Region 9 Pollution Prevention Coordinator 15
Polybrominated Diphenyl Ethers in People
Ron Kites, Indiana University 17
Brominated Flame Retardants in the Environment
Mehran Alaee, Environment Canada 18
Brominated Flame Retardants: Toxicology and Risk
Linda Birnbaum, U.S. EPA/ORD/National Health and Environmental Effects
Research Lab (NHEERL) 21
Status of the VCCEP Consultation re: penta, octa and decabromo diphenyl ethers
Jennifer Seed, U.S. EPA/OPPTS/OPPT 23
Bisphenol A and Phthalate Esters: Potential Sources of Resin Components in the Everyday
Environments of Preschool Children
Marsha Morgan, U.S. EPA/ORD/RTP/National Exposure Research Laboratory
(NERL) 26
Radium in Oil and Gas Piping and Production Facilities
Loren Setlow, U.S. EPA Office of Radiation and Indoor Air (ORIA) 30
Balanced Perspectives Regarding Environmental Levels of Thallium and Platinum
Group Metals
Frank Anscombe, U.S. EPA Region 5 34
Wednesday, August 13, 2003 38
Asbestos and Related Durable Fibers: Too Ubiquitous, Too Persistent, Too Complex to Put
Health Risks to Rest?
Phillip Cook, U.S. EPA/ORD/NHEERL/Duluth, MN 38
PHARMACEUTICALS AND PERSONAL CARE PRODUCTS 42
Pharmaceuticals and Personal Care Products (PPCPs) As Environmental Pollutants
(Pollution From Personal Action)
Christian G. Daughton, U.S. EPA/ORD/NERL-Las Vegas 42
Environmental Monitoring for Chemicals in Waters
Michael J. Focazio, U.S. Geological Survey 47
Veterinary Pharmaceuticals: Potential Environmental Impact and Treatment Strategies
John L. Cicmanec, U.S. EPA/ORD/NRMRL/Cincinnati 49
Assessing the Environmental Risk of Substances Under the US Food and Drug Act
Charles Eirkson, U.S. Food and Drug Administration (FDA) 53
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ENDOCRINE DISRUPTING POLLUTANTS IN EFFLUENT DOMINATED
STREAMS 56
A Regional Case Study of Alkyl Phenol and Ethoxylates
Peter Howe, U.S. EPA Region 5 56
Field Observations of the Contributions of Alkyl Phenols on Fish Endocrine Disruption
Cliff Rice, U.S. Department of Agriculture
Dr. Carys Mitchelmore, University of Maryland 59
Effects of Wastewater Treatment Effluents on Fish Endocrine Disruption
Larry Barber, U.S. Geological Survey 61
Aquatic Toxicity, Estrogenicity and Treatability of Nonyl Phenol and Ethoxylates in
Waste Water Effluents
Charles Staples, Assessment Technologies, Inc 63
Thursday, August 14, 2003 65
Objectives of the Final Session
Dan Hopkins, Toxics Reduction Manager, U.S. EPA Region 5 65
Biotechnology: A New Frontier, The Promise, Potential Risks, and How Can We Find
Out?
John A. Glaser, U.S. EPA/ORD/NRMRL - Cincinnati 65
Environmental Futures: Nano Technology and Genomics Coming Over the Horizon
Gerardo (Pasky) Pascual, ORD/Office of Science Policy, Environmental Futures
Workgroup 69
Wrap-Up Roundtable of Speakers
Dan Hopkins, Toxic Reduction Team Manager, U.S. EPA Region 5 72
Feedback From Environmental Journalist - An Outsider's Perceptions
Janet Raloff, Science News 72
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APPENDICES
APPENDIX A: AGENDA A-l
APPENDIX B: LIST OF PARTICIPANTS B-l
APPENDIX C: SLIDES FROM PRESENTATIONS C-l
APPENDIX D: FLIP CHART NOTES D-l
APPENDIX E: PARTICIPANT EVALUATION SUMMARY E-l
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FOREWORD
The U.S. EPA ORD/Regional Emerging Pollutants Workshop was the twelfth in a series of
Regional Science Topic Workshops sponsored by the Office of Science Policy in the Office of
Research and Development at the United States Environmental Protection Agency (EPA). Other
workshops in this series have included the following:
• Asthma: The Regional Science Issues
• Communicating Science: Waves of the Future Info Fair
• Fully Integrated Environmental Location Decision Support (FIELDS)
• Non-Indigenous Species
• Pesticides
• Endocrine Disruptors
• Emerging Issues Associated with Aquatic Environmental Pathogens
• Aquatic Life Criteria
• Critical Ecosystems
• Air Toxics Exposure Assessment
• Cumulative Risk Assessment
The ORD/Regional Science Topic Workshops have two complementary objectives: 1) establish
a better cross-agency understanding of the science applicable to specific region-specific human
health and/or ecological topics; and 2) develop a network of EPA scientists who will continue to
exchange information on these science topics as the Agency moves forward in planning
education, research, and risk management programs.
Each year, EPA Regions identify high priority science topics on which to conduct workshops.
The workshops address the science issues of greatest interest to the regions on the selected topic
areas. Each workshop is planned and conducted by a team of regional, ORD, and interested
program office scientists, is led by one or more Regional Science Liaisons or ORD, and is
facilitated by a regional chairperson. Participants maintain the cross-Agency science networks
they establish at the workshops through planned post-workshop projects and activities such as
identifying collaborative research opportunities, creating information sharing mechanisms (e.g.,
interactive web sites), and developing science fact sheets for regional use.
For additional information on a specific workshop or on the Regional Science Topic Workshop
series in general, contact David Klauder in ORD's Office of Science Policy (202-564-6496).
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EXECUTIVE SUMMARY
The U.S. EPA ORD/Regional Emerging Pollutants Workshop was hosted by Region 5 and held August
11-14, 2003, in Chicago, Illinois.
The workshop was organized into multiple sessions covering a number of diverse topics, all of which
addressed chemicals/substances considered to be either emerging pollutants, or substances for which
additional research may be warranted based upon recent risk evaluation research or for other reasons.
Break out and roundtable discussion sessions to explore specific topics - and the overall issue of tracking
and researching emerging pollutants - were held at intervals throughout the course of the workshop.
Topics discussed in the workshop included the following:
• Case Study - Triclosan: One Example of How Emerging Pollutants Come to Our Attention
• Perfluoro Octane Compounds in the Environment
• Toxic Chemicals Resulting From the Disposal of Electronic Equipment
• Brominated Flame Retardants
• Bisphenol A and Phthalate Esters
• Radium in Oil and Gas Piping and Production Facilities
• Exposures to Thallium and to Platinum Group Metals
• Asbestos and Related Durable Fibers
• Pharmaceuticals and Personal Care Products in the Environment
• Environmental Monitoring for Chemicals in Waters
• Veterinary Pharmaceuticals: Potential Environmental Impact and Treatment Strategies
• Assessing the Environmental Risk of Substances Under the US Food and Drug Act
• Endocrine Disrupting Pollutants in Effluent Dominated Streams
• Biotechnology: The Promise, Potential Risks, and How Can We Find Out
• Environmental Futures: Nano Technology and Genomics Coming Over the Horizon
• Feedback from an Environmental Journalist
Scientists from EPA (Regions; Office of Research and Development; Office of Pollution Prevention and
Toxics; Great Lakes National Program Office; Office of Radiation and Indoor Air; Office of Science
Policy) and invited speakers from academia, government laboratories, Environment Canada, U.S.
Geological Survey, U. S. Food and Drug Administration, U.S. Department of Agriculture, and the media
presented research information and discussed additional research needs and strategies for ensuring that
emerging pollutants are addressed.
The diverse presentation topics covered in the workshop allowed participants to explore these topics as
well as the issue of ensuring that emerging pollutants receive Agency attention and are adequately
researched and monitored. The roundtable and break out sessions, which addressed the presentation
topics, sought to answer the following questions:
• Are risks to human health and the environment from the substances being discussed
quantifiable, and are they likely to increase over time?
• What knowledge gaps need to be filled to clarify present and projected risks? and
• Are there pollution prevention/risk reduction or other risk management options for these
pollutants?
According to the workshop evaluations, most participants found the workshop very useful, and many
expressed interest in making such dialogs a more regular feature of ORD activity. Planned outcomesfred
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include continued communication among participants and others on the emerging pollutants discussed in
the workshop.
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WORKSHOP SESSION SUMMARIES
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Monday, August 11, 2003
WELCOME AND INTRODUCTORY REMARKS
Bharat Mathur, Deputy Regional Administrator
U.S. EPA Region 5
Mathur welcomed attendees and said the workshop is one of the first held by U.S. EPA's Office
of Research and Development (ORD) on emerging pollutants. He added that emerging pollutants
is an important topic for ORD and for EPA headquarters (e.g., as a factor in developing strategic
plans). The topic is also important to the regions, because they are on the front line to respond to
new pollution concerns raised by the public.
Region 5 also is taking an increasingly active role in science issues and dialogue with ORD.
Mathur added that Region 5 has held other workshops on topics such as pesticides and TMDLs
and has collaborated with other Regions to hold additional workshops. "It is my hope that
Region 5 and other regions can influence the Agency's science interests to meet our own needs,"
he said.
ORD/Regional Workshops - Videotape
Paul Gilman, Assistant Administrator, Office of Research and Development (ORD), U.S.
EPA Agency Science Advisor
Gilman began by saying that this is the 13th in a series of workshops on selected topics involving
the Regions. ORD has 2,000 employees and a $700 million budget, including $100 million in
external grants that it administers. It has 13 labs and research facilities located throughout the
regions. At EPA, science is used to make good decisions. High priority research areas are
human health and ecological health.
The workshops are driven and planned by the Regions to help promote cross-agency networking
and to integrate EPA science into Region decision making. The next workshop will address
inhalation risk. Gilman said one objective of the current workshop is to identify emerging
pollutants in U.S. EPA regions.
The Agency would like to use scientific knowledge and research for the decision making needed
to address regional programmatic areas. Some of the topics that have been identified in the past
for research include the following: particulate matter, drinking water, global climate change,
endocrine disrupters, and ecological systems. Past workshops have addressed such topics as
cumulative risk assessment and asthma.
ORD's goal is to anticipate future or emerging issues, to determine whether there are human
health or environmental concerns, and to develop a research agenda to quantify impacts. Most
emerging pollutants are as yet unregulated, he said, and the Agency must explore whether data
on these substances currently exist and what additional data may be needed to identify such
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pollutants and their effects. "The public will need to be educated" about the existence of
emerging pollutants and their impacts "to provide an action agenda for the future," he said.
Introduction to the Emerging Pollutant Workshop
David Macarus, U.S. EPA Region 5, Regional Science Liaison to ORD, Chair, Workshop
Planning Group
Thousands of chemicals are used in products that provide beneficial uses. But along with the
beneficial uses there also are wastes or negative consequences that must be addressed.
Additionally, there can be delayed consequences, as in the case of PCBs, which are no longer
manufactured, but are still bioaccumulating in fish.
One of the goals of the workshops is to bring EPA science into regional decision making. This
particular workshop also has some industry representatives in attendance. Macarus noted that
industry has more information about some substances than does EPA, so a dialogue with them is
important.
An important question to ask is whether EPA's processes are adequate for dealing with all of the
chemicals that come onto the market. These products are beneficial, but can we prevent negative
consequences of their manufacture and use? "We must maintain the beneficial uses and keep the
impacts on the environment from affecting us," he said. Macarus ended his comments by saying
that it is important to identify unanswered questions - and unquestioned answers.
Case Study - Triclosan: One Example of How Emerging Pollutants Come to Our
AttentionEmerging Pollutants Come to Our Attention
Steve Reimer, U.S. EPA Region 10
This case study briefly describes the serendipitous discovery of an emerging pollutant, Triclosan,
while seeking to identify and quantify other suspected contaminants in the environment.
During 1997 and 1998, the Region 10 laboratory was involved in the Columbia River Intertribal
Fish Commission Project (CRITFC). This was the first large-scale survey offish consumption
in the area. For the study, 300 fish samples were analyzed for organic and metal contaminants.
The lab was involved in identifying the target list of chemicals. The usual pollutants were
found, such as Arochlor (PCBs), DDT, mercury, and some other metals.
When analyzing for Aroclor with electron capture detectors (EDC), extra peaks were detected
eluting after Aroclor 1260. These peaks didn't match anything researchers had experience
analyzing. They didn't match Aroclor 1268 or a chlorinated terphenyl pattern, and analysis on
the gas chromatograph (GC) with an atomic emission detector showed bromine rather than
chlorine. These late eluting peaks were detected in bottom-dwelling and older fish (e.g.,
sturgeon and white fish).
Analysis determined that the peaks represented brominated compounds, with polybrominated
diphenyl ethers (PBDE) as the probable compounds. PBDE is used as a flame retardant in
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upholstery foam. Because, at the time, there were no commercially available standards, the lab
produced its own homemade "Bromkal 70" to make a standard. This allowed the lab to report a
value for total PBDE in the fish samples.
By 2001, standards were available commercially through Cambridge Isotopes, and the research
team decided to revisit the fish samples using both the homemade and the commercial standard.
At this time they also began to look for sources of PBDE in the environment. Potential
environmental sources of PBDE were identified based on a literature search. They included
storm water runoff, industrial effluent, and wastewater treatment plant effluent.
Samples from five wastewater treatment plants (water and sludge) were collected along with
sediment from above and below outfalls from plants treating wastes for industrial (Tacoma),
agricultural (Yakima), and residential (Port Orchard) areas. Because bio-solids from treatment
plants can be used as a soil conditioner, samples also were collected from several farm fields.
Analytical procedures included solvent extraction, fiorisil treatment, acid treatment, sulfur
removal, and GC/ECD analysis.
Using gas chromatograph/mass spectrometer (MS) analysis, researchers found, among other
compounds, 5-chloro-2-(2,4-dichlorophenoxy)phenol, or triclosan. This unexpected finding
again required innovative thinking and methods development. In order to create a quick
standard, they used a toothpaste (Colgate) extract, which contained 0.3% triclosan, to make a
standard for the GC/MS. Triclosan was detected in wastewater treatment plant sludge in
concentrations as high as 23 ppm. The compound was found in concentrations in the low parts
per billion in some sediment samples. Bio-solids that had not yet been spread showed 29 ppm
triclosan. Triclosan was detected in soil from one of the hop fields at 150 ppb. The compound
was not detected in the control hop field at 0.04 ppb.
In summary, the laboratory was able to find the triclosan in the environment for several reasons.
The analysts had time to work on the problem and the necessary equipment, including an AED
and an MS to identify the unknown peaks. The lab also was able to develop and find standards
for the analysis, though the PBDE standards weren't commercially available in 1997. Also
credited for making the finding were "picky" analysts, who wanted to identify the initially
unidentified peak, and luck.
PERFLUORO OCTANE COMPOUNDS IN THE ENVIRONMENT
PFOS Toxicity Studies
Christopher Lau, U.S. EPA/ORD/National Health and Environmental Effects Research
Laboratory (NHEERL)TResearch Triangle Park (RTF)
Perfluorinated organic chemicals such as perfluorooctane sulfonate (PFOS) and
perfluorooctanoic acid (PFOA) have been in the news over the past few years. At one point the
New York Times reported, albeit erroneously, that some of these compounds were posing health
risks to young women and girls. PFOS also is discussed on the website for the book Our Stolen
Future. Some have commented that PFOS will be the PCB of the 21st century. Perfluorooctane
sulfonate is an organic compound that does not easily break down. It is hydrophobic (does not
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bond to water) and oleophobic, so it is ideal for use as a surfactant in many industrial and
consumer applications. Perfiuorooctane sulfonate has been mass produced for the past 50 years.
Two major processes are used to make PFOS. One involves electrochemical fiuorination in the
presence of hydrofluoric acid, favored by 3M, that produces a mixture of straight-chained and
branched isomers. The other process is telomerization, favored by DuPont to produce straight-
chained telomer alcohol. Hence, PFOS compounds exist in a mixture in the environment.
PFOS is a very useful chemical found in more than 200 products. The best known is probably
3M's Scotchguard™. It also has been used commercially in a variety of other products as: paper
coatings, floor polish, alkaline cleaners, denture cleaners, shampoos, fire-fighting foams,
aviation hydraulic fluid, mining/oil well surfactant, acid rust suppressant, metal plating,
electronic etching bath, and ant/roach insecticides.
PFOS came to EPA's attention because of its presence in the blood serum of workers involved in
the manufacture of the product (300 - 8,000 ppb. mean 2,500 ppb). Once they began bio-
monitoring for the compound, they found it in non-production employees (29-96 ppb, mean 47
ppb), human serum samples (7 - 82 ppb, mean 28 ppb), blood bank pools (9 - 56 ppb, mean 30
ppb), and children (7-515 ppb, mean 44 ppb).
The mean concentration level in children of 44 ppb was somewhat alarming, because low levels
of contaminants are typically found in this sub-population. Additionally, researchers have found
the compound in the environment, in plasma and in liver samples from many types of wildlife
animals - from dolphins, fish, and birds to polar bears in the arctic.
PFOS is readily absorbed orally but remains in the body for a long time; the half-life in humans
was estimated at 8.7 years, compared to 200 days for monkeys and 7.5 days in rats. Exposure
results in body weight loss, liver hypertrophy/lesions, and reduced serum/liver cholesterol. Such
effects are pretty consistent among the species examined.
U.S. EPA is concerned about PFOS for the following reasons: the chemical is widespread in
humans and wildlife; it is stable, persistent, and bio-accumulative; it is developmentally toxic in
lab animals; levels in children are relatively high; modes and mechanisms of toxicity are not well
defined; and fate and transport of the compound is unknown at this time.
3M voluntarily stopped its manufacture of PFOS as of December, 2002, though there are still
some companies in Europe and Asia that make it. In addition, alternative fiuorochemicals
substituting for PFOS are under development and being marketed.
Studies of maternal toxicity, developmental toxicity (including pre- and post-natal evaluation),
and mechanisms of pathophysiology were undertaken using Sprague-Dawley rats and CD-I
mice. Researchers found maternal toxicity in pregnant rats with the level of the chemical
increasing over the period of gestation. The liver was found to have a PFOS level about four
times higher than the blood serum. There was a weight gain deficit for the pregnant rat when
given higher doses (3-10 mg/kg) due to reduced food and water intake. Reduced serum thyroid
hormone levels also were observed in the rat.
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In pregnant mice, PFOS at the end of gestation was four times higher in the liver compared to
serum levels, and the liver was enlarged. Liver enlargement was not observed to the same extent
in rats. A weight gain deficit also was observed to a lesser extent in the mice. The reductions in
maternal weight gains for both rats and mice corresponded to administered doses and body
burden.
In regard to developmental toxicity, PFOS exposure during pregnancy in the test animals did not
cause the fetuses to die or to be low in weight, suggesting that the mother protected the fetus. In
utero exposure did not significantly alter implantation or the viability and weight of the fetus at
term. At the highest doses, some structural malformations were observed (enlarged right atrium
of the heart and cleft palate).
The postnatal evaluations were a different story, however. All of the test animals gave birth live,
but the pups born to mothers which had been administered high doses of PFOS began turning
gray and dying shortly after birth. Other newborns in the lower dosage groups lived a while
longer, but also died within the ensuing days. Thus, postnatal survival was severely
compromised by exposure to PFOS, in a dose-dependent fashion, corresponding to body burden.
Pharmacokinetic findings suggested that there was no placental barrier in the mother to keep
PFOS out of the fetuses; and that PFOS is found in the milk, as well, so the pups received
additional doses. Moreover, at birth, the serum and liver levels of PFOS in the pups are the
same, indicating a lack of hepatic accumulation at this stage. Certain developmental effects
were observed, such as a small decline in growth (some stunting) in the surviving pups, and a
delay in the opening of the eyes of both the mice and the rats.
Hypothyroxinemia was observed in the PFOS-exposed neonates. Liver hypertrophy was seen in
the developing mice. Both the mice and the rats showed an identical pattern in regard to the
postnatal effects, except that the lethal dose for the mouse was 20 mg/kg, while the lethal dose
for the rat was 10 mg/kg.
At this point, little is known about how this chemical works. Researchers are now exploring
several mechanisms. Putative mechanisms of PFOS toxicity include the following: interference
of cholesterol and lipid synthesis/transport; impedence of cell-cell communication through gap
junctions; alterations of mitochondrial bioenergetics; hepatotoxicity: peroxisome proliferation;
and thyroid hormone imbalance. Yet, these mechanisms are unlikely to account for the neonatal
mortality.
For an on-going study, researchers also examined whether there were critical periods of PFOS
toxicity during gestation. For this portion of the study, a four-day treatment, with a high dose of
25 mg/kg, was given. Findings thus far indicate that if the exposure occurs early in gestation,
deaths are attenuated; in contrast, if the exposure occurs late in gestation, all of the pups die.
Because development of the lung tissues occurs late in gestation, researchers hypothesize that
the PFOS may have adversely affected the maturation of the pulmonary system.
In summary: the mechanism of developmental toxicity for PFOS is largely undefined, but is
currently under active investigation, and our preliminary findings suggest that PFOS may
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compromise the structures and/or functions of the developing lung and liver, potentially leading
to neonatal morbidity and mortality.
Researchers are hoping to include PFOS in the Center for Disease Control's (CDC) NHANES
monitoring program. Long-range research plans at NHEERL/ORD would relate body burden to
reproductive and developmental toxicity, clarify mechanisms for PFOS developmental toxicity,
and use computational toxicology to explore the mechanisms of toxicity for the perfluorinated
organic chemicals as a class. The evaluation of toxicity using small fish and amphibian models
also is planned
Studies of Human and Animal Toxicity
John Cicmanec, U.S. EPA/ORD/National Risk Management Research Laboratory
(NRMRL)/Cincinnati
Ammonium Perfiuorooctanate, C-8, is like a hydrocarbon with hydrogen atoms replaced with
fluorine. The compound is very stable and repels water and oil and reduces surface tension
dramatically. More than 100,000 pounds are produced each year. NASA is the primary user of
PFOA for space applications.
The research results presented here came out of a risk assessment performed under a consent
order for a site in West Virginia.
The focus of occupational studies conducted on PFOA included liver function, pancreatic
function, the endocrine system, and lipid metabolism. There were "possible" endocrine-related
findings in workers - increased cholecystokinin levels in two workers and elevated estrogen
levels in four male workers, though these levels were correlated with body fat index ratios.
PFOA was detected in workers' blood at levels ranging from 0 -114 ppm, with a mean of 5 ppm.
PFOA was present in the groundwater near the plant. Investigators believe that these
concentrations were the result of an aerosol dispersion of the compound. Thus, airborne
transmission appears to be important.
PFOA has a biopersistence of 94 days and a biodegradation rate of 13% at 28 days.
A quantitative non-cancer risk assessment was performed. In the case of PFOA, non-cancer risk
drove the case involving PFOA more than cancer risk did. The non-cancer risk assessment
involved analysis of critical studies for identification of critical effects, supporting data, and
uncertainty factors, so that the reference dose (RfD/RfC) could be derived and screening values
for water, soil, and air calculated. Uncertainty factors were extrapolated.
There was a desire to correlate the occupational exposures to the data gathered through animal
studies. The PFOA screening levels developed were as follows: water - 150 micrograms/liter
(ppb), soil - 240 milligrams/kilogram (ppm), and air - 1 microgram/cubic meter (ppb).
Despite the fact that non-cancer risk was the main driver in the PFOA case, researchers also
looked at animal carcinogenicity studies that had been performed. These studies indicated that
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animals exposed to PFOA developed fewer cancers than animals exposed to many other
compounds.
An interesting finding of the studies indicated that there are significant differences in PFOA
metabolism for humans and rats. For example, there is a marked gender difference in serum and
tissue half-lives in rats that is not shared by humans. In rats, PFOA has a much shorter half-life
in females than in males. In humans, the half-life is about equal in both males and females.
Additionally, peroxisome proliferation is much more significant in rats than humans.
The risk characterization involved the following steps: describing the scientific data base;
describing the exposure scenario; listing key assumptions that were made; describing how the
process was performed, including calculations; describing other approaches and conflicting data;
and considering uncertainty versus variability.
A comparison of experimental monkey blood levels to environmental human exposure levels
provided the following data: a 26-week monkey study resulted in blood concentrations of 10
ppm; occupational human exposure levels - 0 to 114 ppm (mean 5 ppm); and environmental
human exposure levels - 0 to 40 ppb.
In summary, the results of animal studies and environmental monitoring indicate that PFOA is
not presently an environmental health threat. Although some endocrine effects have been
observed, they are not the critical adverse effect.
Risk Information UpdateRisk Information Update: Overview of Assessment and Activities
ofPFOSandPFOA
Jennifer Seed, U.S. EPA/Office of Prevention, Pesticides and Toxic Substances
(OPPTSyOffice of Pollution Prevention and Toxics (OPPT)
PFOS came to the attention of U.S. EPA in 1999 when 3M used blood samples of workers and
animals in toxicology studies and compared the samples to controls from blood banks.
Researchers found that "the blanks weren't blank." They found PFOS, suggesting that exposure
is widespread. Control animals also had high background serum levels that were traced to fish
meal feed. These results launched a series of studies.
PFOS was even found in polar bears. The source was likely the U.S. Navy, which has its sailors
wash ships at sea with fire fighting agents. 3M showed EPA data with concentrations of the
compound in blood samples, so 3M phased out PFOS in December, 2002. Although there was
no need to go through a formal risk assessment, as 3M was discontinuing production, there was a
concern that other manufactures would enter the PFOS market once 3M ceased production.
Thus, the Office of Pollution Prevention and Toxics (OPPT) published Significant New Use
Reports (SNURs) in 2000 and 2002 to prevent other manufacturers from producing PFOS. An
OECD hazard assessment was completed in 2002, and an IRIS assessment is in internal review
and will be out in the next six months.
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EPA is now looking at PFOA, a C-8 perfluorinated compound that might be used as a substitute
for PFOS. PFOA was thought to be chemically inert, however, this is not the case. In
September 2002, the director of OPPT announced a priority review process for PFOA. In
November 2002, OPPT released a hazard assessment of PFOA. After the data began coming in,
EPA found PFOA in humans and animals, though in lower concentrations than PFOS.
By April 2003, OPPT released a preliminary risk assessment of development toxicity for PFOA.
After the data for the two-generation study came in, they decided to do a formal risk assessment
to determine whether they had to act under the Toxic Substances Control Act (TSCA) against
PFOA for developmental toxicity. By Spring 2004, the Science Advisory Board is expected to
review a revised risk assessment covering all endpoints.
There are tremendous uncertainties on how to do a quantitative risk assessment on these
compounds. The preliminary risk assessment was based on post-weaning mortality and delayed
sexual maturation in a rat, using a two-generation reproductive toxicity study. The rat is not a
good model for humans, however, because of the gender differences in how rats metabolize
PFOA. The female rats get rid of the PFOA to which they are exposed in four hours while the
males take eight days to rid themselves of the PFOA.
DuPont and 3M are currently studying the role of exposure to pups via serum and milk. They are
also looking into the gender differences rats exhibit in how quickly they eliminate this
compound. A two-year bioassay shows liver, pancreatic, leydig cell, and mammary tumors with
uncertainty regarding human relevance. The ILSI Risk Science Institute has formed an expert
workgroup to summarize the state of tumor science.
Critical reviews in toxicology will take place in November 2003 or January 2004 and an OPPTS
policy paper on induced liver tumors will be issued for a joint SAP/SAB review in Dec. 2003.
The paper will focus on how to look at different tumor types. U.S. EPA has nominated several
perfluorinated compounds to CDC for the next NHANES, and a class study of perfluorinated
compounds to the National Toxicology Program (NTP). International producers and
communities also need to be aware of the problem.
PFOS and PFOA Program Office Update Program Office Update
Mary F. Dominiak, U.S. EPA/OPPTS/OPPT
Perfiuoroalkyl sulfonates (PFAS) are acids, salts, halides, etc. including perfiuorooctylsulfonate
(PFOS), which was produced in quantity before the end of 2000 and widely used (over 300
chemicals on inventory, including polymers). The chemicals have been produced since 1950 for
use in surface treatment, paper protection, and performance chemical (surfactant and insecticide)
products.
Perfluorooctanoic acid (PFOA) is used only as an essential processing aid to make
fiuoropolymers in an enclosed process with controllable releases. PFOA is not expected to be
found in final fluoropolymer products except as a trace contaminant but testing is needed to
determine if this is true. Fiuoropolymers are widely used in electrical, chemical, automotive,
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aerospace, military, medical, and construction applications. They are also used to coat cookware
and in fabric waterproofing.
U.S. EPA began investigating perfluorinated compounds in 1999 based on new data on
perfluorooctyl sulfonate (PFOS). The Agency expanded the investigation in 2000 to include
PFOA and fiuorinated telomers. EPA published SNURs in 2000 and 2002 to close out the return
of PFOS after 3M's phase-out.
The SNURs require prior notice before any new manufacture or import of 88 PFAS, including
PFOS, with exceptions only for three high-tech, low-volume, low exposure/release uses for
which there are no good substitutes. These uses are semiconductor manufacture, aviation
hydraulics, and limited imaging. Industry began voluntary research on PFOA and telomers in
2000. This research produced additional concerns, and EPA released draft hazard assessments
on PFOA in September 2002 and November 2002.
In March 2003, industry submitted letters of intent (LOIs) for voluntary research. In April 2003,
EPA released a Preliminary Draft Risk Assessment on developmental concerns and solicited
parties for enforceable consent agreements (EGAs). EGAs are useful because they allow EPA to
move faster than under more traditional processes. The EGA focuses on understanding sources
of PFOA in the environment and pathways leading to human and environmental exposure.
The EGA negotiations substitute for the Toxic Substances Control Act (TSCA) subsection 4 test
rule. Industry LOIs promise data on market and use, product and article contamination analysis,
monitoring/modeling for releases, test chemical, and product selection. The EGAs also seek data
on incineration, degradation, article aging, additional chemicals, and additional sampling.
In June 2003 EPA held an initial public meeting with 191 attendees and 50 interested parties.
The parties included: FDA, CPSC, industry, environmental groups, local and state government
entities, and plaintiffs in a class action suit involving PFOA contamination of local water
supplies in Ohio and West Virginia. Technical workgroups were formed to pursue possible
EGAs. The next plenary public meeting will be in October 2003. Agreement on one or more
EGAs should be reached during this session. The process is expected to continue into the
future. Additional EGA negotiations will be pursued on remaining data issues.
The EGA process is open to public participation and comment. The on-line docket may be
found at www.epa.gov/edocket/: use "Quick Search" to locate docket OPPT-2003-0012. There
is an extensive data repository in file AR-226 at oppt.ncic@epa.gov.
Additionally, EPA has proposed that CDC include PFOS, PFOA, and other perfluorinated
chemicals in the next NHANES study. A decision on this is expected soon. An NHANES study
will provide a baseline of human exposures to compare with current data and track future trends
to assess release/exposure reductions. EPA also is nominating this class of chemicals for study
to the National Toxicology Program (NTP).
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TOXIC CHEMICALS RESULTING FROM THE DISPOSAL OF ELECTRONIC
EQUIPMENT
Examining the Pollution Potential of Discarded Electronic Equipment Disposal
Timothy Townsend, University of Florida
Researchers have been investigating leaching from discarded electronic equipment (e-waste) to
determine what is released and under what types of conditions. Electronic devices such as
computers, cell phones, DVD players, and other electronic equipment contain metals and
metalloids as well as organic and inorganic chemicals in their circuit boards, wire boards, and
plastic housings.
Lead is a major potential contaminant. Its most prominent use is in cathode ray tubes (CRTs).
Lead-tin solders also are used in printed circuit boards. Other solder elements can include
bismuth, copper, silver, indium, and antimony. Semiconductors contain arsenic and selenium,
and batteries contain nickel and cadmium. Laptop flat screens are lit with lamps contain
mercury.
Other e-waste constituents that have been identified (primarily by environmental groups),
include the following: beryllium, palladium, tantalum, zinc, polychlorinated napthalene, gallium,
and liquid crystals. Plastics contain brominated flame retardants. The electrical and electronics
industries consume 56% of BFRs produced with building construction consuming 31%. In
regard to potential exposure pathways, researchers did not look at potential exposure during use.
Instead, they considered exposure after disposal, through landfilling (impact on leachate,
groundwater, gas), waste-to-energy (impact on air emissions, ash quality), and demanufacturing
and recycling. Human exposure can occur during dismantling of electronic equipment to sell
parts. In some facilities in Europe where they grind up electronics, some workers have elevated
brominated compound concentrations in their blood.
A concern exists that e-waste may leach toxic chemicals into the leachate of lined landfills or
contaminate groundwater near unlined landfills There also is concern that chemicals such as
mercury may escape through landfill gas. EPA Regions 4 and 5 are studying the leaching of
hazardous chemicals from discarded electronic devices.
The current study is focusing on Toxicity Characteristic Leaching Procedure (TCLP) methods
development for discarded electronic devices and toxicity characterization of computer CPUs.
During other research funded by the Florida Center for Solid and Hazardous Waste
Management, the leachability of cathode ray tubes was examined. An assessment is also being
conducted into the true impacts of e-waste disposal in Florida.
TCLP is designed to represent what is leaching from a landfill under a worst-case scenario of
acid leaching. In summary, a solid waste is leached in an acid solution for 18 hours and the
resulting "leachate" is analyzed. If the concentration of certain pollutants in the leachate exceeds
a standard in the rules, it is a TC hazardous waste, unless otherwise exempted. However, it is
hard to do TCLP on e-waste, because of the way the testing is currently done (requires small
particles of a representative sample).
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Researchers studied the questions of how best to accomplish size reduction and how to
determine a representative sample. In some cases, the researchers resorted to cutting up pieces
of the individual components by hand, and in others, they resorted to modified procedures that
allowed characterization of entire devices (e.g., immersing the entire device in a 55-gallon
drum).
Researchers found that 21 out of 30 CRTs failed TCLP for lead when they used the standard
TCLP methodology. However, when they used the modified TCLP methodology, three of three
samples failed TCLP for lead. When they used the standard TCLP methodology on cell phones,
five of 10 failed for lead, but when they used a modified TCLP methodology, 23 of 33 samples
failed.
Researchers used three different methods for analyzing computer CPUs. When they used the
standard methodology and hand cut pieces for analysis, all eight samples passed TCLP (they did
not exceed the 5 mg/L standard). When they used the standard methodology and shredded the
pieces for analysis, all seven samples passed TCLP. When they used the modified TCLP
methodology involving immersion of the entire device, however, 9 out of 10 failed (exceeded 5
mg/L).
All of the laptops analyzed using either the standard or the modified methods failed TCLP
(exceeded 5 mg/L for lead). Interestingly, the laptops failed for lead, but not for mercury. One
problem is that when equipment is shredded, it exposes steel, which causes lead not to leach as
much. So policy makers may need to decide if the TCLP test is appropriate for this use.
Future research should be conducted using real landfill leachate. Researchers are constructing
simulated landfills with and without co-disposed e-waste devices. They are also looking for
brominated flame retardants in the leachate and they are working on developing data to support
keeping CRTs out of landfills. Currently, more than 25 landfills have been sampled and
compliance monitoring data have been reviewed. Toxics in e-waste can be reduced by using
lead-free solders and alternatives to BFRs, and initiatives have been proposed for these. Silver
or copper solders may, however, be worse due to silver toxicity.
Emissions from the Incineration of Electronics Industry Waste Combustion Issues
Eric Stewart, ORD/NRMRL/RTP
At least 2.1 million tons of e-waste was generated in 2000. About 1.9 million tons entered U.S.
landfills or incinerators. E-waste may contain leachable toxic metals and BFRs. In addition to
disposal/recovery in the U.S., some of the remaining waste goes to developing countries for
recovery operations.
Open burning releases these chemicals, which may result in exposures. For example, recovery of
valuable metals from e-waste in China may involve open burning of plastic encased parts to
reduce the wastes to metal. This may release the metals as well as persistent organic compounds
such as polybrominated dioxins and furans.
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Researchers have looked at controlled combustion to determine the emissions when e-waste was
burned. They expected metals and the brominated flame retardants, as well as the potential for
brominated furans and dioxins and, because chlorine also is present, bromo-chlorinated dioxins
and furans.
The research involved tests conducted over a kiln temperature range of 570 - 830 degrees
Centigrade. The lower temperature combustion was intended to simulate a scenario in which
more of the metal was kept in the ash so it could be recovered. The higher temperatures were
intended to simulate incineration in which the resulting ash is landfill ed. As part of the study,
the researchers varied the kiln preheating time.
Heat generated from the combustion of the waste accounted for 17% of kiln firing rate.
The e-waste used in the tests was equal parts (by weight) shredded keyboards, motherboards, and
cases. Flue gas measurements included the following: continuous emissions of O2, CO2, CO,
NO; volatile organic compounds (VOCs) (measured with an on-line gas chromatograph); and
sampling trains for modified method 5 (semi-volatiles), method 26 (halogens), method 23
(PCDD/Fs, PBDD/Fs), and method 29 (metals).
The NO concentration averaged 55 ppm. VOC emissions were independent of kiln temperature
over the range tested and consisted primarily of bromobenzene and other brominated organics.
No PCDD's were detected using LRMS. Emissions of PCDFs were near the detection limits
using LRMS. PBDFs were detected, but due to a lack of standards, results for brominated and
mixed bromochloro-DF are semi-quantitative at best. MCDF was detected during low-
temperature runs at 4 ng/dscm. OCDF was detected during one of the high-temperature runs at 2
ng/dscm.
Some brominated furans appeared to be present in higher concentrations than those of MCDF.
MBDF appears to be present at 5-10 times the concentration of MCDF. In general, PBDF was
greater than PB-MCDF, which was greater than PB-DCDF. Metal concentrations were
significant, consisting primarily of copper, lead, antimony, cadmium and manganese. TCLP
results for bottom ash showed no chemicals above standards. Controlled incineration may be an
alternative method of e-waste disposal.
In the future work will be done with Baptist University in Hong Kong to determine the size,
type, and composition of e-waste. They are also scoping tests in an open burn facility to
quantify emissions of metals, VOCs, SVOCs, and PXDDs/Fs.
Toxic Chemicals Resulting From the Disposal of Electronic Equipment
Jason Swift, U.S. EPA Region 5 RCRA Program
There is a growing waste stream of electronic equipment. Nearly 250 million computers will
become obsolete in the next five years. Mobile phones will be discarded at a rate of 130 million
per year by 2005, resulting in 65,000 tons of waste. Many chemicals are used in electronics,
including mercury for the back lighting in fiat screen displays in laptop computers, and lead in
the cathode ray tubes and solder.
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It is estimated that twenty-two percent of the world's consumption of mercury goes into
electrical and electronic equipment. Approximately four pounds of lead can be found in each
computer. Beryllium is used in computer, telecommunications, and automotive electronics
industries.
Many unused computers end up in stockpiles in people's homes and offices. This will add to the
e-waste streams when they are finally disposed. In California an estimated 18% of households
stockpile TVs and 19.4% stockpile computer monitors. The National Safety Council (NSC)
estimates that three-quarters of all computers ever sold in the U.S. remain stockpiled. In 2001,
11% of PCs retired in the U.S. were recycled.
According to the Basel Action Network and Silicon Valley Toxics Coalition, about 80% of the e-
waste that is supposed to be recycled is sent overseas to China and other such places. Electronic
equipment recycling processes include grinding, shredding, manual disassembly, metal
reclamation, and glass cutting.
According to the Basel Action Network and Silicon Valley Toxics Coalition, approximately
100,000 migrant workers labor in Guiyu, China, breaking down imported computers. Cathode
ray tubes are smashed to remove copper. The glass is dumped in irrigation canals and along
rivers where it could possibly leach lead.
It is estimated that more than 3.2 million tons of electronic waste is put in landfills each year.
Around 70% of heavy metals (mercury, cadmium) in landfills is thought to come from e-waste.
Plastics, such as those used in electronics casings, have a high BTU value and are incinerated in
cement kilns or other combustion devices for energy recovery.
Chemicals and metals can escape into the environment during disassembly. Are risks
quantifiable? Inhalation of beryllium dust can cause chronic lung disease at concentrations as
low as 0.01|_ig/m3. Beryllium exposure and dose response data are needed. Waste samples
collected a few feet from the Lianjiang River near Guiyu, China, showed high levels of many
metals, including cadmium, chromium, copper, lead, mercury, nickel, silver, and zinc.
Research is needed to determine where e-wastes go, and what happens to hazardous substances
released from it during recycling, incineration, and landfilling. Monitoring is needed during
processing. There also are insufficient data on liquid crystal toxicity, substance interaction
during incineration, and effects of low dose exposure over time.
The environmental impacts of alternatives to using toxics in equipment also must be explored.
There are some lawsuits that allege that chemical exposures in the semiconductor industry have
caused cancer, birth defects, and miscarriages. The Common Sense Initiative proposed
comparing California health records to employment records in an effort to find any increased
incidence of chronic illness. The project never went further than discussions.
To manage risk, the options include disclosure of hazards, material selection, proper handling,
and controlled pre-treatment.
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Comments/Questions and Answers
Q - Do you have a personal preference for incineration or landfilling for disposal?
A - Unable to give an opinion in regard to incineration, the incineration emissions data have
only recently become available. However, testing of leachate from lined, subtitle D landfills is
not showing much leaching of lead. But you may not want to use a landfill for other reasons.
Q - Are you seeing fugitive emissions of mercury?
A - Mercury may not show in TCLP because of its interaction with other chemicals in the
sample.
Q - Do you expect to see a relationship between the metals that leach with the pure metals
within the waste?
A - The metals do interact, which can influence analytical results, but there is a relationship.
Other metals can affect how much copper or lead can leach, for example.
Q - Is there mercury in landfill gas? What about other metals?
A - We have found mercury and also molybdenum.
A comment was made that the ORD lab in Cincinnati is working on the recycling of CRT glass
to keep the lead out of landfills and incinerators. This project will expand next year.
Q - Can you relate furans and dioxins in the combustion of e-waste?
A - We can relate it for mono-BDF, but not for the others.
Q - With a mixed waste stream, would you expect dioxins and furans?
A - Yes. We don't know why we didn't see more, possibly because we had more bromine than
chlorine in this case.
Q - How typical is it to have waste with five parts bromine to one part chlorine?
A - Atypical. There is more furniture and other such waste in municipal waste so the bromine is
in much lower quantities relative to chlorine.
Q - Did you think that the metals reacted with the bromines to strip the bromines out of the
waste itself leaving a metallic form of halide?
A - Responder did not understand the question.
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Tuesday August 12, 2003
BROMINATED FLAME RETARD ANTS
Welcome & Introduction
Ted Smith, U.S. EPA/Great Lakes National Program Office (GLNPO)
Brominated Flame Retardants (BFRs) have been in the news a great deal because of the penta,
octa, and deca forms. The European Union is banning the penta and octa forms and California
has passed a bill that is awaiting the governor's signature banning penta, octa, and deca. Region
9 has spearheaded efforts that have led to the formation of an EPA ad hoc work group to address
the BFR issue. EPA has held two multi-stakeholder meetings in San Francisco: in 2002 on
BFRs/electronics and in 2003 on BFRs in residential furniture.
Overview of Brominated Flame Retardants
Leif Magnuson, U.S. EPA, Region 9 Pollution Prevention Coordinator
Magnuson began by saying that this workshop is a great opportunity to renew a commitment to
researching emerging pollutants. This is a very tough challenge because of the overwhelming
number of pollutants. U.S. EPA has limited staff and resources available to address new issues.
"We must raise the profile of these chemicals in the agency. They are as important as dioxin and
mercury. How do we spend our research dollars and recruit involvement from participants? We
need your input to determine where to spend the next available dollars," he said.
According to Magnuson, Region 9 has gotten involved in the BFR issue in California because
the Region has received many comments about BFRs directly from the public. Thus, they have
been pulled into the issue by their constituents. Because California has stringent fiammability
standards for residential furniture, the Region gets some of the more worrisome BFRs.
In the past, more products were made of wood and metal. Today, numerous products are made
with plastic or other petroleum-derived materials that are quite flammable. As a result, the
government - especially California - has set high standards for flame retardancy, particularly for
furniture. Flame retardant additives are used to treat plastics, foams, and other materials to keep
them from burning so fast. For example, if a room is filled with plastics, "flash over" can occur
in which everything catches on fire at once. There is no doubt that BFRs save lives by slowing
down "flash over" and giving people more time to get out of buildings during a fire.
There are dozens of chemical BFRs with different properties. These include brominated
bisphenols, diphenylethers, cyclododecane, and others. When plastics catch fire, the long-chain
polymers in them heat and break up very quickly, releasing flammable gases that combine with
oxygen to spread the fire. When BFRs are introduced into plastics, they act by suppressing the
release of free radicals, which slows the fire. The BFRs are released very quickly in a narrow
temperature range as they heat up, which makes them effective flame retardants, unlike chlorine.
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BFRs of recent concern include polybrominated diphenylethers (PBDE),
hexabromocyclododecane (HBCD), and tetrabromobisphenol A (TBBPA).
Products in which BFRs are used are found everywhere. BFRs are used in polyurethane foam,
textiles, plastics, rubber, resins, etc. Home products include couches, beds, chairs, TVs, stereos,
microwave ovens, carpets, curtains, etc. Office products include computer casings and circuit
boards, printers, fax machines, lighting, furniture, etc. The Americas account for 95% of the
world's use of PentaBDE at 15.7 million pounds per year. PentaBDE is highly bioaccumulative.
Around 86-99% of the total PBDE congeners found in human tissues are present in this product.
The basis of concern regarding BFRs arises from the increasing concentrations of BFRs (mainly
PBDEs) in the environment, humans, and wildlife. The European Union has banned/is phasing
out certain PBDEs. Toxicity concerns include the following: endocrine disruption (PBDE,
TBBPA, HBSD), dioxin formation (PBDE, TBBPA, HBCD), altered behavior and learning
(PBDE). More testing is needed to determine suspected sensitive endpoints.
Currently, it is not known how PBDEs and other BFRs are released into the environment, but
they can be found in samples taken virtually anywhere (indoor and outdoor air, surface waters,
sewage sludge, foods, and biota). PBDEs are related to a number of important topics warranting
special attention, including children's health, endocrine disruption, persistent organic pollutants
(POPs), emerging environmental challenges, and high production volume chemicals.
Regulations for BFRs are appearing along with reporting and monitoring requirements. There is
interest in developing a substitute for BFRs. Europe is ahead of the U.S. on the issue of BFRs,
and will ban penta and octa across the EU by August 15, 2004. They have gathered a lot of
information on production and are working on plans for mitigation. The Europeans are currently
conducting a risk assessment for deca and draft risk assessments for TBBPA and HBCD have
been released for comment. U.S. EPA has included three BFRs in the Toxic Release Inventory,
and under TSCA, the Agency can require testing of certain chemicals. Three BFRs (Deca-,
Penta-, and Octa-BDE) have been submitted for voluntary testing under the Voluntary
Children's Chemical Evaluation Program (VCCEP).
Another action U.S. EPA has taken is the issuance of a requirement that BFRs be evaluated
under TSCA's "Significant New Use Rule" (SNUR). The SNUR was driven by the California
and CPSC proposed residential furniture standards. It will likely cover only flame retardants for
fabrics, but those used in foam are possible candidates as well. The Agency also could require
more toxicity data and risk assessments and could restrict use.
Several European eco-labels prohibit BFRs in electronics and some American groups promote
the purchase of BFR-free electronics. Some electronics manufacturers are working on
alternative chemicals. In the 1990s, Japanese companies took BFRs out of many products.
Furniture manufacturers, including Ikea, Eddie Bauer, and Crate and Barrel have requested
alternatives to PentaBDE, and Hickory Springs has converted a plant to produce a non-
halogenated phosphorous-based compound. There have been some problems with this new
process, however, as some of the treated foam comes out scorched and discolored. BFRs keep
the foam white. Some buyers won't accept the discoloration. Public and manufacturer
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education is needed on this topic so producers and consumers will understand that there is a
health issue involved.
Environmental Presence and Known Sources
Polybrominated Diphenyl Ethers in People
Ron Hites, Indiana University
At a Stockholm, Sweden, conference in 1998 a presentation was given on the concentration of
BFRs in human milk, showing a doubling in concentration, of PBDE 47 over a five-year period
at the same time that DDT concentrations were going down. Hites thought the compound had a
strong resemblance to PCBs. The Stockholm presentation was so shocking it is likely
responsible for the focus, within the emerging pollution workshop, on BFRs.
After seeing the Stockholm presentation, Hites decided to look at PBDE concentrations in
human maternal and umbilical cord blood (to represent the baby's blood). In this study, which
took place at Indianapolis hospitals in 2001, paired mother-cord blood samples were taken
randomly from 20 pairs with the goals of finding the range of PBDE levels and the extent of
placental transfer and correlating levels with environmental factors and health indices.
The concentrations of total PBDE were about the same in both mothers and umbilical cord
blood, indicating that the compound moves through the placenta. Concentrations were detected
in all samples, although a couple showed very high concentrations (350 - 450 ng/g lipid).
During analysis, researchers had some problems with the lab blanks, because foam - and BFRs -
are everywhere.
Brominated biphenyls (BB-154) were found consistently in all the samples, though researchers
didn't know why. The mothers in public hospitals were under age 31, and smoking did not
appear to be responsible for incidence of this compound. All of the mothers and babies had
concentrations of this compound in their blood, with an average of around one ng/g lipid, though
some samples had concentrations ranging from 5 to 16 ng/g lipid. There was a problem with
brominated biphenyls in Michigan cows' milk some years ago, but this problem was supposedly
resolved.
After conducting the Indianapolis analysis, researchers began to pull together other available
data on PBDEs. A full literature search on PBDEs in people and the environment was
conducted. A tabulation of all concentration data by congener was made, omitting papers that
did not report congener-specific data. One difficulty in this research was that not all papers
reported or measured the same set of congeners.
Papers on human samples (blood, milk, tissue) were sorted out for additional review, noting the
years the samples were taken. Ambient samples included the following: 41 data sets from
Europe (mostly from Sweden); 14 data sets from Japan; and nine data sets from North America,
(including 2 or 3 from Canada). Occupational samples (of people who worked as dismantlers of
electronic equipment) included 12 data sets from Sweden and Norway. The data were organized
by time, totals, averages, and congener distribution, and were calculated by percentage.
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The data were plotted from 1970 to 2000. The data show a doubling time in detected
concentrations of 4.4 years since 1970 all over the world, though Japanese levels are relatively
low and North American levels are much higher than elsewhere in the world. Researchers also
looked at individual PBDE congener concentration distributions in human samples. These
congeners included PBDE 47, 99, 100, 153, 153, 154, 183, and 209.
Congener 47 appears in the highest concentrations throughout the world. Mean concentrations
for BDE-47 in North America were 28 ng/g lipid - which was significantly higher than
occupational exposures in the EU, which had a mean of 4 ng/g lipid compared to a mean of 2
ng/g lipid for non-occupational EU samples. The samples from North America also had higher
mean concentrations of congeners 99, 100, 153, and 154 than found in Japan or in EU non-
occupational samples.
Researchers don't know why concentrations of BDE-47 are higher than the other congeners -
whether this is due to having a higher vapor pressure, which allows it to be transported more
readily, or if it metabolizes differently than the other congeners.
In another plot of recently collected data (2002 and 2003), concentrations of total PBDE for
North American neonates and mothers were 35 ng/g lipid in blood (and in milk taken from
mothers in Texas) compared to 2 ng/g lipid for Sweden. The wide difference between the
concentrations in the two areas is most likely due to the fact that Americans use 95% (or 7,100
metric tons) of the world's penta product.
Some conclusions and recommendations from this work include the following:
• PBDE levels are 10 to 20 times higher in people from North America than in Europeans
(or at least in Swedes). Levels in Japan seem to be about half of those in Europe.
• This finding is consistent with the market for the Penta-BDE product, 95% of which is
used in North America.
• Levels in people worldwide seem to be increasing exponentially with a doubling time of
four to five years.
• The congener pattern is dominated, especially in North America, by BDE-47;
occupational samples also show BDE-183 and 209.
• In the future all congeners should be measured all of the time.
• PBDEs cross the placental barrier, but are there any effects?
• The range of concentrations is wide - what accounts for high outliers?
• Begin a regular program of annual monitoring of PBDE (at least) in people, in selected
food, and in Great Lakes fishes.
• Don't forget about the polybrominated biphenyls (PBBs).
Brominated Flame Retardants in the Environment
Mehran Alaee, Environment Canada
The latest issue of Environment International contains an article on BFRs. PBBs were
introduced in the 1970s as flame retardants. PBBs were found in 1981 in samples collected
along the Viskan River in Sweden. Others have found PBBs throughout the world. In 1987
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Jansson and his colleagues first indicated that PBDEs are "global contaminants" by
demonstrating their presence in samples collected from the Baltic Sea, North Sea, and Arctic
Ocean.
U.S. researchers were aware of the presence of these compounds, as well. In 1983, Stafford
reported the presence of PBDEs in eggs and tissues offish-eating birds from the Great Lakes
Region, and in 1991, researchers from EPA reported 180-220 ng/g of PBDEs in blubber from
bottlenose dolphin on the south Atlantic US coast. In 1995, EPA researchers reported up to 8000
ng/g PBDEs in bottlenose dolphin from the Gulf of Mexico.
In 1997 research on PBDEs was started at the Canada Centre for Inland Waters (CCIW) and the
Institute of Ocean Studies (IOS), located in Sidney B.C., but people were still skeptical until the
Swedish data were released in 1998. In 1999 research was expanded to include PBBs, HBCDD,
and TBBPA.
In the U.S., EPA Method 1614 is used for the determination of PBDEs. Isomer specific/isotope
dilution method is used for the determination of HBCDD and the isotope dilution method for
TBBPA. Researchers have made a lot of progress in identifying PBDEs; however, no method is
perfect. Each BFR has its own analytical requirements. PBDEs are amenable to GC analysis,
though there are 209 possible congeners (less than 45 are commercially available), and there can
be co-elution among various congeners.
GC/ECD is the simplest and least selective detector used in determination of PBDEs. It requires
careful sample preparation and there is the potential for interference from PCBs and other
organohalogen contaminants. GC/ECN/MS (which is the ISO method) monitors bromine anion
formed by dissociative capture. This method is more selective than BCD, but there is
susceptibility to interference from organobromine compounds. GC/HRMs is the more selective
technique (US EPA method 1614) but it is susceptible to interference from PCBs.
A new EPA method 1614, which is due to be released shortly, will use a high resolution GC. It
will be based on eight BDE congeners (28, 47, 99, 100, 153, 154, 183, and 209) and is intended
to reduce the variability among the results achieved by different laboratories. Alaee encouraged
everyone who is involved with PBDEs analysis to conduct isomer-specific analysis so they will
know what they are analyzing.
Concentrations of BDE-209 in sediment cores from the St. Louis Estuary showed that PBDEs
are increasing and that PCBs were high in the 1980s but are now decreasing. TBBPA was found
in sewage sludge samples from various cities in Canada. Suspended solids samples from the
Detroit River showed more concentration on the western or industrial side of the river.
Temporal trends in marine mammals and Great Lakes biota show increasing levels from north to
south.
In testing of birds with a heavy fish diet (osprey, herring gull, bald eagle), PBDEs were found in
egg specimens. Peregrine falcons, which were also tested, showed much lower levels of PBDEs,
apparently because they have a primarily terrestrial diet. PBDEs have been shown to be
increasing in Great Lakes walleye between 1980 and 2000. In marine seas, the levels in beluga
whales from Baffin Island are increasing exponentially.
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Over time, PBDE levels in Sweden and Japan rose until the mid-1980s and have since dropped.
The increase and decrease correspond to bans of some of these substances. Analysis of various
species occupying increasing positions up the food web indicates that PBDEs bio-magnify, and
that PBDEs follow a similar increasing trend within the lake's food web as PCBs. HBCDD also
biomagnifies within the food web. Unlike the other congeners, however, 60 days after exposure
through spiked food, BDE 209 was no longer detectable in fish. More analyses indicate that the
PBDEs are being metabolized.
In summary, PBDEs are ubiquitous, global environmental pollutants. Levels of PBDEs are
rising in North America. TBBPA has been observed in suspended sediments from the Detroit
River and in sewage sludge across Canada. HBCDD has been observed in fish from Lake
Winnipeg and in the Lake Ontario food web. There will be more information on BFRs presented
at a conference June 6-9, 2004.
Comments/Questions and Answers
Comment - One attendee took issue with the Lake Ontario food web information because data
on lake trout are mixed.
Q - Were the mothers with high PBBs the same ones who had high PBDEs?
A - There is no correlation. The data on the Texas women were very limited. About one-third
were Hispanic, but there was no difference in outcomes. The number of births and age was
considered, but there was no relationship to compound levels. The sample size was small.
Q - Did you have information on their diets?
A-No.
Q - Were the Texas women from the Texas/Mexico border?
A - No - they were from Dallas and Austin.
Q - Is laboratory contamination an issue with the state and regional laboratories?
A - Yes, it's an issue. In one commercial lab, they went into a new area of the lab to perform
the analysis and the concentrations in the blanks went out of sight. It turns out the contractor had
put foam in the air ducts to cut down on noise. You need to perform some ambient air sampling
to determine what type of problem you might have.
Q - In the work on the BDE-209 core samples, how certain is the data? It looks like 209 was
there before it was being manufactured.
A - It may have been produced on an experimental basis at one time. There are strong
indications of BFR manufacturing in the area since World War II.
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Brominated Flame Retardants: Toxicology and Risk
Linda Birnbaum, U.S. EPA/ORD/National Health and Environmental Effects Research
Lab (NHEERL)
Birnbaum felt that BFRs were being ignored, but now interest is growing. She believes,
however, that it is important to look at all of the congeners.
Flame retardants save lives, but BFRs are a global, transboundary problem. These compounds
are persistent and they have a potential for bioaccumulation. There are more than 75 different
BFRs, which comprise 40% of the total usage of bromine. Worldwide, approximately 200,000
metric tons are used each year, with half of the use in the U.S. At this time, there is a limited
data base on BFRs when compared with other compounds, such as PCBs and dioxins.
Br-Bisphenols, especially TBBPA, are detected in air, sediment, sludge, and biota. TBBPAhas a
relatively short half-life in the environment and a low chronic toxicity. It is not teratogenic or
mutagenic and, based on limited data in biota, little is retained in tissues. Limited data on
TBBPA indicate that it may be immunotoxic, and it appears to be hepatotoxic. The data also
suggest that it could be neurotoxic (inhibits dopamine uptake and generates free radicals). In
regard to endocrine disruption, AhR effects do not appear to be relevant for commercial products
though it can affect thyroid hormone. Because it also inhibits sulfotransferase (decreases
estrogen clearance), it could theoretically lead to higher estrogen levels.
U.S. EPA has regulated TBBPA under TSCA. There is concern for air (long range transport),
clean water (sediment), and waste (sludge). There has been a Region 9 workshop, Region 5
grants, GLNPO and cross-agency workgroup (Region 9), and an agency "what we know"
statement (though it may now be out of date).
Hexabromocylododecane (HBCD) exhibits ecotoxicity to algae, daphnia, and fish. In regard to
general toxicity, it is highly absorbed and is a mild irritant and skin sensitizer, with liver effects
after repeated doses. More information is needed on repeated dose studies and reproductive
toxicity. It may be developmentally neurotoxic.
Because it has been detected in the blood of workers, there are concerns regarding occupational
settings. HBCD has been found in human breast milk and is persistent, bio-accumulative, toxic,
and capable of long range transport. The Europeans have substituted HBCD for the penta group
of PBEs - which may be an example of jumping from the frying pan into the fire.
Polybrominated Diphenyl Ethers (PBDEs) include DBDE (the deca mixture), OBDE (the octa
mixture), and PeBDE (the penta mixture). The BDE-47 in the penta mixture appears to be
bioaccumulative. The penta is more toxic to the environment than the octa, which, in turn, is
more toxic to the environment than the deca. PeBDE (penta) is highly toxic to invertebrates.
Deca and octa may be of low risk to surface water organisms and top predators, but there is
concern for wastewater, sediment, and soil organisms. There also are concerns about lower
brominated congeners in octa for the potential for debromination and the generation of
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PBDDs/PBDFs (dioxins and furans). Adult rodent studies show PBDEs to be hepatotoxic and to
lower thyroid T4 levels. At high doses, deca is hepatocarcinogenic.
Some people thought that deca couldn't be absorbed, but new data shows that it can. Deca also
can be metabolized into reactive intermediates and can undergo debromination. Deca can be
found in human blood and milk. It may be developmentally neurotoxic and it may be breaking
down in fish. Europe, which is banning penta and octa, is looking at deca, as well.
New information on penta (SOT, 2003) indicates that it can affect the endocrine and
reproductive systems and have developmental neurotoxic effects. In regard to endocrine
disrupting effects, there is a question as to whether AhR effects are relevant to BFRs. Thyroid
homeostatis has been reported in rats and mice in many labs. There are still questions regarding
estrogen homeostatis, because OH-PBDEs may be anti-estrogenic while sulfotransferase
inhibition could be estrogenic.
In regard to developmental reproductive effects, you won't see them if you look only at adult
animals. Pubertal exposures of DE 71 have been shown to delay puberty and to have effects on
male organs. In utero exposure of BDE-99 has been shown to delay puberty, cause ovarian
toxicity and produce male organ effects and decreased sperm levels.
In regard to developmental neurotoxicity, rats exposed perinatally to DE-71 showed deficits in
sensory and cognitive function. Other studies on mice in Sweden and Italy showed that when
infantile exposure to BDE-99 occurred (during a critical window of rapid brain growth), there
were permanent effects on learning. Perinatal exposures appear to delay sensory-motor
development. Recently, studies at other labs also are showing developmental toxicity. A
Swedish study of mice exposed to BDE-99 and PCB-52, appears to suggest that effects may be
more than additive, though more testing needs to be done on this.
In regard to pharmacokinetics of PBDEs, DBDE is poorly absorbed. Lipid binding is important,
with accumulations in fat showing more 47 than 99, and relatively little, if any, 209, because it is
a bulky molecule. Covalent binding of 99 and 209 is seen in the liver. Metabolism involves
hydroxylation, debromination, and O-methylation. Feces are the major route of excretion.
Different organizations are involved in other ongoing PBDE research. Dose/response research is
being conducted by NHEERL, NIEHS, USDA, and Sweden. Cell signaling in vitro, involving
altered calcium associated with changes in learning and memory, is being conducted by
NHEERL.
Developmental toxicity of PBDEs is seen in both mice and rats. Mice are very sensitive in the
infantile period. Sensory and cognitive effects also are seen. The mechanism of these effects is
unknown. PBDEs alter cell signaling in vitro by altering calcium-dependent release of
arachidonic acid, which is associated with learning and memory.
Potential health risk of PBDEs can be summarized as follows:
• In a comparison of animal and human data, daily dose isn't important, while the body
burden is important (body burden allows cross-species comparison for PBTs).
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• The most sensitive effects to date include developmental neurotoxicity and effects on
thyroid hormones (0.8 mg/kg). Preliminary reports indicate that developmental
reproductive toxicity is seen at an even lower dose (0.06 mg/kg).
• The top five percent of human exposures in the U.S. result in concentrations of more than
400 ng/g lipid. If humans are 25% lipid, then their "dose" is approximately 0.1 mg/kg.
A significant dose causing developmental neurotoxicity in mice is 0.8 mg/kg, thus,
mouse tissue concentrations are only about 10 times higher than total PBDE
concentrations in human tissues. We are not seeing the same distribution in terms of
exposures as with PCBs. We don't know why we have highly exposed people, because
we don't know the pathways by which they are being exposed.
• Margin of exposure for PBDEs appears low.
• Additional concern: are PBDEs interacting with other PBTs?
Comments/Questions and Answers
Q - Can the presence of PCBs indicate the presence of PBDEs?
A - There is no correlation between PCBs and PBDEs. They are from different sources.
Status of the VCCEP Consultation re: penta, octa and decabromo diphenyl ethers
Jennifer Seed, U.S. EPA/OPPTS/OPPT
The Voluntary Children's Chemical Evaluation Program (VCCEP), a pilot program to test 20
chemicals, was set up over the course of 18 months of meetings with various stakeholder groups
representing children, industry, the environment, government, and others. Through these
meetings, these stakeholders developed a program with which they felt they could live. In this
program, a special emphasis will be placed on gathering exposure data.
Within the program, exposure and toxicity data is to be gathered in three stages. Tier 1 will
involve bringing forth all of the information available to date on the 20 chemicals. Much of the
data will be offered up by the industry participants. Often, much information is available on
toxicity, with exposure data lagging behind. Tier 2 will involve obtaining additional information
on toxicity and exposure. Tier 3 will involve elaborate studies. At this point, the industry
stakeholders have only committed to provide data for Tier 1. Other stakeholders want
independent evaluation of these data.
The entire assessment is focused on children. The underlying question: Are there adequate data
about these chemicals to determine risk to children?
The VCCEP has a cooperative agreement with Toxicology Excellence for Risk Assessment
(TERA) to perform peer evaluation of the data. Thus far, information on four chemicals,
including penta, octa, and deca BDEs have been submitted. TERA will write up summaries of
the information and post them on its website. These won't be EPA recommendations - EPA has
agreed to wait until the peer consultation.
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Issues that have thus far arisen from all three assessments of exposure studies suggest that for
children, the major routes of exposure are breast milk and fish consumption. Most of the
exposure appears to come from tetra BDE, although this compound is not part of the VCCEP's
pilot activities. One of the important questions we must answer is, how can we relate what we
have in commercial mixtures to exposures in children?
Comments/Questions and Answers
Q - We need to move upstream and look at the parents' exposures also.
A - Under EPA's definition of children, we also look at exposure of parents and prospective
parents.
Q - What is the web site?
A - www.tera.org Click on peer review for peer consultations information.
Roundtable Discussion on PBDE Research Needs
Comments/Questions and Answers
Comment - There is no central repository for BFR research. There are 14 research projects with
$12.5 million being spent, but these studies are not coordinated.
Comment - We need to get out in front of this issue so that the data gaps will be filled in the
next few years.
Comment - Leif Magnuson asked workshop participants to complete an exercise asking how
they would distribute $100 of new research money into various categories. The BFR breakout
session group did this and it is included under the breakout session reports.
Comment - We haven't yet formalized a research strategy. We need to get a sense from the
workshop participants of what type of research strategy we should have and then determine who
should do the research.
Q - What research is being done?
A - We don't have it broken out, but a smattering of research is being done.
Comment - What would help is not just a laundry list of research needs, but to decide what are
we trying to accomplish.
Comment - Wants more input into a research strategy. People who have been working on this
topic have ideas, but they have a general sense of what is lacking. Want to prioritize the
research. So far, the research is very ad hoc, with no strategy or prioritization. The Great Lakes
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Program is involved, the pollution prevention people, and the Science to Achieve Results
(STAR) grants. Different groups are involved.
Comment - We need a way of deciding how best to fund this research - not just fund projects as
they come up.
Comment - The VCCEP program will come up with specific data needs. We will need coherent
Agency research.
Comment - The VCCEP data will have concrete drivers. That will give reasons for what
research should be done.
Comment - The VCCEP stakeholder round tables looked at research needs.
Comment - Want broader categories of research needs.
Comment - We also should add in what the strategy will be for figuring out substitutes for
BFRs.
Comment - We also need a data management strategy and standardization to make sure that we
are analyzing all of the congeners, for example, to make sure data are comparable.
Comment - They held a session with the Design for the Environment people on alternatives.
Q - Can we switch to a less toxic chemical? Should this be part of the study?
(A 10-minute discussion followed on how to develop a research strategy- and when a strategy is
developed, how to get it funded.)
Comment - ORD has a different approach to planning for research. The ORD planning process
involves getting representatives from all of the program offices and one representative from all
the Regions. It involves a balancing act between research needs and capabilities. If there aren't
capabilities in the Agency, they use a STAR grant to go outside. There is often some conflict in
budgeting.
Comment - There are a number of cross-agency initiatives that don't necessarily come up
through this process.
Comment - If this research is for the Regions, then we need to put the dollars into answering the
sorts of questions people are asking them.
Q - Are they requesting proposals on BFRs for the next STAR grants?
A - The Regions have been meeting on how they can raise awareness of the science issues that
need to be raised. People should go through Paul Oilman. We ought to bring forward what we
have in the way of data now, what the data gaps are, and determine where we need help and
what we want.
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Comment - We are looking for Region support. Region 4 is the lead region for ORD .
Comment - Also looking for multimedia research.
Comment - Regions need to get into the Agency's strategic planning. Some Regional issues are
being addressed.
Q - If they put together ideas, where should they take them for funding?
A - Bring them to the regional science council. There is also a national regional science council.
We can use this mechanism to get the ideas up to the Deputy Regional Administrator level. If
they want to move forward, then we give them more.
Comment - The pollution prevention people are interested in looking at alternatives to BFRs.
Comment - To find studies, look at the science inventory on the ORD intranet.
Comment - It is the responsibility of the project officers on these project to take the information
to the BFR group. We should put all of these projects into the science inventory so people will
know about them.
Comment - It is important to keep people who are working on BFRs in contact with each other.
Comment - Whoever is writing a strategy needs to make use of the questions people are raising
so that other groups that are already doing other work can be involved. Put questions out so that
many can answer them. It may be beneficial to make a clear matrix presenting the projects.
Have a BFR conference in two years to bring all of these people together with the goal of
answering these questions.
Comment - Want to mesh the strategy with what comes out of the VCCEP.
Bisphenol A and Phthalate Esters: Potential Sources of Resin Components in the Everyday
Environments of Preschool Children
Marsha Morgan, U.S. EPA/ORD/RTP/National Exposure Research Laboratory (NERL)
Previous research on a small number of children suggested that ingestion (dietary and indirect) is
a major route of exposure to environmental chemicals. Exposure routes differ by class of
chemical:
Inhalation > indirect ingestion » dietary ingestion for PCBs
Dietary ingestion > indirect ingestion > inhalation for B2 PAHs, phthalate esters, 2,4,D herbicide
Dietary ingestion > inhalation > indirect ingestion for Total PAHs, phenols, OP and OC
pesticides.
Potential doses maybe greater for children than for adults in the same households.
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The Children's Total Exposure to Persistent Pesticides and Other Persistent Organic Pollutants
(CTEPP) study is the first large aggregate study in the country, a pilot of approximately 260
preschool children in North Carolina and Ohio. CTEPP was a large, multimedia, and
multipathway exposure study of young children in both residential and daycare settings that
looked at the potential exposures that preschool children may have to common pollutants in their
everyday environment. The study considered more than 50 different types of pollutants.
CTEPP is significant because it is seeking to provide a greater understanding of children's
aggregate exposure to pollutants, particularly pesticides, in their homes and in daycare centers.
The study seeks to identify important sources and pathways of exposure that contribute to
children's exposures to pollutants and to provide improved approaches for estimating children's
exposures to and potential doses of pollutants. It also is intended to fill in critical data gaps
under the Food Quality Protection Act of 1996.
The objectives of CTEPP were as follows:
• Measure the aggregate exposures of a small set of preschool children in their everyday
environments to persistent pesticides and other persistent organic pollutants
• Apportion the exposure pathways and identify important exposure media, and
• Identify and formulate important hypotheses to be tested in future research.
The study involved 257 preschool children and their adult caregivers. The study was conducted
on subjects in six different counties in both North Carolina and Ohio. In both states, four of the
counties were urban and two were rural. Half of the children were in daycare and half were in
residential settings. The study also considered socioeconomic factors by selecting subjects from
lower income and middle/upper-income households. Thus, the stratification of the study
involved daycare versus residential, urban versus rural, and low income versus middle-/upper-
middle income households.
The sampling periods were 48 hours. Care givers collected food, beverages, urine, and hand
wipe samples, while the field staff collected drinking water, indoor air, outdoor air, play area
soil, and indoor floor dust samples. Additionally, if pesticides were applied with seven days of,
or during, the 48-hour monitoring period, other samples also were collected. These included
transferable residues (collected with a polyurethane foam roller), hard floor surface wipe, food
preparation surface wipe, and urine (not pooled).
Supplemental information also was collected, including food diaries, child day care menus,
activity diaries, and videotapes of 10% of the children to monitor hand-to-mouth and object-to-
mouth behavior. Information on aggregate exposures and absorbed doses was collected with
urine as the biomarker of exposure.
Targeted pollutants for the CTEPP study include the following:
• Polycyclic aromatic hydrocarbons (e.g., benzo[a]pyrene)
• Phthalates (benzyl, butyl, dibutyl)
• Phenols (e.g., pentachlorophenol, bisphenol-A)
• Polychlorinated biphenyls (PCBs)
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• Organochlorine pesticides (e.g., lindane, DDT, heptachlor)
• Organophosphorus pesticides (chlorpyrifos, diazinon)
• Acid herbicides (e.g., 2, 4 - D, dicamba)
• Triazine pesticides (atrazine)
• Pyrethroid pesticides (e.g., cyfluthrin, cis/trans-permethrin)
These compounds were selected because they are possible carcinogens, endocrine disrupters,
teratogens, and/or neurotoxins, and are ubiquitous or residues are common indoors or in food or
water.
Phthalate esters are used as plasticizers in polyvinyl chloride (PVC) products, such as floor tiles,
children's toys, synthetic leather, carpet backings, shower curtains, and adhesives. These uses
employ large molecular weight phthalates (e.g., benzyl butyl phthalate). Phthalate esters are
also used as solvents and fixatives in personal care products, such as perfumes, hairsprays, and
nail polishes. These uses employ the smaller molecular weight phthalates (e.g., dibutyl
phthalate).
Bisphenol-A is an industrial chemical commonly used to make polycarbonate plastics and epoxy
resins for use in reusable bottles (bottled water, baby bottles), tableware (plates, cups), digital
media (DVDs, CDs), electronics (cell phones, computers), dental sealants, and protective liners
in metal cans (food, beverages).
There are some analytical issues in looking for phthalate esters, such as background
contamination of phthalates in the field and in lab blanks for all media. Possible contamination
sources include gauze pads, latex gloves, solvents, nitrile gloves, filtration cartridges, and pipette
holders. To minimize background contamination, researchers tried to use as much glass or
Teflon as possible and to minimize the handling of samples by using cotton gloves over the
plastic gloves.
In regard to the surrogate recovery standard - benzyl butyl phthalate-d4, there were major
interferences in certain media (wipes, air, dust, soil). As a result, researchers changed to an
alternative surrogate recovery standard (e.g., benzyl butyl phthalate-dlO), which had a higher
molecular weight and could reduce interferences.
There also were analytical issues in regard to Bisphenol-A. The surrogate recovery standard -
bisphenol-A-d6 - also was subject to major interference in certain media (wipes, air, dust, solid
food). As a result, researchers changed to an alternative surrogate recovery standard (e.g.,
bisphenol-A-dlO) that could reduce interference. Additionally, researchers had to deal with
background contamination in the field and lab blanks and in a few wipe samples.
The preliminary results revealed that dibutyl phthalate was detected at or above method
quantification limits in 99% of the indoor air samples collected from homes and 100% of the
indoor air samples collected from daycare centers, in 100% of the samples collected in homes
and daycare centers, in 83% of the hand wipe samples collected in homes, and 84% of the hand
wipe samples collected in daycare centers. Additionally, DBP was detected in 100% of the
samples of floor wipes and 85% of the food preparation surface wipes collected in homes.
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BBP was detected at or above the method quantification limits in 100% of the indoor floor dust
samples collected from homes and daycare centers, 60% of the hand wipes collected in homes,
and 96% of the floor wipes and 67% of the food preparation surface wipes collected in homes.
Bisphenol-A was detected at or above the method quantification limits in 93% of the hand wipes
collected in homes and 100% of the hand wipes collected in daycare centers, 72% of solid food
collected in homes and 74% of the solid food collected in daycare centers, 75% of the floor
wipes from homes, and 89% of the food preparation surface wipes collected in homes.
There were no statistically significant differences between the concentrations of DBF and BBP
in indoor floor dust samples at preschool children's homes and daycare centers. BBP was found
in higher concentrations in homes, while DBP was higher at daycare centers. There was little
difference in concentrations of BPA between homes and daycare centers. BBP was detected in
much higher concentrations in floor wipes than in other samples at preschool children's homes.
The preliminary conclusions of the study are that DBP, BBP, and BPA were detected in all
media; however, they were detected the most often in the following:
• DBP - indoor air, indoor floor dust and wipes
• BBP - indoor floor dust and wipes
• BPA - solid food and wipes.
Hard floors (e.g., vinyl flooring) in homes maybe important sources of BBP exposure for
preschool children.
The results suggest that these preschool children were potentially exposed to low levels of DBP,
BBP, and BPA in their everyday environments.
Comments/Questions and Answers
Q - Are the urine data available?
A - The North Carolina data is done and will be on the Internet in a year and a half. They are
still working on the Ohio data.
Q - Did you compare play area soil with indoor play areas?
A - The soil contained low concentrations of the target compounds, so researchers didn't want to
make a correlation, because it wouldn't mean anything.
Q - What about sampling grass in grass play areas?
A - In such cases, we would collect surface soil samples from the closest area with bare soil.
Q - When will the results for Ohio be available? Did you adjust the data after completing the
North Carolina data?
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A - They made some adjustments to the data. The data will be completed in the next year.
Q - This is exposure data. Is anyone looking at toxicological effects?
A - Don't know.
Q - Did you determine the sources of pentachlorophenol?
A - Don't know about sources.
Q - Did you look at agricultural areas and urban areas?
A - This wasn't the objective of the study. Researchers looked at urban and rural areas, but
didn't consider agricultural activities in the study design.
Radium in Oil and Gas Piping and Production Facilities
Loren Setlow, U.S. EPA Office of Radiation and Indoor Air (ORIA)
Radium is toxic and a potent carcinogen. Health problems associated with it were first
discovered among the women who used radium to paint watch dials and faces. A high incidence
of cancer of the mouth was found among these women, who would place paint brushes in their
mouths to create a point in the bristles between applications of radium paint. Radium degrades
to cause radon and other radionuclides and is present naturally in soil and water throughout the
U.S.
The presentation covered the problem of radiation in oil and gas production facilities and in
other industrial processes. Radiation at oil and gas facilities is not normally evaluated during
environmental site investigations and cleanups. Such sources of radiation may pose potential
health and safety hazards to inspection personnel and to the public. Because of recycling of
radioactive piping and other materials from oil and gas production facilities, radiation is present
in many unexpected residential and industrial settings.
Technologically Enhanced Naturally Occurring Radioactive Materials (TENORM) are materials
containing radionuclides that are present naturally in rocks, soils, water, and minerals and whose
radioactivity has become concentrated and/or exposed to the accessible environment as a result
of human activities.
Because of concerns about TENORM, a Regional EPA Guidance, "Potential for Radiation
Contamination Associated with Resource Extraction Industries," was issued on April 15, 2003 to
EPA Regional radiation personnel, regional Superfund staff, the National Hardrock Mining
Team, and On-scene Coordinators. This guidance informs EPA staff of radiation associated with
specific minerals resource extraction, processing, or manufacturing industries. The guidance
will help EPA field staff to contact key EPA regional radiation staff personnel to implement
radiation safety measures and conduct radiation surveys, as appropriate. The guidance can be
found at www.epa.gov/radiation/tenorm/about.htm.
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Some industries with TENORM contamination include the following: aluminum (bauxite),
copper, fluorspar, gypsum, molybdenum, phosphate, phosphorus, potassium (potash), precious
metals (gold, silver), rare earths including monazite, tin, titanium (leucoxene, ilmenite, and
rutile), tungsten, vanadium, zircon, coal (and coal ash), oil and gas, and geothermal energy.
Water and sewage treatment facilities also can be contaminated with TENORM.
In regard to oil and gas facility TENORM, radium levels can range from non-detectable to more
than 100,000 picoCuries/gram. Five picoCuries is the allowable limit for radium in pipe scale.
It should be noted that radium is much more dangerous than uranium or thorium ore. In 1996,
the American Petroleum Institute (API) estimated that the equivalent of 30,000 m3 of TENORM
was generated in 1993. This same study, using radiation survey data, estimated that there is the
equivalent of 3.4 million m3 in total legacy inventory. In some cases, TENORM has gotten into
facilities that recycle steel. Such facilities have had to install radiation monitors to reject
radioactive materials. Some contaminated pipe has been used in homes and businesses.
In regard to TENORM in Region 5 oil and gas facilities, oil field equipment with 5,000
microR/hr was found at one Michigan pipe yard. An API study found that 92% of production
facilities in Illinois had radiation contamination.
Radium is selectively soluble in underground formations and is mobilized in production waters
in preference to uranium and thorium. The radium precipitates out at the surface because of
changes in temperature and pressures compared to underground conditions and it plates the
interior of pipes, separators, storage tanks, gas lines, etc. On the basis of a 1989 API report and
other studies, it is believed that one-third of all producing U.S. oil and gas wells have elevated
radiation.
The first oil wells were drilled in the 1860s. According to the Illinois State Geological Survey,
155,000 wells have been drilled in the Illinois basin alone. A hot trend now is to drill natural gas
wells into coal beds to recover coal bed methane. Because coal contains radioactivity,
TENORM can be generated. Contaminated water also is a problem that must be managed.
There is a problem managing TENORM contaminated water in the Powder River Basin coal
fields because a lot of water is produced.
By anecdote, Setlow has heard that scrap yards have been under orders to not accept oil field
pipe, and there have been some problems in the automotive industry from radioactive metal used
in cars. Contaminated metal made from scrap has been used in many places, including
playgrounds. Exposure to TENORM in pipe scale has been a problem for pipeyard workers.
Until the 1990s, workers at pipeyards used to knock the scale out using hammers; now, chemical
and hydraulic pressure means are used.
Exposure to the scale and disposal of the TENORM-contaminated scale is an issue. When
radium is in the mineral scale, it is locked up in the mineral matrix and not readily leachable.
But when it is broken out of the pipe or tanks or other vessels and ground up, it becomes an
inhalation hazard and a toxin that gets into the ground.
TENORM also can contaminate soil. The MCL for Radium-226 in soil is 5 picoCuries/gram.
At one site in Michigan, soil samples contained up to 2700 picoCuries/gram.
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Oil and gas TENORM waste disposal methods include injecting wastes into the original
producing formation, deep injection well disposal, disposal at licensed facilities, land and road
spreading, and re-use and recycling of equipment. TENORM cannot be sent to RCRA Subtitle
C or D landfills (except under some special cases). It usually has to be disposed of at a facility
for low level radioactive wastes.
There have been more than 5 million oil wells drilled in the U.S. and any of them may have
TENORM that may never have been dealt with or even recognized. Modern environmental
protection methods didn't commence until the 1970s. Pre-1970s legacy wastes may remain at
sites that could be converted to home and building sites. As residential communities move into
former oil and gas production areas, the need to identify and address TENORM becomes
increasingly important.
As already mentioned, potential hazards exist from TENORM contaminated recycled metal
scrap, mineral scale, and pipes. In one case in New Orleans, 26 acres of land was leased to a
pipe yard. The pipeyard company did not clean up the radium scale on the property, and the
owner of the land sued the pipeyard company and the oil companies which supplied the pipe to
be cleaned. In 2001, a $1 billion judgment was handed down in the case for both compensatory
and punitive damages. The workers at the pipe yard were exposed to radiation while they broke
the scale out of the pipes and several of them subsequently sued their employer saying they were
never told of the risks associated with this activity.
In regard to TENORM contamination associated with current production sites, RCRA may not
apply, but other U.S. EPA authorities are available (CERCLA, CWA, SDWA, and TSCA).
Petroleum industry associations, individual companies, and some states have developed
guidances for handling TENORM. EPA ORIA is investigating ways to partner with industry
and other stakeholders to address this issue.
More research is needed on the occurrence of legacy oil and gas radium wastes and current
operational and disposal practices. This research is needed to reduce potential for public,
professional, and worker radiation exposures.
Comments/Questions and Answers
Q - What levels of radiation can be found in the pipe scale?
A - The scale can have levels of hundreds of picoCuries/gram. Scrap metal companies are
supposed to have zero tolerance for radioactivity.
Q - Do the automobile manufacturers look for radioactivity in the metal they receive?
A - Don't know.
Q - Why don't scrap companies use Geiger counters?
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A - It depends on the company. Not all train their workers on how to deal with pipe scale.
Q - What is the level of exposure to radiation to workers in oil fields? Are there any effects?
A - Don't have data on this. OSHA has standards. OSHA and the Nuclear Regulatory
Commission say occupational exposures can be five times the level of exposure allowed for the
public.
Q - Is radon a degradation product of radium?
A - Yes. In many cases radon emissions become the driver of risk assessments that are
performed. Radium dust contaminates soil. It is a problem if contaminated soil is used for a
playground. Radiation also can occur if a house is built over a contaminated site.
Q - Are there any pollution prevention remedies to this problem, like using water softeners?
A - Some producers use scale inhibitors, but this just moves the problem further down the line
toward the refineries.
Comment - Institutional controls could limit it.
A - At this point, 37 states have oil or gas wells, but only 10 states have regulations for
TENORM. The issue is whether there are controls built into the production process.
Q - Is radium leachable into the new steel in which the scrap is recycled?
A - Some of the radium goes into the slag, some of it goes into the steel. The percentages
depend on the smelting temperature.
Q - Have you found radioactivity in the natural gas used to burn in our homes? Is it then air
borne?
A - Some has been found in gas lines, but it isn't a risk in most homes. The radium goes into
the air when the gas is burned.
Q - Is lead 210 a scale that develops?
A - Yes, it is deposited over time.
Q - Is radium a problem in drilling mud?
A - It can be. It can also be a problem in produced water. Producers try to recycle the drilling
muds. There are pits (including dried out pits) containing produced muds and water all over the
country.
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Balanced Perspectives Regarding Environmental Levels of Thallium and Platinum Group
Metals
Frank Anscombe, U.S. EPA Region 5
(This talk is available in full from the presenter (anscombe.frank(5),epa.gov) and represents his
views, which may in places depart from those of EPA. This summary is provided for the
Proceedings.)
This talk discusses environmental exposures to two metals, thallium and platinum. To have
perspectives on their risks, it seems useful to place them within the broad context of trace
environmental exposures to chemical compounds.
Trace Exposure Risk Primer
Our dominating doses are to the chemicals that comprise foods that we eat and medicines that
we take. Approaching 1,000 different chemical compounds have been analytically
distinguished in a cup of coffee. A National Research Council study has affirmed it plausible
that our exposure to carcinogens naturally contained within foods dwarfs risks presented by trace
residues of synthetic chemicals on these foods. There is no comprehensive program to evaluate
the carcinogenic potency of the natural ingredients within foods.
The gentlest substances are regarded by pharmacology as "practically non-toxic." If one drinks
enough water, this will dilute your electrolytes to a lethal degree. Thus water can be a toxicant.
So is oxygen. Long-term respiration generates free radical oxidants thought to be the most
important cause of age-related diseases. We require oxygen minute-to-minute, yet in the long
run it kills us. We are the physical manifestations of many chemicals. All chemicals can be at
least somewhat toxic. Toxicants R Us.
It is comforting to think of certain chemicals as "bad." Some are indeed virulent poisons,
devoid of biological value. It is comforting to think that other chemicals are safe. The truth is
murkier. A large dose of a practically safe substance can be just as deadly as a tiny dose of a
deadly poison. We learn of chemical harm to humans owing to high-dose tragedies. It is hard
to assess what risks may be presented by low doses of these same chemicals, given myriad
possible biological outcomes without acute symptoms.
With sufficiently sensitive and selective analytic technique, with available reference standards,
and with funding, an analytical chemist could distinguish thousands of synthetic chemicals, at
trace levels, in us. What risks to these trace exposures present, individually or collectively?
How can we evaluate this situation prudently and thoughtfully, ranking one risk against another,
and set logical priorities? Low analytic detection capabilities create a frustrating problem.
Chemists can detect myriad chemicals at levels lower than our capacity to estimate robustly what
risks might be entailed. We can find a part per billion, but does it threaten us? We can make
estimates, but they must be predicated on assumptions.
Should we fully inform citizens that they are exposed to myriad trace chemicals, predominantly
natural, yet many others synthetic in origin? Or should we narrowly inform the public of just
one trace chemical exposure at a time? Generally, the latter choice seems to be made.
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Simplicity is a mighty virtue in messages to the public. Yet is it to some degree misleading not
to mention the full range of chemical exposures? Is this ethical?
If the honest situation is that we genuinely do not know how to compare all the risks presented
by a host of trace chemical exposures, would acknowledgment of this be worthwhile? Are we
best served to avert our eyes from the complexity of the real world's trace exposures? Or
should we acknowledge reality, however inconveniently perplexing and troubling?
An intrinsic mission of EPA is to be skeptical about chemical exposures, especially ones
involuntarily presented via food, water, or air. It seems a responsible idea to hold this
workshop, regardless of profound uncertainties. But it would be irresponsible not to be mindful
of these same uncertainties.
EPA-derived food consumption advisories tend not to factor in the health benefits of all the
chemicals that are natural constituents within food. Does such narrow framing beget advice that
is defensible on medically holistic grounds? Do advisories depend on a premise that there are
alternative healthy foods readily available? If so, does this premise deserve to be expressly
acknowledged?
Thallium
On the periodic table, thallium lies between lead and mercury, two other potent neurotoxins.
Owing to the observed symptoms, thallium was the first suspect for the neurological poisoning at
Minamata, Japan. Within our bodies, thallium mimics an essential metal, potassium. It affects
potassium-activated enzymes in the brain, muscles, and skin. Symptoms of thallium poisoning
include slurred speech, numbness, and hair loss. A fatal dose for an adult is about one gram.
This qualifies as extremely toxic. Thallium's abundance in the earth's crust is 59th among
elements, ten times more common than silver, in contrast. EPA canceled all pesticide uses of
thallium in 1972, partly owing to a survey that found 24 percent of sick or dead bald eagles had
been poisoned by thallium. Global air emissions of thallium from coal combustion have been
estimated at 650 to 1,600 tons per year. Cement production may yield much more: 2,700 to
5,300 tons. Plants absorb thallium through their roots.
Thallium has long been undetectable by conventional analytic means. This is an important
factor in explaining why this dangerous metal is virtually ignored. Lin and Nriagu have found
that the average concentration of thallium in 37 lake trout taken from Lake Michigan during
1994 was 140 ng/g. In 1992, EPA suggested a reference dose for thallium of 5 ug/70kg/day.
High consumption fish consumers exceed this safe dose by several fold.1 The margin of safety
for thallium in fish seems modest, as it does for methyl-mercury. The two substances together
may pose additive risk greater than either alone. Recent advances in analytic methods can
empower more understanding of thallium exposures.
Platinum Group Metals
The platinum group metals (PGM) Platinum, Rhodium, and Palladium have been used in
catalytic converters installed on U.S. automobiles since 1975. These convert NOx,
hydrocarbons, and CO to CO2, nitrogen, and water, improving air quality. These metals are in
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75th, 76th and 79th place in abundance among the earth's elements. This rareness brings two
implications. Use of these metals in a hot gas stream produces new vapor exposures. Ambient
PGM levels near roads have risen, viewed from the perspective of ultra-low natural background.
The second implication is that there is not a lot of knowledge about inhaling platinum group
metals.
The good news is that the three metals are of low toxicity. Yet, a study of vegetation and soils
beside roads in South Bend, Indiana reports abundance is comparable to many European studies
and approaching levels that would be economically viable to recover." A study from Rome
showed a six-fold increase in platinum levels in top soils between 1992 and 200l.m However, air
concentrations are still three orders of magnitude below levels for which occupational health
limits have been set. The known health risk is sensitization of the airways by soluble platinum
compounds, known as platinum salt hypersensitivity. This has been suffered by platinum
workers, who develop runny noses and asthma. Given that present exposure limits offer a 1000-
fold safety margin in relation to this condition, inhalation of platinum group metals does not
seem to pose a health risk to the general population, based on existing understanding.
Yet neither should we assume that we understand all human or ecosystem outcomes for these
metals. Our experience with them is not extensive. I have tried to make the general case that all
substances, in sufficient dose, can create harm. We should always be wary of chemical
exposures.
Closing
We humans are made up of many chemicals and we are exposed to many more, both natural and
man-made. When you next hear of a synthetic chemical being banned, you may wonder: what is
the public health gain, in a holistic sense? Does anyone know of the totality of the risks that
will be presented by its replacement? How does the risk of this one chemical exposure compare
to the many others?
In writing these remarks, I chanced on a paper regarding caffeine in some lakes in Switzerland."
Caffeine is contained in coffee, tea, soft drinks, chocolate, and pharmaceuticals, from cough
syrups to No Doz. Caffeine is likely the most consumed drug in the world. It is found in
municipal wastewater effluents, and in surface and ground waters worldwide.
I looked at the National Toxic Pollutant repository of the National Institutes of Health. Under
caffeine, I read "at higher doses, symptoms include convulsions, Cheyne-Stokes respiration,
apnea of preterm infants, arrhythmias....Overdoses may cause death, convulsions.. .Continued
excessive use may lead to depressed mental states. Symptoms may include pulmonary edema,
myocardial infarction.'" A report from the Massachusetts Poison Center by a doctor at the
Boston Children's Hospital: "The issue of fetal toxicity of caffeine remains controversial. The
drug has been demonstrated to induce chromosomal mutations in vitro, but not in vivo. Clinical
trials in humans have shown heavy coffee drinkers to have an increased incidence of
miscarriages and premature birth, however these differences lose significance when adjusted for
other factors such as smoking. Further study is needed.VI
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What would happen if it were reported that one chemical, yet only one, deemed toxic by the
respected National Institutes of Health were present in our drinking water supplies? , Many
people have to have caffeine. Yet what if there were another chemical and it had an unappealing
name? What if someone invokes the precautionary principle?
Conclusions
• Thallium is intrinsically unhealthful. The same seems true for lead, mercury, cadmium,
and beryllium. This is an evolutionary perspective that living things have not
incorporated and made use of these metals. This natural avoidance seems a useful
insight about them. Many other metals are used gainfully by the human body. I do not
claim that thallium exposures constitute a problem worthy of action. Yet more studies
seem warranted.
• As regards all chemicals, dose (including pathway, quantity, chemical forms, timing, and
the vulnerability of an exposed person) determines harm. I am skeptical of all chemical
exposures, from a holistic perspective and bearing in mind uncertainties.
• The world abounds in risks from chemical exposures. It seems reasonable to focus on
ones that seem most important. Chlorides may be a long-term threat to the Great Lakes,
for instance. We and our planet contain ingredients that can be regarded as good or ill,
depending on dose. Health consists of striking the best balance.
Break Out Sessions
Break out sessions were held to discuss the following topics:
• BFRs and Electronic Equipment
• Radium, Thallium, Platinum, and other metals, and
PFOS/PFOA.
Flip chart and discussion notes from these break out sessions can be found in Appendix D of this
document.
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Wednesday, August 13, 2003
Asbestos and Related Durable Fibers: Too Ubiquitous, Too Persistent, Too Complex to Put
Health Risks to Rest?
Phillip Cook, U.S. EPA/ORD/NHEERL/Duluth, MN
Health effects from exposures to microscopic durable fibers is not an old issue - it is a
continuing issue. An extensive history of research, discussion, and debate, which focused on
occupational exposures to a few types of asbestos fibers, has not lead to an understanding of all
risks. "Asbestos" is more a slowly expanding pollutant problem than a re-emerging one. It
hasn't gone away, even if it no longer commands a lot of attention. A hallmark complication for
risk assessment in the case of asbestos is the very long lag time between exposure and effects. It
may take 30 to 50 years from exposure to the development of pulmonary disease.
Objectives of the presentation are to provide an overview of asbestos health risks, to give
examples of EPA's experience with asbestos-like fibers, and to describe why we need and how
we can develop a relative potency model to assess risks from complex mixtures of different
mineral fibers and new synthetic fibers. Asbestos is a persistent, bioaccumulative toxin, much
like PCBs. We need to look at asbestos the same way we have looked at PCBs. Some synthetic
nanofibers that are being developed are similar to asbestos. We should take what we know about
asbestos risk to look at nanofibers so we can avoid developing substances that would pose
asbestos-like risks.
Chrysotile asbestos is the main type of asbestos used in the U.S. Some say it is not a carcinogen.
Cook believes that it is a carcinogen. Amphibole crystals are present in taconite (iron ore) from
Northeast Minnesota - ferroactinolite replaces hornblende in some rocks with cummingtonite-
grunerite being the most common amphibole overall. Ferroactinolite appears to be the amphibole
which is most consistently fibrous. Amphibole can't be extracted from the rock for use, but it
has fiber-like characteristics and can be released in dust when the rock is crushed. Particles of
chrysotile or amphibole asbestos occur as thin fibers or in bundles that can enter the lungs and
cause asbestosis. However, short fibers that can break off of larger rodlike bundles can be
respirable, as well. In the past, scientists have tended not to consider the risk from the short
fibers, and science today still rests on dose-response relationships based on light microscopy,
which was inadequate for detecting short and thin fibers. The assumption was that only the
longer and thicker fibers pose a health risk.
Once the transmission electron microscope (TEM) became available, it enabled researchers to
see very small particles and to even analyze the chemical composition of individual fibers. It is
still difficult to tell whether individual fibers grew as a single crystal or were fragments of single
crystals. Some researchers believe that cleavage fragments aren't a problem and should not be
counted. Cook believes that the cleavage surfaces would be no different than the natural fiber
surfaces and that they also can cause disease if sizes and shapes are similar to asbestos fibers
which cause disease.
Cancers in the respiratory tract develop when the fibers reach the alveoli and are retained for
many years. The fibers can also cause fibrosis and the lung changes responsible for asbestosis, a
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fatal condition. There also is a significant incidence of gastrointestinal cancers in highly
exposed occupational settings, but researchers don't know whether the cause is inhalation or
ingestion of the fibers.
Previously, health officials thought asbestosis was associated with high exposure levels, and that
cancer resulted from lower exposures of harmful fibers. The highest rates of asbestosis in the
1990s were clustered around seaports or industrial sites where occupational exposures were high
in the 1940s and 50s. There also were some hot spots in less industrial areas, such as Lib by,
Montana, where vermiculite mining was associated with amphibole fiber exposures. Cancer loci
associated with asbestos fibers exposures include the lung (with smoking a strong co-factor), the
pleura and peritoneum (mesothelioma), gastrointestinal tract and kidney.
A conceptual model is needed for development of methods for prospective assessment of health
risks associated with exposures to mineral fibers. Researchers need to know what dose in the
tissues/lung should not be exceeded and to explore temporal exposure issues, such as the effects
of life-time, short-term, or early life exposures (from environmental exposures). Existing data
on the dose-response in tissues is based only on long fibers and light microscopy. Data is needed
on relative potencies, respiration response, retention/clearance, and fate/transport issues.
Vermiculite mining in Montana started in the 1920s about six miles from the town of Libby.
About 80% of the world's vermiculite was produced there, involving the processing of more
than 300,000 pounds a day. Around 5,000 Ibs/day of amphibole fibers were released into the
Libby airshed. W.R. Grace bought the mine in 1963 and closed it in 1990. Products made from
the fiber included construction aggregate, fireproof coatings, insulation, and soil additive and
fertilizer. EPA's primary focus is on insulation, because it is present in thousands of homes
across the U.S. Exposures weren't just limited to Libby, however, because approximately 300
plants across the U.S. and in Canada processed the vermiculite ore. Many workers were affected
and some children who played in the waste piles from the processing activities got
mesothelioma.
Iron formations are found in the Lake Superior region. Amphibole, a potentially fibrous
material, exists in the taconite rock at the eastern end of the Mesabi Iron formation. Iron ore
from the Peter Mitchell Pit was processed at Silver Bay, Minnesota. Taconite tailings from
processing 67,000 tons of fine crushed rock were deposited into the lake each day. Not all of the
fine tailings went to the bottom of the lake. The transport of fine tailing particles caused
noticeable increases in turbidity in western Lake Superior, leading to ecological concerns in the
1970s. When particles in water samples were viewed with an electron microscope, the
resemblance of amphibole particles to amphibole asbestos fibers in these tailing particles was
noted.
Tailings particles were tracked through the lake and uses of water from the lake. Researchers
found amphibole in toilet bowls and in the drinking water of Duluth, Minnesota in 1973. The
connection to asbestos first emerged through a citizen's comments made in opposing the tailings
discharge into the lake. Later, Cook examined the literature and found that indeed there was a
report of high incidence of gastrointestinal cancers in Japan in association with ingestion of
similar amphibole fibers. Thus, what was first thought to be a case of ecological concern turned
into a case of human health risk after the fibers were found in the drinking water. EPA moved
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quickly and people were given the option of filtered water or well water. Risk from ingestion of
fiber in water is still considered controversial as the evidence remains largely circumstantial.
With litigation pending, EPA took action immediately on human health concerns. The
Minnesota Pollution Control Agency was involved in issues associated with fibers in the air.
Cook found that people who ingested unfiltered water uniquely had amphibole fibers in their
urine, probably as a consequence of penetration of the gastrointestinal tract by a small fraction of
ingested fibers. Tailings discharges to the Lake were stopped and air emissions regulated. There
is, however, a proposal to use the dry cob tailings, which contain amphibole fibers, as aggregate
for road construction. This raises anew issue in regard to possible future exposures and health
risks.
Concerns about risks associated with non-occupational exposures to mineral fibers (e.g., Reserve
Mining Case) and interest in the effects of synthetic fibers led to EPA research on the effects
associated with a wide variety of durable fibers during the period of 1978-85. A major objective
was to determine the carcinogenic potencies relative to known asbestos materials. The Duluth
EPA lab provided electron microscopic characterizations of samples used in biological tests,
quantitative measurements of fiber doses in test animals, and determinations of dose-response
relationships. Researchers determined that amphibole fibers from taconite could cause cancer.
In the intratracheal and intrapleural exposures of Fischer-344 rats study, the primary objective
was to determine relative potencies of different fiber types for carcinogenesis. The studies
included two samples of amphibole from taconite at the Peter Mitchell Pit - ferroactinolite
(fibrous) and grunerite (non-fibrous). For details, see Coffin et al. Toxicology Letters, 1982, and
Cook et al. Toxicology Letters, 1982.
Results showed that ferroactinolite fibers were dissolving and splitting longitudinally while
residing in rat lung tissues over time. The dose was changing because fibers were splitting,
producing more and thinner fibers. In a hypothetical relative potency model proposed by Pott in
1978, long fibers were assumed to be most potent, but short fibers were also assigned finite
potencies which could be significant when many more short fibers were in an exposure.
In fiber carcinogenicity equivalence dose (CED) studies comparing relative carcinogenicity
factors (RCFs) based on Pott's hypothesis, data show that RCFs for short and thin fibers greater
than those proposed by Pott should be investigated and considered.
Conclusions from rat studies include:
• Fiber splitting in vivo greatly enhanced the potency of ferroactinolite in rat studies.
• Short and thin amphibole fibers appear to affect toxicity. If they do not, long ferroactinolite
fibers would have to be regarded as many times more potent than long amosite or crocidolite
fibers.
• Because risk is a function of cumulative fiber dose, exposures should be measured on the
basis of all fiber sizes with consideration of relative carcinogenicity and fibrogenicity of
different size and shape categories.
• Similarly, exposure predictions should be based on all fiber sizes so that relative potencies
can be included in risk assessments.
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Narrow definitions of hazardous fibers perpetuate risk assessment limitations:
• No methodology for assessing risks from short fibers - we need a relative potency model.
Weak links to mechanism of action data.
We are unable to provide precise definition of undesirable synthetic fibers so that safe
alternatives can be developed (we need to define risk in a generic way so we can predict risk
from new products, such as nanofibers).
Human dose-response relationships are very uncertain and may be inaccurate.
Properties of microscopic fibers that indicate the potential for causing asbestos-like pathologies
include the following:
• Size and shape that allows respiration, retention in lungs, and translocation to the pleura.
Durable, persistent in tissues.
Reactive surfaces, ability to induce ROS (reactive oxygen species).
High collective surface area.
Propensity to split into thin fibers in vivo.
An example of how our general knowledge of effects caused by different durable fibers can be
helpful in predicting potential emerging health risks is provided by carbon nanofibers which are
being used to produce zeolite tubes resembling the most potent asbestos fibers. These fibers are
proposed for use in monitoring and filtering applications, but should not be produced in sizes
that allow them to be respired and retained in human lungs. We should use our knowledge of
asbestos to work with industry to develop fibers that aren't respirable. Effective environmental
protection requires that each new generation advances the knowledge passed on by the previous
generation.
Comments/Questions and Answers
Q - Is the relative potency based on fiber size or weight basis?
A - Cook believes relative potency should be measured on a per particle basis.
Q - Would the zeolite fibers that are manufactured split?
A - They have a high tensile strength, which is why they are so attractive. Like the
carbon nanofibers they are produced from, they would not have an internal structure that would
promote splitting.
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PHARMACEUTICALS AND PERSONAL CARE PRODUCTS
Pharmaceuticals and Personal Care Products (PPCPs) As Environmental Pollutants
(Pollution From Personal Action)
Christian G. Daughton, U.S. EPA/ORD/NERL-Las Vegas
The focus of this research, funded by U.S. EPA, is primarily on Pharmaceuticals and Personal
Care Products (PPCPs) in the environment, originating from end-use rather than from
manufacturing. The emphasis is on the use/disposal of PPCPs primarily from activities/actions
of individuals and to a lesser degree from hospitals and industry - not from the PPCP
manufacturing sector, whose waste streams are much better defined, confined, and
controlled/controllable.
Another class of potential pollutants, the Endocrine Disrupting Compounds (EDCs) are also a
concern. A plethora of terms have often been used interchangeably with EDCs (rightly and
wrongly): environmental estrogens, endocrine-disrupters, endocrine-modulators, estrogenic
mimics, eco-estrogens, environmental hormones, xenoestrogens, hormone-related toxicants,
hormonally active agents (HAAs), endocrine-active chemicals (EACs), endocrine active
substances (EASs), and phytoestrogens (a naturally occurring subset). Estrogens represent but
one mode of action. Others include androgens.
PPCPs and EDCs are not synonymous. They are intersecting sets, and confusion regarding their
relationship must be avoided. Only a small subset of PPCPs are known/suspected of being
direct-acting EDCs (e.g., synthetic steroids); toxicological concerns usually differ. EDCs
comprise members from many disparate chemical classes.
PPCP-relevant goals for the U.S. EPA's ORD include the following:
• Identification of potential environmental concerns: anticipatory research, and emerging
issues. Identifying pivotal sources of uncertainty that affect risk estimates.
• Proactive vs. Reactive - pollution prevention vs. remediation/restoration: identifying and
fostering investigation of "hidden" or potential environmental issues/concerns before they
become critical ecological or human health problems.
• Foster interdisciplinary research and collaboration: catalyze research by academe, private
sector, government. Attempt to determine whether certain classes of chemicals deserve more
attention in rule-making.
• Ruling-in/out vs. Uninformed rules: Provide bases for informed decisions. Ensure that
science leads to eventual decisions for guidance or to regulate/not regulate.
Since the 1970s, the impact of chemical pollution has focused almost exclusively on
conventional "priority pollutants," especially on those collectively referred to as "persistent, bio-
accumulative, toxic" (PBT) pollutants, "persistent organic pollutants" (POPs), or" bio-
accumulative chemicals of concern" (BCCs). The "dirty dozen" is a ubiquitous, notorious subset
of these comprising highly halogenated organics (e.g., DDT, PCBs). The conventional priority
pollutants, however, are only one piece of the larger risk puzzle. More attention must be devoted
to the unregulated chemicals.
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PPCPs come from industry, agriculture, and household maintenance activities. Chemicals are
overlooked because there is no analytical framework to define them. The set of neglected or
omitted/overlooked chemicals is constantly expanding with many new chemicals being
introduced to the market, and with the poorly characterized influence of environmental
weathering and transformation thattakes place.
Regarding the prevalence of xenobiotic occurrence, some possible generalizations may be made
about its ubiquity:
• The lower the concentration, the higher the probability of larger numbers of distinct
chemicals occurring.
• Exponentially more types of chemicals occur at exponentially lower concentrations.
• At the very lowest concentrations (septomolar to yoctomolar (zM-yM), the off-the-cuff
truism may apply that, "Everything can be found everywhere."
According to Einstein, "Not everything that can be counted counts, and not everything that
counts can be counted." Daughton reflects on the state of the art of environmental monitoring by
saying, "Not everything that can be measured is worth measuring, and not everything worth
measuring is measurable."
Further truisms regarding environmental monitoring hold: what one finds usually depends on
what one aims to search for; only those compounds targeted for monitoring have the potential for
being identified and quantified; those compounds not targeted will elude detection; and the
spectrum of pollutants identified in a sample represent but a portion of those present and they are
of unknown overall risk significance.
There is a major unanswered question regarding the toxicity of complex environmental mixtures.
Is the overall toxicity (or the spectrum of unique toxic effects) of a complex mixture caused by
few or many chemical constituents? And do these constituents comprise a small or large fraction
of the total dissolved mass? PPCPs in waters is likely not a new phenomenon, but has become
widely evident in the last decade because continually improving chemical analysis
methodologies have lowered the limits of detection for a wide array of xenobiotics in
environmental matrices. There is no reason to believe that PPCPs have not existed in the
environment for as long as they have been used commercially.
PPCPs are a diverse group of chemicals comprising all human and veterinary drugs available by
prescription or over-the-counter. People are largely not aware that their daily actions affect the
environment in this way. Certain pharmaceutically active compounds (e.g., caffeine, aspirin,
nicotine) have been known for over 20 years to occur in the environment, primarily from treated
and untreated sewage effluent. Now we know that numerous PPCPs can occur at very low
concentrations. Prior discovery was delayed by limitations in analytical environmental
chemistry (ultra-trace enrichment and detection).
Confined animal feeding operations (CAFOs) are a major source of antibiotics.
Portions of most ingested drugs are excreted in varying unmetabolized amounts, primarily via
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urine and feces. Other portions sometimes yield metabolites that are still bio-active or are
excreted as conjugates. Free excreted drugs and derivatives can escape degradation in municipal
sewage treatment facilities; the conjugates can be hydrolized back to the free parent drug.
Undegraded molecules are then discharged to receiving surface waters or find their way to
groundwaters through leaching and recharge.
Continual input of PPCPs to the aquatic environment can lend persistence to compounds that
otherwise possess no inherent environmental stability. The full extent of their impacts is
unknown. Most ecological monitoring studies to date have been performed in Europe (except
for USGS). The use/release of antibiotics and natural/synthetic steroids to the environment has
generated most of the controversy to date, but a plethora of other PPCPs have yet to be
examined. The scope of the overall issue is ill-defined.
Regarding pharmaceuticals in the environment, toxicological significance for both humans and
ecological exposure to multiple chemicals at trace concentrations (ppb-ppt) for long durations is
poorly understood. If PPCPs eventually prove to be an environmental concern, it is unknown
whether sewage treatment facilities could be cost-effectively modified to reduce emissions.
Source control aimed at both disposal and medical practices ("environmental stewardship"
programs) may prove more effective. The focus should be on proper and sufficient science for
establishing occurrence, exposure, and susceptibility/effects, so that sound decisions can be
made regarding human and ecological health.
Other potential routes to the environment include leaching from landfills, runoff from CAFOs
and medicated pet excreta, loss from aquaculture, spray-drift from agriculture, direct discharge
of raw sewage (from overflow events and residential "straight piping"), sewage discharge from
cruise ships (millions of passengers per year), oral contraceptives used as soil amendment and
plant growth tonic (urban legend), and transgenic reduction of proteinaceous therapeutics by
genetically altered plants (aka "molecular farming" - "biopharming"). Discharge to the
environment also occurs via dislodgement/washing of externally applied PPCPs to the skin.
Unanticipated routes of inadvertent ecological and human exposure to drugs is likely via water
(and secondarily, sludges and sediments). In certain localized situations, however, inhalation
exposure through sorption of drugs to respirable particles could occur despite the low volatility
of these compounds. . Dust from confined animal feeding operations where drugs are used to
supplement feed and given directly to animals also could contaminate the environment. Pig
house dust in samples collected over 20 years contained five antibiotics in concentrations up to
12.3 mg/kg.
In 1999-2000, USGS implemented the first ever U.S. national reconnaissance of "emerging
pollutants" in waters. In 2001 the first ever study was published on geographic variation across
the U.S. of prescription drug use. These occurrence data demonstrate the potential for ANY
consumer-use chemicals to enter the environment and warn us to be watchful for drugs with new
mechanisms of action and ever-increasing biochemical potencies.
Some drugs have double uses as medicines and pest controls. The potential significance of these
alternative uses as sources of environmental release has never been explored. Examples include
4-aminopyridine, an experimental multiple sclerosis drug and an avicide, or warfarin, an
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anticoagulant and a rat poison, among others. In September 2001, U.S. EPA allowed an
exemption from FIFRA for caffeine use to control the reproduction of coqui frogs in Hawaii,
which were out-competing birds by massive consumption of insects and producing a piercing
and annoying chirp.
Acetaminophen as been used on Guam to control brown tree snakes, which were reproducing in
great numbers without a natural predator and decimating bird, bat, and reptile populations and
causing economic losses to agriculture. Acute effects of larger doses of acetaminophen on local
non-target species have not been detected. Vultures (Gyps bengalensis) in Pakistan and India
may have declined in the 1990s due to pesticide use, diclofenac poisoning, or from pathogens.
The pesticide is used for cattle in India, and carcasses are a major food source of vultures.
All municipal sewage contains PPCPs. Local doctors' prescribing customs and cultural habits
vary the types of PPCPs found in receiving waters. Illicit and abused drugs also may be found.
Groundwaters maybe affected. Sources of raw sewage in the U.S. include combined sewer
overflows, sanitary sewer overflows, leakage from sewage transport infrastructures, failing
septic systems, unpermitted privies, and straight piping. The American Society of Civil
Engineers (ASCE) gave a grade of D in 2001 to U.S. drinking water and wastewater
infrastructures. More than $20 billion may be needed to repair them to a suitable level.
Subtle effects of PPCPs emanate from their numerous receptors, with response being exquisitely
specific and sensitive. Receptors of exposure and resulting effects can differ greatly from those
of currently regulated pollutants. Receptors in non-human species could differ from those in
humans. Researchers believe that acute effects may be less important than chronic effects to low
concentrations over time. Receptors could be different in aquatic environments, but this is
difficult to predict.
Subtle effects also include impacts on development, spawning, and other behaviors in shellfish,
ciliates, and other aquatic organisms. Calcium-channel blockers can inhibit sperm activity.
Antiepileptic drugs could trigger apoptosis in the developing brain. Very small amounts of
NSAIDS, glucocorticoids, and anti-fibrotics affect collagen metabolism in teleost fish, leading to
defective fin regeneration. Multi-drug transporters (efflux pumps) are common defense
strategies for aquatic biota, but may compromise aquatic health.
Latent damage in humans could cause subtle shifts in behavior or intelligence. Advances are
required in developing and implementing new aquatic toxicity tests to better ensure that such
effects can be detected. Slow poisoning of a victim with low doses administered over a long
time period was a popular practice in Europe in the 1600s and in the 1800s, akin to what may be
going on in the environment today with PPCPs.
Aquatic organisms are captive to continual, life-cycle, and multi-generational exposures of
chemicals via sewage released to surface waters. The supply of chemical contaminants is also
continually replenished. The risk cup body burden can be great due to additive effects from
multiple agents sharing common mechanisms of action (MOAs).
There may be possible interactive effects, especially synergism, which is difficult to
demonstrate. Non-target species receptor repertoires are not well characterized. Hormesis, or
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unknown effects, can accrue from doses below the therapeutic level. There has been little
research done at extremely low concentration levels. There maybe susceptible genetic outliers
within species. MO As are not fully understood.
The major collateral benefits of research and development efforts with PPCPs include
optimizing or improving existing wastewater/sludge treatment technologies (primarily for
POTWs) and developing or implementing new, cost-effective technologies for further lowering
the trace levels of PPCPs. Any improvements to remove trace levels of PPCPs also will likely
remove numerous other unregulated pollutants from water.
Pollution prevention efforts like source reduction could have significant consequences for
improved consumer health and the economy. These "cradle-to-cradle" stewardship efforts could
originate from the healthcare industry or from the individual consumer. Voluntary compliance
with a life-cycle stewardship approach also could improve medical healthcare outcomes and
consumer safety as well as reduce healthcare costs. (See Environmental Healthcare Perspectives
111,2003.)
There is a wealth of materials and links addressing environmental stewardship of PPCPs at the
U.S. EPA's web page on the Green Pharmacy:
http://www.epa.gov/nerlesd 1 /chemistry/ppcp/greenpharmacy.htm. In communicating risk more
effectively, perhaps there will be growing public acceptance of wastewater re-use for human
consumption ("toilet to tap" re-use programs). It also is important to forge collaborations
between scientists and the medical community. (See "Environmental stewardship and drugs as
pollutants," C.G. Daughton, The Lancet, 2002, 360:1035-1036).
In the future, the safety of drinking water supplies must be ensured by removing PPCPs and
other unregulated pollutants from treated wastewater. The decaying water/sewage infrastructure
must be improved and cost-effective technologies developed for optimal removal of PPCPs.
Concerns regarding the introduction of PPCPs to the environment from molecular farming must
be investigated. Integrated industry-consumer stewardship programs for minimizing the
introduction of PPCPs to the environment must be developed. A cohesive national or
international guidance must be developed for disposal/recycling of PPCPs.
Comments/Questions and Answers
Q - Confined animal feeding operations (CAFOs) use lots of antibiotics. Is there any
information on altered microbiological communities downstream of hog farms and resistance to
antibiotics?
A - U.S.D.A. has done a lot of research into this. There is no doubt some resistance - but are
they pathogens that could affect people? There are some people who worked in animal
operations who have died of resistant pathogens.
Q - Have we engaged Proctor & Gamble or the pharmaceutical industry, such as Johnson &
Johnson, in cradle-to-grave stewardship programs?
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A - The trade associations look at this. Most companies have their own stewardship program
relative to production processes, but not the introduction of drugs into the environment by
consumers. They may look at this somewhat, because they are concerned for other reasons.
Environmental Monitoring for Chemicals in Waters
Michael J. Focazio, U.S. Geological Survey
Since 1998, the U.S. Geological Survey (USGS) has been developing analytical capabilities to
measure pharmaceuticals and other organic wastewater contaminants (OWCs) in a variety of
environmental matrices. USGS' objectives were to develop sensitive and specific methods to
measure trace organics at low levels and to evaluate environmental occurrence in "susceptible"
waters.
Initial efforts to perform national reconnaissance studies for OWCs in water resources addressed
streams (1999-2000, 139 sites in 30 states); drinking water sources (2001, 76 sites in 27 states,
U.S. EPA); and groundwater (2000, 56 sites in 17 states). Data can't be compared except for
specific compounds among the reconnaissance studies, however, because researchers developed
analytical methods and added compounds as they moved forward. Ninety-five chemicals were
initially targeted, including drugs, antibiotics, lotions, detergents, antioxidants, plastics, PAHs,
fragrances, pesticides, fumigants, disinfectants, and fire retardants.
The stream monitoring studies focused on susceptible settings, including downstream of
wastewater treatment plants (WWTPs), confined animal feeding operations (CAFOs), and a
small number of undeveloped or natural settings. About half the sites were urban and half were
rural, with 17 sites having mixed use and eight being minimally developed. The most commonly
detected compounds were the naturally occurring sterols coprostanol, which was detected in
85.7% of the samples, and cholesterol, detected in 84.3% of the samples; N-N-diethyltoluamide
or DEBT, in 74.1% of the samples; and caffeine, in 70.6% of the samples. The chemicals found
in the highest median concentrations weren't the most frequently detected chemicals. Triclosan,
which was found in 57.6% of the samples, had a median concentration of 0.14 ppb, (the highest
median concentration of any of the compounds), and the detergent 4-nonylphenol, which was
detected in 50.6% of the samples, had a median concentration of 0.8% ppb (the next highest
median concentration for non-naturally occurring chemicals).
For drinking water sources reconnaissance, similar chemicals were targeted, 124
pharmaceuticals and other OWCs, plus sterols (but no synthetic hormones). A total of 49
surface sites and 25 groundwater sites serving both large (e.g., 8 million) and small (e.g., 1,000)
populations were sampled in 25 states and Puerto Rico. Results of the study are not yet
published. Many of the chemicals were not detected and when they were detected, the frequency
of detection was low due to source strength and the effects of treatment.
The most commonly detected chemicals were caffeine, at a frequency of 54% of all samples, and
the herbicide metolachlor, in 43% of the samples. The insecticide diazinon was detected in 19%
of the samples. An anti-convulsant drug, carbamazepine, was detected in 22% of the samples.
There was a higher frequency of detections in surface water, including caffeine at 69%,
metolachlor at 53%, and diazinon at 27%. The most frequently detected compounds were the
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same as those in the combined surface water and groundwater results, though the order of
frequency varied somewhat.
The frequency of detections in groundwater was significantly lower than in surface water. For
example, caffeine was detected in only 24% of the samples and 1,7 dimethylxanthine (a caffeine
degradate) in 16% of samples. Lower frequencies maybe due to source strength or to
absorption. Chemicals that appeared among the top 10 in frequency in the groundwater that
differed from the top 10 detected in surface waters included the solvent tetrachloroethylene, in
24% of the samples, the plasticizer bisphenol A, in 20% of the samples, and the antibiotic
sulfamethoxazole, in 20% of the samples. Besides diazinon, several other OWCs found are
suspected endocrine disrupters, including ethanol 2-butoxy-phosphate and bisphenol A.
Preliminary results of source-water reconnaissance included the following findings:
• At least one OWC in 55% of samples
• Mixtures of OWCs common
• Concentrations generally low (
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U.S. Environmental Protection Agency
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A - We just did stream bed sediments. As expected, some compounds were found in high
concentrations.
Q - Do you get sediments in your water samples because of unfavorable partitioning?
A - We tried to minimize those effects through the sampling methods we used.
Q - Can you identify sources when you publish your reports?
A - When we prepare such reports, we will say that there was a wastewater treatment plant
nearby, but we don't name it.
Q - Did you look for any hormones that are used in the veterinary industry for animal
production?
A - Yes. We looked specifically for some, but we looked primarily for a broad spectrum of
compounds.
Q - Did you look at microbial breakdown of compounds?
A - At WWTP outfalls, but we did not look at this extensively. It may explain the white or
nondetection areas on graphs.
Comment - If you took data on the frequency of detections plotted against the proximity to
WWTP outfalls, maybe you would know if some plants are better at removing chemicals or
dilution effects.
A - Iowa and Colorado are looking at this.
Comment - Look at the sources of wastewater going to the WWTPs.
Q - Could you look at the input into the POTWs and calculate what you'd expect to see in the
outfall?
A - Yes, we're heading toward this. We have a list of compounds based on prescriptions and
Pharmaceuticals produced.
Veterinary Pharmaceuticals: Potential Environmental Impact and Treatment Strategies
John L. Cicmanec, U.S. EPA/ORD/NRMRL/Cincinnati
In the late 1970s, the increasing occurrence of antibiotic-resistant organisms was recognized in
Europe and the U.S. The source was most likely the large-scale treatment of animals for
infectious disease as well as for growth enhancement. More than 3,200 tons of antibiotics were
used in 1998 for humans and animals in Europe and the U.S.
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More concern arose when the topic of endocrine disrupters was introduced. In many farm
operations, long-acting drugs such as trenbolone acetate and melengestrol acetate are routinely
used to enhance weight gain in beef cattle and, unfortunately, these compounds persist in the
environment. The public also is concerned about the use of bovine somatotropin to increase
milk production in dairy cattle.
Data gathered in watersheds with large, confined animal feeding operations (CAFOs) showed
that this way of doing business in American agriculture was having a significant environmental
impact, and that new practices need to be developed. This presentation will define the problem
and present some treatment or remedial strategies.
The veterinary group of compounds includes the following categories: antibiotics, anthelmintics
(worming agents), hormones, steroids and bovine ST, pesticides, vaccines, and x-ray contrast
media - iodine and barium-based. Potential endocrine disrupting chemicals include the
following: trenbolone acetate, melengestrol acetate, estradiol benzoate, ractopamine, testosterone
propionate, human chorionic gonadotropin, and pregnant mare serum.
Little is known about the fate of trenbolone and melengestrol after excretion by animals. The
half-life for trenbolone when stored as liquid manure is 267 days. In farm field studies,
trenbolone was detected at the end of the fertilization period, and melengestrol, which is even
more persistent, was detected at harvest. Ractopamine is a beta adrenergic agonist. It partitions
energy from fat growth to lean growth, increases protein accretion and muscle growth, and
increases muscle fiber diameter.
Swine are confined in gestational buildings and in growth/finishing buildings throughout their
lives, and related steroid hormones have been found in a study of human and farm animal waste.
Swine exceeded human sources for estradiol five-fold (swine 152 ppb, compared to municipal
sources at 31 ppb). For testosterone, municipal sources showed 29 ppb, compared to 21 ppb for
swine. Estradiol was measured in cattle waste at 19 ppb.
While the antibiotic tylosin is used most in swine, others include: sulfonamides -
sulfamethoxazole, etc.; quinolones - ciprofioxacin; beta-lactams - penicillins and
cephalosporins; aminoglycosides - streptomycin and gentamycin; and macrolides -
erythromycin and tylosin.
Europe uses more antibiotics for humans, 7,000 tons in 1998, compared to the U.S., 4,800 tons
in 1997, but Europe's population is 390 million compared to 270 million in the U.S. Europe uses
one-third as much antibiotic in farm animals, but has a much lower population than the U.S. -
19.8 million cattle in Europe (3,902 tons of antibiotic) compared to 97 million in the U.S.
(15,100 tons of antibiotic).
In Europe the ratio is 7:4 in favor of humans because of relatively low animal populations. In
the U.S. the ratio is 15:5 in favor of animals because of larger animal numbers. An adjustment
for all animal populations was made for body size: four pigs = one cow; 100 chickens = 1 cow.
In 1997, before controls, the annual use of antibiotics as growth promoters, not as treatment for
microbial diseases, was 1599 tons in Europe. In 1999, after controls were introduced, the annual
use dropped to 786 tons.
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In Europe, only four antibiotics - monensin, avilamycin, fiavomycin, and salinomycin are
presently approved for animal use. Primarily the macrolides and sufonamides persist in the
environment. Tetracyclines, penicillins, and fiuoroquinolones rapidly degrade. Concentrations
found were usually 1-5 ng/L but ranged up to 300 ng/L.
Tylosin is used as a feed-additive for swine. It is a macrolide antibiotic called Tylan made by Eli
Lilly & Company, and is administered at 20 g/ton dry feed. Its mechanism and resistance is
similar to lincosamide and streptogramin B type. One lagoon screening study showed tylosin
tartrate at 10 mg/L. This compound is used to reduce the amount of methane, but methane could
be harvested for electricity generation.
A study of resistance in E. coli in different species showed that swine operations had much more
antibiotic resistence relative to humans and cattle. Geese also showed more antibiotic resistance
than humans or cattle, and bacterial samples were positive from animal, bedding, and transport
cages. Sixty percent of chickens have streptogramin resistant E.faecium (SREF). There is some
geographical variation, but it was present at all sites tested.
For both Europe and the U.S., a study of resistance in retail meat showed that 30 to 60% of
samples had streptogramin resistant SREF. This also was evident in pork and beef products.
Among humans, 0.4 to 1% of people in the U.S. have SREF. Up to approximately 10% SREF
was reported in humans in Europe.
Linking animal and human use- The animal drug virginiamycin, streptogramin (Group B), has
been used for more than 26 years as a growth promoter at sub-therapeutic levels. In humans
synercid, streptogramin - quinupristin/dalfopristin combination - was approved for therapy in
the U.S. in 1999 as a "drug of last resort" to save lives when resistance has been developed to
other drugs. This is a family of drugs that should work on resistant strains, but now we find that
there are bugs that are resistant to it.
Antibiotics can have an adverse effect on some field crops. Chlorotetracycline, metronidazole,
and sulfamethoxine are toxic to plants such as soybeans, poinsettia, and corn at concentrations of
10-160ppm.
There are a number of processes to remove pharmaceuticals from water. The common ones
include: sorption to particles, ultraviolet light, bacterial degradation, and reverse osmosis.
WWTPs were not designed, however, to sterilize wastes or to remove pharmaceuticals. In some
industries, such as printing, waste must be pre-treated, but hospitals are not required to do so.
Pre-treatment also should be considered for large CAFOs.
Pharmaceuticals occur in U.S. wastewaters at levels of 61 |ug/L for acetominophen; 37 |ug/L for
ibuprofen; 27 for |ug/L amoxicillin; 14 |ug/L for cephalexin. These compounds are used in both
animals and humans. Sorption data for selected veterinary pharmaceuticals include tetracycline
at -1.19 log Kow; cipro at 0.4 log Kow; avermectin at 3.19 log Kow; tylosin at 3.5 log Kow;
sulfamethazine at 0.89 log Kow; metronidazole at 0.02 log Kow; and chloramphenicol at 1.14
log Kow.
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Ceftiofur (Naxcel R) is a new drug approved by the FDA for treating respiratory disease in
cattle, with no withholding time for milk required. However, a bacillus stearothermophilus test
will detect levels of 50 ppb in milk. But when used according to directions, none is detected in
the milk. Flunixin (banamine) is used in horses to treat inflammation, pyrexia, and colic. It is a
non-steroidal anti-inflammatory analgesic agent, and is approved for use in cattle to treat bovine
respiratory disorder.
What can we learn from studies of human pharmaceuticals? The most persistent drugs are
diazepam, carbamazepine, bezafibrate, and lopromide. Elimination of these drugs from
wastewater depends primarily upon sludge retention time. For activated sludge systems, 4 -5
days are needed; for nitrogen removal, 8-20 days are needed.
Presently, antibiotic resistance and endocrine disrupting chemicals have been shown to have the
greatest potential for causing environmental damage. The vast quantities of compounds used
and their widespread distribution make veterinary pharmaceuticals a significant environmental
challenge. Product control and distribution is more complex than for human pharmaceuticals.
Comments/Questions and Answers
Q - What is the likelihood that CAFOs can bear the cost of adding wastewater pretreatment?
A - We looked at the cost in Europe. It would cost more than twice the profits and put operators
out of business. However, we came up with six wastewater treatment processes that, if scaled
down, could be used. But there is no really cost effective method yet. In the Chesapeake Bay
area (Maryland, Delaware, and Virginia), there are heavy concentrations of waste and not
enough land for disposal, so wastewater pretreatment of animal waste is necessary. For poultry,
composting and treatment is more cost effective.
Q - Are human and farm wastes sources of steroid hormones?
A - From raw waste, levels were found at 140 mg for cattle and 20 mg for humans. High doses
cause death in humans.
Q - There are so many different chemicals. Should we focus on one group of pharmaceuticals
over others?
A - Antibiotic resistance and endocrine disrupters should be the first emphasis, but there is
danger in generalization, because pharmaceuticals can have different effects on different species.
We have to balance against the quantities and where they are being used.
Q - Wouldn't it cost more to build a wastewater pretreatment plant for CAFOs than just not
using antibiotics?
A - An economist would have to answer that.
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Q - Regarding antibiotics in wastewater - what about the biosolids? Should we look at the
effects of spreading them on the land? Are they looking for these types of compounds in
biosolids?
A - Work is being done to look at sites where biosolids are being spread. Is there aerosol
spreading? USGS has started studies, and these compounds should be included, but priorities
may need to be set.
Q - Is anyone trying to balance the tons of antibiotics being fed to animals, metabolized, and
released to the environment?
A - Someone must be looking at this. For example, sulfas are given in concentrations to saturate
the body, so a lot would be excreted. Many medications get bound to molecules in the body.
Efficient use in animals and shedding to the environment has not been studied yet.
Q - Are veterinary pharmaceuticals lower grade than human products? Is there a disposal
protocol for ear implants?
A - You must dispose of the ears that have held implants very carefully, but there are no
regulations over disposing of the waste -just the implants.
Comment - Although there are only a few drugs approved for use in Europe, a lot of other ones,
bought on the black market, are also being used. The presence of these drugs comes up when
testing is performed.
Assessing the Environmental Risk of Substances Under the US Food and Drug Act
Charles Eirkson, U.S. Food and Drug Administration (FDA)
In addition to looking at effects of substances on humans and animals, the FDA has been
performing environmental assessment since 1975. The Food and Drug Administration's main
authority comes from the Federal Food, Drug, and Cosmetics Act (FFDCA), which provides the
legal authority for assuring the safety and effectiveness of drugs, food/feed additives, devices,
biologies, and cosmetics.
The FDA, like all government agencies, also must comply with the National Environmental
Policy Act (NEPA) and assess the environmental impacts of their "actions." Under this statute,
the FDA performs reviews for assuring the safety of drugs and food additives to the
environment. FDA regulations implementing NEPA appear in 21 CFR25. These regulations
were revised in 1997 under the ReGO Initiative.
Although the EPA's Toxic Substances Control Act (TSCA) doesn't look at environmental
effects - and drugs are specifically exempted from pre-market approval under TSCA - the FDA
does work on issues involving aquaculture and drugs used in aquaculture.
Under NEPA, the FDA considers the environmental impacts (use and disposal) from the federal
"action" of approving a drug or food/feed application. In regard to veterinary products and
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drugs, veterinarians do a lot of the review. The environmental review under NEPA incorporates
environmental issues into FDA decision making.
It is important to note that NEPA does not require that the most environmentally beneficial
course of action be taken. Instead, the FDA looks at alternatives, and what looks best for what
one wants to do. Additionally, the FDA is required to comply with FFDCA requirements before
NEPA - and if there is a conflict, FFDCA prevails. Thus, the FDA can't refuse to approve
something just because of environmental impacts if it meets all other requirements.
There are some "categorical exclusions" under NEPA. Classes of actions that individually or
cumulatively do not significantly affect the quality of the human environment are ordinarily
excluded from the requirement to prepare an environmental assessment (EA) or an
environmental impact statement (EIS). Categorical exclusions include investigational new
(animal) drug applications (ESfD/INAD). These are excluded based on the small amount of the
drug being produced for investigational purposes.
Another categorical exemption is approval of natural substances when approval does not
significantly alter the distribution of the substance, its metabolites, or degradation products in the
environment. It should be noted that in this case, the "natural substance" has to be natural for
the area in which it is distributed (e.g., something that exists in Africa but not in the U.S. is not
"natural" to the U.S.).
Examples of categorical exclusions include the following: approval of a drug when the approval
will not increase the use of the drug; drugs for use in nonfood animals (because of the low
volume of use); drugs for minor species, including wildlife and endangered species, when
previously approved under similar animal management practices (e.g., drug used on cattle then
used on deer); and therapeutics, under veterinarian order or prescription.
An environmental assessment is required for an excludable action if extraordinary circumstances
indicate that the specific proposed action may significantly affect the quality of the environment.
Examples include actions for which available data establish that, at the expected level of
exposure, there is the potential for serious harm to the environment. FDA has used this on some
parasiticides. They also may go back and take a new look at products if the company decides to
make changes or a new application. EAs also are done if there are adverse effects to
species/critical habitat/endangered species.
Non-excluded applications include the following: therapeutic drugs used to treat whole
herds/flocks (e.g., anthelmintics: ivermectin); production drugs (e.g., subtherapeutic
antibiotics/synthetic hormonal growth promotants); coccidiostats (anticoccidials and growth
promotants: e.g., arsanilate); aquaculture drugs (FDA routinely assesses these); biotech products
(including genetically modified organisms (GMOs): e.g., transgenic salmon) and use of wild
plants/animals (harvesting). FDA frequently performs assessments on these last two categories.
The focus of the environmental assessments FDA performs is on environmental fate and
ecotoxicology based on drug use pattern. The EAs are publicly available documents, however,
they only become available after the product is approved under FFDCA. The FDA has also
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prepared Environmental Impact Statements on selenium in animal feed; subtherapeutic
antibacterial agents in animal feeds; taxol; and chlorofiuorocarbon propellants.
The FDA uses basically the same standard approaches as EPA for its EAs; however, they have,
in the past, sometimes included mitigations, such as labeling requirements or reducing dosages,
within the EAs rather going to an EIS to do this. Putting mitigations in the EA can save them
from having to do an EIS, but the FDA's General Counsel is disputing whether this is
appropriate.
When the FDA looks at effects, the agency uses a tiered approach - acute toxicity testing is
conducted first and then chronic toxicity if the data so indicate. Researchers also perform
chronic toxicity testing if they see that a compound is particularly persistent. When testing
human drugs, the FDA typically runs from 2 to 4 effects studies. They also look at introduction
into the environment through wastewater. When testing animal drugs, the FDA typically
performs 4 to 5 effects studies, including terrestrial studies because of the dung that animals
generate. Special studies the FDA may undertake include antibiotic minimum inhibition
concentrations (MIC), dung beetles, sediment toxity, avian toxicity, wash-off studies, and gene
transfer.
The main emphasis in testing animal drug effects under NEPA is on ecology. Issues having to
do with public health would be handled under FFDCA. Animal drug effects testing may involve
the aquatic environment, using daphnia, algae, and fish; the terrestrial environment, involving
plants (typically five species), microbial function, and earthworms; and pasture parasiticides,
including dung insects (flies and beetles). EAs for human drugs normally focus on the aquatic
environment.
Under the regulations, human drugs are categorically excluded if the expected introductory
concentration (EIC) in the aquatic environment is less than 1 ppb (absent extraordinary
circumstances). The data on human drugs routinely demonstrated, based on data for EAs done
between 1987 - 1996, no effects at concentrations of less than 1 ppb. Approximately 90% of the
toxicity effects occurred at levels at or above 1 ppm, while approximately 10% of the toxicity
results were reported for levels between 1 ppb and 1 ppm.
Of those, approximately one-third were antibiotics and one-third were central nervous system
drugs. Animal drugs do not have a categorical exclusion based on an EEC; however, less
information can be provided if expected environmental concentrations (EECs) are less than 1
ppb at release from an aquaculture facility or less than 100 ppb in soil. One hundred ppb is
below the level shown to have effects in studies conducted with earthworms, microorganisms,
and plants.
Various sources of information are available through FDA's website. EAs on human drugs are
available through FOIA requests. FOIA summaries also are available about how FDA made
decisions on the safety of a product, how it is used, and its efficacy. Information about
veterinary drugs is available through the FDA website, as well.
Two issues that FDA needs to look at are endocrine disrupting compounds and microbial
interaction. Trenbolone and its metabolites are under investigation.
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Comments/Questions and Answers
Q - If you have multiple sites using these drugs in water, do you look at cumulative risk?
A - Yes. Though if you have multiple sites using a chemical, it will still dilute to the same
amount.
Q - What about additive effects?
A - These are almost impossible to consider. It's hard to look at effects in a single species and
then extrapolate to the environment.
ENDOCRINE DISRUPTING POLLUTANTS IN EFFLUENT DOMINATED STREAMS
A Regional Case Study of Alkyl Phenol and Ethoxylates
Peter Howe, U.S. EPA Region 5
Approximately 500,000,000 pounds of alkylphenol is used each year in the U.S. These
compounds are used in industrial, institutional, and domestic surfactants, as antioxidants in
plastics, PVC stabilizers, oil additives, in oil field recovery, and in metal extractants.
Alkylphenolpolyethoxylates (APEs) have degradation products that are extremely toxic to
aquatic organisms (will probably be the regulatory end point), though not to humans or other
animals. The degradation products from APEs also are responsible for endocrine disruption to
aquatic organisms, though to date, the water quality standards have not addressed this endpoint.
The common environmental metabolites of nonylphenol ethoxylates include short chain
ethoxylates that are very toxic and also are endocrine disrupters. The European Parliament has
banned sale of nonylphenol (NP) and nonylphenol ethoxylates (NPE) to the general public and
restricted industrial use to specific, authorized purposes based on toxicity, not endocrine
disruption. Environment Canada has proposed that NP and ethoxylates be considered "toxic"
under the Canadian Environmental Protection Act.
NP bioconcentration factors are: bluegill - 220; fathead minnow 271 and 293 as reported by
Keith et al (2001). NP is not highly bioaccumulative, but is, however, very toxic. Depuration
half-life (hours) are: gammerus pulex - 38; killifish - 9; mussels - 7; salmon - 96 as
summarized in Gross-Sorokin et al (2003). The NP aquatic criteria document (draft March
2003) provides a freshwater chronic criterion of 5.9 ppb, and an acute criterion - 27.9 ppb, while
the saltwater chronic criterion is 1.4 ppband the acute criterion is 6.7 ppb. These values do not,
however, include toxicity of ethoxylates nor dothey address endocrine disruption. A study using
Japanese killifish indicates that as ethylene oxide chains increase in length, toxicity decreases.
A Canadian risk assessment was based on the cumulative toxicity of all APEs and estimates the
toxicity of NP1EO and NP2EO at half that of NP. Although this risk assessment recognized
endocrine disruption, it was not the major regulatory end point. Apparently APEs are to be
controlled through mandatory pollution prevention.
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ORD has provided funds for the Region 5 Central Regional Laboratory to conduct acute toxicity
testing on NP1EO and NP2EO to develop a TEQ for aquatic toxicity. At this time, the QAPP for
this work is under development.
A study of British streams hypothesized endocrine disruption effects in fish outside the
immediate discharge zone due primarily to 17 a-ethinylestradiol (EE2), a synthetic estrogen used
in birth control, and alkylphenols. A major issue in regard to EE2 is how far downstream it
persists.
Biomarkers for endocrine disruption in fish include decrease or cessation of egg production,
imposex (oocytes in testes), and vitellogenin (VTG) - egg yoke protein formed primarily in
female fish produced by the liver in response to estrogen or produced by male fish in response to
exposure to estrogen or estrogen mimics. (If researchers find VTG in males, they know they are
being exposed to estrogen). NP exposure is known to cause all of these effects, though
researchers do not yet know the relevance of the effects on fish populations.
Findings of NP endocrine disruption in fathead minnows (Miles-Richardson et al [1999]) are that
the NOAEL estimated from effects on endocrine disruption is six-fold less than standard chronic
toxicity for the early life stage of the fathead minnow. There is a question as to biological
relevance of endocrine disruption to fish populations, though, and this risk assessment does not
include APEs other than NP.
Hormones are another major factor in endocrine disruption in effluent dominated streams. In
one study, exposure to 17 B-estradiol (E2) to male fathead minnows showed a threshold for
histologic changes in the testes equal to approximately 0.04 ppt. Additionally, the threshold for
VTG induction also was equal to approximately 0.04 ppt. Testing of effluent concentrations of
E2 at four Michigan sewage treatment plants showed an average concentration of 1.5 ppt (range
= nd - 3.7 ppt). VTG induction in 14-day exposures to juvenile female rainbow trout indicate
that EE2 is more potent than E2, which, in turn, is more potent than El (estrone).
Studies of male fish exposed to effluent from the Minneapolis Metro Plant show inconsistencies.
Carp and walleye collected in the effluent showed VTG increase and testosterone decrease;
however, goldfish exposed to effluent samples for 10 weeks exhibited no change in testosterone.
Walleye collected from the Metro Minneapolis effluent showed total APE concentrations in fish
tissue at 6.2 ppm. Data gathered in 1995 on APE concentrations in the effluent of 15 paper mills
along the Fox River (Wisconsin) ranged from a low of 0.03 ug/L to a high of 26.60 ug/L for
nonylphenol and from alow of 1.28 ug/L to a high of 712.0 ug/L for total NPE.
Another study conducted in 1995 of concentrations of APEs from Publicly Owned Treatment
Water (POTW) along the Fox River (Wisconsin) yielded a range from a low of 0.18 ug/L to a
high of 15.9 ug/L for nonylphenol and a low of 8.8 ug/1 to a high of 78.8 ug/1 for total NPE. Fox
River APE concentrations (ug/L) upstream of the Green Bay wastewater treatment plant showed
NP at 0.58; NPE at 2.78; NP1EO 1.70; NP2EO 11.8 for a total concentration of 16.88 ug/L.
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Because of concerns about the APE levels in the effluent of wastewater treatment plants,
researchers looked at eight other large POTWs. They found little removal of alkylphenols in
plants with only primary treatment (less than 10% removal), while plants with secondary
treatment removed from 30% to almost 100%, and plants with tertiary displayed treatment
removal rates were in the above 90%.
Effluent streams are very important in the Chicago area because the combined effluent from the
major Chicago wastewater treatment plants is greater than the flow of most of the rivers in the
region. Eighty percent of the water that flows through the Lockport lock and dam, for example,
is effluent. The amount of effluent is influenced significantly by precipitation in the area,
because much of the area is served by a combined sewer system (stormwater runs through the
wastewater treatment system).
The Region 5 Central Regional Laboratory, working with ORD, developed a methods initiative
proposal for APEs for water and sediment. Concentrations of NP and NPEs in carp from the
North Branch of the Chicago River also have been tested.
Although water quality based effluent limits (WQBEL) control traditional toxics, there is a
question of whether they facilitate recovery of large effluent-dominated streams. Cooperative
whole effluent toxicity (WET) testing at the three major Metropolitan Water Reclamation
District of Greater Chicago (MWRDGC) plants show no chronic toxicity (though all effluents
were toxic 10 years ago). Toxicity testing of water collected at the Lockport lock and dam,
which also used to be toxic, also shows no chronic toxicity. Despite these decreases in toxicity,
these waterways still don't have good fish populations. Some of the factors that may contribute
to the poor fish population include: combined sewer overflows; contaminated sediments; barge
traffic; and habitat limitations.
Conclusions include the following: there is widespread APE occurrence in Region 5 water,
sediments, and fish tissue; there appear to be some effluents that may exceed the proposed water
quality criteria for NP; the Region 5 Central Research Laboratory has an SOP for NP, NP1EO,
and NP2EO; Region 5 is developing TEQs for NP, NP1EO, and NP2EO to account for the
toxicity of ethyxolates; consideration should be given to phasing out APEs in the U.S. due to the
increased costs associated with removing them from POTW effluents.
Comments/Questions and Answers
Q - What about the Canadian study on nonylphenol in Atlantic Salmon?
A - Didn't have time to get into that.
Q - Have you heard about a plan to use NP as an emulsifier as a petroleum substitute?
A - Haven't heard of this.
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Field Observations of the Contributions of Alkyl Phenols on Fish Endocrine Disruption
Cliff Rice, U.S. Department of Agriculture
Dr. Carys Mitchelmore, University of Maryland
Cliff Rice gave the presentation. Many chemicals mimic natural estrogen. For this study, they
used nonylphenol ethoxylates (NPEs) as the token endocrine disrupting chemical (EDC).
Numerous effects can occur that are detrimental to normal endocrine functioning, such as
disrupting sex ratios, impairing fertility, infertility, and even changing behavior. There are often
high levels of EDCs in rivers, due to industry, agriculture, and urbanization, though the EDCs
resulting from agricultural pesticidal applications as extenders/wetting agents are unlikely point
source problems in this river.
There are especially high levels of EDCs found in the discharges of some wastewater treatment
plants, though some other plants provide treatment that removes or reduces many of these
compounds. For the study, researchers used biomarkers to determine exposure to and effects of
these chemicals, such as the presence of the female yolk protein, vitellogenin (VTG), in male
fish, and changes in normal steroid profiles (estrogen (E2) and 11-ketotestosterone (11-KT).
The study site was the Cuyahoga River, which is famous for an oil slick that caught on fire in
1969. This incident played a critical role in the crafting of the 1972 Clean Water Act. The
species sampled for the study was the common carp, a benthic bottom feeders, because the top
predator fish haven't re-established in the river. The researchers looked for NPEs, since these
are especially prevalent in wastewater treatment plant (WWTP) discharges and are known to
have estrogenic effects on resident wildlife.
The aims and objectives of the study included the following: determining levels of nonylphenol
ethoxylates in sediment, water, and carp tissues, including nonylphenol (NP), NP1EO, NP2EO,
and total NPEs (tNPEs) (this was actually part of a larger study by the Ohio Environmental
Protection Agency to determining whether these compounds were there); determining if there is
a difference between levels of NPEs in pristine (headwaters) versus possibly affected sites
(downstream); determining whether there is a correlation between levels of NPE and possible
WWTP discharge sites; and determining whether there is a correlation between biological
parameters and levels of NPEs, in particular in regard to measures of VTG, E2, and 11-KT.
There were seven sampling sites along a 74-mile stretch of the Cuyahoga River. Site 4 was near
the confluence of the Little Cuyahoga River and several abandoned hazardous waste sites. For
the study, 12 fish, half male and half female, were sampled at each site for levels of NPEs in
their tissue. Additionally, general biological and health measures were determined for each fish,
including length, weight (whole fish and gonad weight), gonadal somatic index, condition factor
(weight divided by length), and percentage lipid. Endocrinological parameters measured
included circulating steroid levels and VTG levels in the blood.
The lowest levels of total NPEs in the fish were found at site 1, which was the uppermost site
along the river. Peak total NPE concentrations were found just downstream from the Akron
WWTP (site 6). High levels were also found at sites 7 and 8, the farthest downstream of the
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sampling locations. In all locations, similar levels of total NPEs were found in males and
females.
Similar results were found for NP, NP1EO, and NP2EO, with the following differences: NP
levels were highest in fish from sites 6 and 8, downstream from WWTPs, but there were highly
variable concentration levels; NP1EO provided the greatest contribution to total NPE, though
NP2EO was detected in the greatest concentration at site 6, with high levels also shown at sites 7
and 8.
In regard to biological parameters, a reduction of weight and length in the sampled fish, both
male and female, was noted in progressing down the river. Although there was no difference in
gonad weight in females as they moved downstream, there was a difference in males (bigger
upstream). There were, however, no differences in GSI or percentage of lipid. Because NP,
particularly, is lipophilic, researchers thought there would be a correlation, but there was not.
For males, there was no difference between the sites in levels of E2 or 11-KT, though there is a
suggested difference in levels of VTG. Higher levels of VTG at site 6 correlates with the highest
total NPE, NP1EO, and NP2EO downstream of the Akron WWTP, but NP was highest at site 8,
rather than site 6, although this was not significant at P > 0.05, due to the low number of samples
and variability. Overall, there were very poor correlations between NPEs and male VTG levels,
and total NPEs, NP1EO, and NP2EO. There is also a poor correlation between NP and VTG
levels.
To increase the sample size, researchers grouped the sampling sites into five zones. When they
did this, they found that higher levels of VTG correlated with high NPEs downstream of the
Akron WWTP.
In regard to female fish, there were no differences among the sites in levels of VTG or E2.
There were significant differences in levels of 11-KT and the ratio of E2 /11-KT between sites,
though there was no correlation/patterns with levels of NPEs, leading researchers to wonder
about the role of other chemicals or factors.
The summary and conclusions include the following observations: Levels of NPEs are
comparable to those reported in other studies for a moderately contaminated river; the highest
NPEs are downstream of the Akron WWTP, except for NP - the highest levels of NP were at
site 8; NPEs especially NP have been shown to affect fish endocrine parameters (e.g., elevated
VTG in males - though this study showed a weak correlation - and changes in steroid hormones
for males and females - though this wasn't seen in the study.); WWTPs also have been shown in
other studies to affect the fish endocrine parameters; there was a clear estrogenic impact along
the whole length of the river as all male fish have some VTG present; there was no obvious
impact of NPEs on females; and more data are required, suggestions include increasing the
sample size and sampling during a different season.
The percentage of contribution of plant discharge from the Akron WWTP to the Cuyahoga River
for the sampling period was anywhere from 40 to 60% of the river flow at that location.
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In another study of female carp in the Des Plaines River (Illinois), a reduction in VTG did
appear to correlate with an increase in NP.
Comments/Questions and Answers
Q - In the last graph, it looks like all of the data is driven by one point.
A - Maybe.
Comment - You should call that point an outlier.
Q - Were the fish collected in the spring?
A - No. They were collected in July.
Comment - Female weights maybe affected by the discharge of eggs.
Q - Given that you were looking at effluent dominated streams and we know that NP is 100,000
times less potent than natural estrogens, did you look for natural hormones?
A - No. We didn't have the data or the funding for that.
Effects of Wastewater Treatment Effluents on Fish Endocrine Disruption
Larry Barber, U.S. Geological Survey
Determining chemical impacts in the environment requires an interdisciplinary approach
involving hydrology, chemistry, and biology. Chemicals can enter waterways in either urban or
rural settings through industrial discharges, publicly owned treatment works (POTW), combined
sewer outfalls, landfills, agricultural activities, and animal production activities. Rural areas
have sources of chemical pollution, including landfills, manufacturing, and agricultural
activities. One confined animal feeding operation (CAFO) may produce the equivalent amount
of waste as one to two million people. In areas where water is reused, we have to think about
wastewater effluent.
The effects of endocrine disrupting chemicals can include ecosystem changes: population effects
as reproductive output falls below the critical level; individual reproductive effects, as
reproduction is impaired in individual animals; secondary behavioral and morphological effects
(changes in characteristics affecting mating); primary molecular and biochemical responses
(changes blood hormone levels, effects on the neuroendocrine system); and exposure to potential
environmental agents. Researchers are just learning about secondary behavioral effects because
it is hard to see changes in behavior.
Hormones are chemical regulators secreted by glands to the blood that effect a change at a target
site. It is difficult to identify hormones in the environment - and even more difficult when
dealing with congeners.
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In regard to the aerobic degradation of surfactants (linear alkylbenzene sulfonate (LAS) and
alkyl phenol ethoxylates (APEOs), as they degrade, they become less toxic and have a shorter
half-life. These are very high production volume chemicals, however. Interestingly, researchers
often find that concentrations of nonylphenols are higher in river water than in effluent.
The researchers conducted a study of the effects of environmental estrogens on reproduction in
fathead minnows. Fathead minnows were a good subject for this test because paternal nest care
is crucial for reproductive success; fatheads are a widely used fish model for toxicological
studies; and they readily reproduce in the laboratory year round. Researchers performed a "flow
through" experiment at the St. Paul, MN wastewater treatment plant (WWTP) in which 100%
effluent was pumped through 15 tanks containing 100 fish for four weeks. One of the things
they were looking for was competitive spawning behavior between exposed fish and control fish
to see effects on population.
The control exposures were conducted at a separate facility in St. Cloud. The negative controls
involved the use of old groundwater in some tanks and groundwater with XAD-8 treatment. The
positive controls involved 17-b-estradiol and a mixture of AP compounds. The experiment was
performed in July and replicated in October.
The XAD-8 effectively removes hydrophobic compounds and has a high affinity for phenolic
moieties. The columns used were suitable for high flow rates and removed 50 to 95% of AP
compounds. The researchers collected seven XAD-8 fractions, 100% water and 100%
acetonitrile. Characterization was done with the GC/MS/, LC/MS/, FTIR, and NMR.
Researchers removed the gonads upon completion of competitive spawning. Different species
have shown different effects as indicated by gonadal abnormalities reported in fish from many
sites contaminated with environmental estrogens, including the Metro sewage treatment plant.
Histopathology of reproductive tissues documents long-term ontogenetic disturbances in the
endocrinology of the animal (in contrast to vitellogenin analysis).
A portion of the study considered competitive spawning. Only the nest-holding male will
reproduce successfully (confirmed through DNA fingerprinting). Failure to defend the nest site
for the entire egg development period will result in loss of the brood. The endpoint was the
number of observations (two per day, AM and PM) during which the nest was held.
The preliminary results of the study are as follows: no intersex development was found in any
fathead minnow exposed in the study. VTG induction was observed in positive controls and
effluent. GSI and HIS appear to be regulated by temperature. There are seasonal effects of VTG
induction, probably because of changes in the wastewater treatment regime. XAD-8 partially
removes estrogenic effect.
Comments/Questions and Answers
Q - Which male fish won the competitive spawning?
A - The "control" (non-exposed) fish had an advantage and typically won.
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Aquatic Toxicity, Estrogenicity and Treatability of Nonyl Phenol and Ethoxylates in Waste
Water Effluents
Charles Staples, Assessment Technologies, Inc.
Nonylphenol ethoxylate (NPE) surfactants are widely used in applications that are sent to
sewage treatment plants when spent. While NPEs are generally easily treatable in well-run
treatment plants, residues from biodegradation are often detectable in effluents. It is of interest
to examine the potential risks to the environment from these residues. Risk assessment is the
preferred means of addressing these compounds.
Risk assessment requires exposure and ecotoxicity data. The results of risk assessment are used
by risk managers to control and manage potential unwanted risks. The purpose of the
researchers' study was to examine the ecotoxicity database, including endocrine-modulating
effects, for the NPEs, NPEC and NP, that are most common in effluents as shown in wastewater
treatability studies.
In an example of a treatability study for NPE surfactants, the effluent from two Canadian sewage
treatment plants, both of which receive municipal and industrial wastes was analyzed. Plant A
used a process involving activated sludge, nitrification, tertiary treatment, and UV disinfection.
Effluent from this plant showed a removal efficiency for NPE of 97%. Plant B had a non-
nitrifying activated sludge process and chlorine disinfection. The removal efficiency for NPEs
was 86%.
According to earlier studies, the main NPE related products in raw sewage are commercial NPE,
while the main components in final effluents were NPEC with some NPE 1,2 and traces of NP.
Risk assessments of NPE residues from sewage treatment plants in surface water should
therefore encompass NPEs, NPEC, and NP.
The researchers performed a critical review of chronic aquatic toxicity data for NP and NPE.
This included dozens of studies, endpoints, LOEC, and NOEC and considered survival, growth,
and reproduction. The species sensitivity analysis shows that the data support the draft U.S.
EPA WQC for NP of approximately 5.9 ug/L. In addition to these studies, the researchers
looked at a study in which medaka fish were exposed from 1 to 100 days post-hatch to NP,
NPE1, NPE4, NPE9, and NPEC 1 and examined for sex ratio, secondary sex characteristics, liver
VTG, and testis-ova. This study showed effects in the Testis-ova and in the secondary sex
characteristics in the fish exposed to NP and effects in secondary sex characteristics in the fish
exposed to NP1EO.
The conclusions from the medaka study are that NP induced gonadal intersex and mixed
secondary characteristics in male medaka at 20 and 100 ug/L. Mixed secondary sex
characteristics were induced in males at 300 ug/L NPE1. However, there was no evidence of
estrogenicity with NPE4, NPE9, or NPEC up to 1000 or 3000 ug/L and no effect on sex ratio for
any compound.
The ecotoxicity studies show increasing toxicity with decreasing ethoxylation in both chronic
and acute studies. Ecotoxicity studies of NPECs show them to be relatively non-toxic. Only NP
showed estrogenic potential in a long-term developmental study with medaka. Thus, the
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available database of conventional chronic studies should be adequate or nearly adequate to
address the ecotoxicity of the various biodegradation intermediates of NPE surfactants.
Treatability studies show that well-run sewage treatment plants are effective at removing NPE
surfactants, but residues do enter receiving waters. Risk assessments of surface waters receiving
sewage treatment plant effluents should address all biodegradation intermediates. Risk
management to reduce risk from natural hormones in human waste simultaneously addresses
NPE, NP, and NPEC. Risk management to reduce risk from industrial sources should include
best management practices.
Comments/Questions and Answers
Comment - It's not a matter of how well run a wastewater treatment plant is if it doesn't have
the equipment to remove NPEs. A plant may be well run, but if it doesn't have the equipment, it
can only do so much.
A - Agreed.
Q - Some data suggest that NPE becomes NP downstream, so we need to test for that.
A - They don't break down to NP except in anaerobic conditions.
Q - What is the toxicity of ether carboxylates?
A - They aren't particularly toxic.
Q - Is NPE still being considered for use in petroleum applications?
A - The University of Massachusetts did some research in this area a few years ago. Also, there
was an application to the State of Florida at that time but I believe that project was abandoned.
Break Out Sessions
Break out sessions were held to discuss the following topics:
• EDC and Effluent Dominated Streams
• Asbestos and Durable Fibers
• Pharmaceuticals and Personal Care Products
Flip chart and discussion notes from these break out sessions can be found in Appendix D of this
document.
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Thursday, August 14, 2003
Objectives of the Final Session
Dan Hopkins, Toxics Reduction Manager, U.S. EPA Region 5
There are still many unanswered questions in regard to emerging pollutants. Some of the topics
we will be discussing today aren't just emerging pollutants or issues, they are emerging science.
How do we identify emerging chemicals and how do we get them to "stick" on our radar screen?
We need to identify these issues, but we also have to make sure they are pursued.
Biotechnology: A New Frontier, The Promise, Potential Risks, and How Can We Find
Out?
John A. Glaser, U.S. EPA/ORD/NRMRL - Cincinnati
Biotechnology has much to contribute to a sustainable environment. There has, however, been
significant suspicion regarding biotechnology, most recently in Europe. EPA and other agencies
in the U.S. have the mission and the responsibility to assess correctly biotechnological
inventions for their suitability and acceptability for a sustainable environment and to understand
how these inventions fit into our commerce and our environment.
The Promise
Biotechnology promises new products and useful processes that may permit the use of biomass
to serve the demands of society. These include the development of agronomic traits, one of the
first of these type of products to be developed, as well as products for the feed processing,
chemical, and health care industries. We still rely very heavily on microbial activity to make the
products we are interested in or can use. Now we are looking at using enzymes engineered from
microorganisms found in nature to make a wide variety of products, from pharmaceuticals to
chemicals. These advances hold much promise for the future.
Products made using biotechnologies include Nitto's polymer-grade acrylamide, Lonza's
carnitine, and Du Font's key monomer for it's highest performing polyester. The entire high
fructose corn syrup industry was created by enzymes. Hercules' G3 is a product of
biotransformation. Researchers are studying a polymer referred to as biosteel that is made from
the filaments of spiders. The promise of future useful technology lies in areas such as
phytoremediation, biobased conversion technology, agricultural biotech, molecular farming, and
analytical biotech.
With phytoremediation, plants offer unique means to move chemicals in the contaminated soil
phase. Plants also offer a unique means to sequester organic and inorganic pollutants. And
plants offer unique opportunities to degrade organic pollutants in cooperation with soil
microbiota. Through the transpiration of liquids, plants can be used for their ability to pump
subsurface contaminated water. The contaminants in such a scenario can be volatilized from
water and possibly metabolized by the plant. Biodegradation products in the root zone of trees
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could be utilized, as well as the oxygen that trees give off in the root zone. Planted areas could
be useful in wetland filtering.
With biobased conversion technology, biofuels, such as bioethanol and biodiesel fuels, can be
made by the microbial fermentation of sugars from a variety of natural sources and crops.
Large-scale development is underway, with batch conversion using one-million-gallon reactors
making the process commercially viable. This should lead to the use of bioethanol as a major
fuel source. With increasing production capacity of reactors, however, waste stream
management also will be important and challenging.
Bioethanol conversion is mainly based on cellulose hydrolysis for more complete utilization of
the available carbon in the source material. Hemicellulose and cellulose hydrolysis require
different microbial action. Bioethanol has been used as a replacement for MTBE. Two million
gallons were produced in 1998, and this amount is expected to increase to 4 billion gallons in
2010 and 9.5 billion gallons in 2020. Current production is around 1 billion gallons.
For biodiesel, rapeseed oil is used due to its high quality. Triglycerides are broken up to release
fatty acids, which are separated and converted to esters. U.S. production of biodiesel in 2002
was 15 million gallons. In February 2003, the largest biodiesel plant came on line in California
with a production capacity of 35 million gallons per year. A cooking-oil-to-diesel recycle/reuse
program is being evaluated in several locations.
Cargill-Dow is using corn for starch and sugar fermentation to produce lactic acid, which is
polymerized to polylactic acid (PLA) at a production target of about 300 million pounds per
year. About 40,000 bushels of corn per day will be used in this process. Further use of
agricultural biotech lies in molecular farming for commodity and specialty chemicals and
Pharmaceuticals. An application for crop protection includes herbicidal control and Plant
Incorporated Protectants (PIP).
Why should we use plant biotechnology? Traditional breeding depends on inherent genetic traits
that occur within an interbreeding population. Specific desired traits, such as those that enhance
production, may not exist within a particular population. Mutation breeding is inefficient and
cannot be targeted to specific traits. Novel traits can be introduced from other species to produce
new or improved end products and can enable environmentally beneficial agricultural practices.
The ability to use environmentally beneficial agricultural practices is an objective for these new
biotechnology ventures, though it is not achieved in all cases.
Crop engineering might take a desired biological pesticide, for example, and work it into a corn
cell yielding a newly transformed corn plant. DNA from microbes in the soil expressing useful
pesticide traits might be used in the crop itself to give protection and this is the case with
Bacillus thuriengensis. Selection of potential crop traits focuses on those that affect yield or
efficiency, or that lower production costs, rather than the properties of the commodity produced.
Output traits are modifications that affect the composition, quality, or value of the commodity
rather than the ability to produce the crop.
There are a variety of ways to put modifications into plants, such as using male sterility or, for
example, putting modifications into plants such as trees with long life spans so that the trait isn't
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exchanged in nature. Other inducible or delayed-action modifications can be made in seed
composition, the timing of trait expression, tissue localization of expression, or the removal of
unwanted genes.
Molecular farming involves crops that aren't used for food, feed, or fiber but for plant-made
chemicals and pharmaceuticals. Modified plants offer new and possibly more useful ways to
produce valuable molecules and therapeutic agents. Plants make proteins in the same way that
humans do, so we can use plants to put proteins together.
The development of human protein therapies has significantly increased from 1982 to the
present. The driving force is the ability to produce crops for pharmaceutical uses that don't
require fermentation for processing. Pharmaceutical crop developers include Dow, Monsanto,
and Prodigene. Plants figure very strongly in these production systems. The focus of work
today for modifications in the pharma crop area is corn, other monocot and dicot grains, forage
crops, and tobacco.
Herbicide tolerance can be built into plants, such as in Monsanto's Roundup Ready ® Crops.
Herbicides target specific enzymes or processes in the plant metabolism. Engineering herbicidal
resistance into plants involves modifying the target enzyme or introducing an enzyme that
detoxifies the herbicide. The introduced enzyme can be obtained from bacteria, fungi, or other
plants. Rather than using a broad-spectrum insecticide that would kill all insects, including those
that are beneficial, the DNA coding for crystalline bodies (Cry) protein from bacteria can be
installed in a plant to engineer crop resistance to specific insects that affect the crop yield and
health.
Analytical biotech can be used to detect pathogens and toxin expression in Plant Incorporated
Protectants (PIPs) crops, and offer opportunities to replace some animal testing with genomic
and proteomic approaches. Structural genomics looks at information at the DNA level. Protein
engineering can be used with metabolic engineering and other forms of functional genomics to
enhance understanding of biological activities at the functional level. Using simple techniques,
we can amplify DNA in samples to get to useable material in a shorter time frame for analysis
that will lead to more information on microbial species.
Potential Risks
The agency plays a strong role in PIP Bt crops to manage the potential risks associated with
them. Not all PIP crops will be required to implement integrated resistance management (IRM)
requirements. Bt crops are selected for IRM when there is a compelling need to preserve the
toxin, because other growers may be using it in spray form, and there is a need to protect its
efficacy against pests.
Around 140 million acres of genetically modified (GM) crops are produced annually worldwide.
EPA registers all pesticides, including new substances and DNA in the plant when it is pesticidal
in nature, under the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA). EPA must
ensure that pesticides will not pose unreasonable risk to human health or the environment. For
PIPs, EPA considers risk to human health, risks to nontarget organisms and the environment, the
potential for gene flow, and impact to the Insect Resistance/Management Plan.
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Major recommendations for continued research from consultative bodies such as the National
Academy of Sciences include assessment of the following: allergenicity from GM Foods; the
possibility for gene transfer; the ecological risks associated with GM crops; gene transfer; and
resistance management. EPA has initiated a Biotechnology Program through ORD, which
received funding in 2003 and is strongly supported by and coordinated with the Office of
Pesticide Programs.
Food allergies occur in about 5% of children and about 1-2% of adults. Novel proteins
introduced into food could be allergens. EPA's ORD research program is pursuing a rodent
model that is needed to evaluate the allergenicity of GM crops. Researchers also must address
the potential ecological risks related to GM crops regarding the likelihood and impacts of gene
transfer, impacts on non-target species, such as the monarch butterfly, and determine/manage
pesticide resistance.
Because resistance evolves in insects, EPA requires resistance management plans to prolong the
usefulness of Bt crops and avoid the need for broad-spectrum pesticides. Bt spray used in
organic farming maybe rendered ineffective if insect resistance becomes significant. EPA
requires implementation of a "high dose, structured refuge" strategy for resistance management.
How Can We Find Out?
Remote Sensing in Agriculture
One example of research leading to new information is the use of crop spectral features to
discern crop conditions as related to pest infestation. This research involves use the remote
sensing of bioengineered crops to monitor crop status, nutrient and pesticide management
applications, and landscape characteristics. The current Bt corn crop is about 20 million acres.
There is no simple and economic means to gain access to sufficient discrete samples that would
inform us about the development of pest resistance for Bt corn on a statistical basis. Remote
sensing has been used to show different irrigation applications and levels of stress. This same
technology could be applied to developing monitoring information about pest resistance. When
considering monitoring of pests to determine whether any have developed resistance, it is
necessary to assay baseline susceptibility levels for resistance monitoring, changes in the
frequencies of resistance alleles, the presence of any dominant alleles related to resistance, and
effects of resistant insects. Such information is important to dealing with resistance failures.
The current monitoring strategies' use of limited sections of a corn crop as proxies for the entire
crop may not provide adequate information for resistance detection. Infestations of corn pests
are expected to begin as local phenomena and may not be adequately identified. Remote sensing
can be used to check grower compliance with EPA's resistance management requirements. As
an early warning system to strengthen resistance monitoring strategies, remote sensing is based
on stress inference, and for detection of pest infestation as part of resistance monitoring of the
corn.
Airborne and satellite imagery can detect plant pigments and plant stress, and can stratify images
and field surface conditions. Infrared imagery may be able to distinguish between Bt corn and
conventional corn crops. EPA can use this information to organize data for different fields and
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determine whether management plans are being carried out. For ground truthing in Nebraska
and Pennsylvania, remote sensing has been used to monitor the activities of insects that are
released to determine the efficacy of the Bt corn.
Infrared spectral wavelengths are potentially useful for detecting a bioengineered crop and
obtaining the spectral signature crops, but because the signal is a composite of many factors, it
needs to be deconvoluted to make the information useful. The signal-to-noise ratio is important
to define detection constraints. Information needs to assist the use of remote sensing to
transgenic crop monitoring include compliance, inference of resistance, and resistance detection.
Comments/Questions and Answers
Comment - The use of new genomic technology won't replace animal testing, but could reduce
it.
Environmental Futures: Nano Technology and Genomics Coming Over the Horizon
Gerardo (Pasky) Pascual, ORD/Office of Science Policy, Environmental Futures
Workgroup
Under Goal 5 of U.S. EPA's ORD Research and Strategy Plan, the agency will evaluate
opportunities for and, as appropriate, conduct research to anticipate and assess future
environmental stressors before they adversely affect people or the environment. In 1995, EPA's
Science Advisory Board called for an EPA-led effort to anticipate and respond to environmental
change and to provide the public with an understanding of risks and opportunities, both
environmental and economic, and to better define actions needed today to reduce risks and
preserve opportunities.
EPA is building the capacity to develop a "foresight" effort focused on potential issues 10 to 20
years into the future. Terrorist attacks in recent years have added urgency to this effort so that
the hostile use or release of hazardous chemicals or the disruption of environmental systems can
be avoided. EPA endeavors to interpret the future by scanning weak signals, scoping strong
signals and developing foresight tools.
By reading scientific journals, researchers can scan weak signals to identify leads in the domains
of conflict and governance, science and technology, agriculture and food security, natural
resources and environment, and energy use. Experts then rank the leads by their novelty, scope
and severity.
An example of looking at a "weak signal" and using the information to anticipate or prevent
future problems involves work done by Massoud Amin of the Electric Power Research Institute,
in which he examined the cause of a four-state power outage that occurred in 1996. Amin
determined that the outage could have been prevented by shedding 0.4% of the load for 30
minutes.
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He then designed a ubiquitous, real-time sensor system that would detect potential problems
with the transmission system before a major outage so it could be prevented. According to
Wired, 2001, Amin's design would have the following effects: "Every node in the power
network of the future will be awake, responsive, adaptive, price-smart, eco-sensitive, real-time,
flexible, humming - and interconnected with everything else."
The Woodrow Wilson Foresight and Governance Project brings in experts to run symposia on
emerging and future issues. In one symposium, participants considered the issue of
toxicogenomic testing. A presenter at the symposium made the points that if individuals become
capable of detecting their own genetic susceptibilities, this may be the lowest cost risk avoidance
mechanism, because it would allow individualized decisions on whether a person would use
specific products rather than relying on government regulations designed to protect the entire
population when only a few individuals are susceptible.
The concluding question by this symposium presenter was what criteria should be used to shift
primary responsibility for avoiding/preventing risks from the manufacturer to individuals? At
this point, some substances, for example, are simply labeled so that people who have certain
sensitivities will know to avoid them (or can make their own choice about avoiding them).
At this point, there are two impediments to using toxicogenomic testing. One is technological -
results of testing may differ depending on how the lab performs the test, so there are efforts afoot
to standardize toxicogenomic testing. The second is who will drive the demand for this
technology? Pharma companies have basically withdrawn at this point because the small
number of people who would be served may not make it economically attractive.
Some demand may be driven by lawsuits. In one case, employees of a company are suing,
saying that the company should have screened them for susceptibility to certain substances.
Nanotechnology, a setting in which materials are manipulated at the molecular level, is already
here, though some researchers weren't initially thinking in terms of potential ecological or health
effects of using this technology. Some products have already been introduced. ORD has given
out research grants supporting "green" applications of nanotechnology. For example, Clemson
University is working on improving the wavelength to which photocatalysts respond.
The University of Miami is developing nanoscale monitoring of marine toxins through artificial
receptor sites that glow when toxins are present. Rice University, which has been very involved
in nanotechnology research, is focusing on nanotechnology and its effects on the environment.
A recently released request for proposal is soliciting projects into the human effects of
nanoparticles.
The state of Pennsylvania is developing foresight tools to determine where future vulnerabilities
lie - and the extent to which an ecosystem might be harmed by stressors. Researchers are
looking into a system's sensitivity and adaptability, its exposure to stress, and society's valuation
of the system. Because vulnerability is something that varies over time and space, the model
used to make such assessments must be dynamic.
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For more information, the web site address is www.epa.gov/osp/efuture.htm or contact Anita
Street at EPA, phone 202/564-3626.
Comments/Questions and Answers
Q - How much money is involved in the STAR program for emerging issues?
A - It varies from year to year. It started with an open-ended RFP for $7 million, but it wasn't
successful. Last year the focus was on 13 nanotech studies for $6 million. This year it is down
to $5 million. Contact Barbara Cam to find out more.
Q - Regarding how to track Bt resistance and how it spreads to other plants, would
biofiuorescence placed on gene trackers work?
A - We are looking for signals that are not affected by background noise. We need to
distinguish between a Bt crop and a conventional crop. Once we develop a signature for pest
infestation near a Bt crop, then we could go to the field for more information. Because we look
at 20 million acres a year, we can look at the entire crop.
Pest infestation usually occurs where there is stress, which may indicate where to focus
sampling. We use a hierarchical approach with remote sensing. We are willing to have a
fraction of false positives and we can still address the problem early. What we don't want are
false negatives. What we are looking for is to address problems early on.
Q - Is there anything in the current futures program to bridge the gap between the goals of
identifying future problems and focusing the agency on preventive actions?
A - Some of the actions I have described are preventive in nature, such as toxicogenomics.
Also, at Rice University in the fall 2001 a researcher spoke on developing greener ways of doing
things using nanotechnology.
She was then working with engineers and not with public health officials, so we asked her to
build bridges between the two in order to identify human and environmental effects. This spring
her presentation was on looking at human health effects, so awareness is building.
Q - Regarding the workers who wanted a company to do gene testing. Years ago enzyme testing
for coal miners was proposed but unions were against it because they wanted management to
take the responsibility for providing protection for workers, so jobs wouldn't be endangered.
Women also don't want to be denied jobs because of concerns about being exposed to chemicals
known for fetal toxicity. How would that play out in this situation?
A - Lawsuits are voluntary acts of employees. The employees have taken it on themselves to
ask for genetic testing. Do we slip down that slope where employers use or require tests to
screen people out? A percentage of the funds in the Human Genome Project is being used to
look at such ethical, legal, and socio-economic issues.
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Wrap-Up Roundtable of Speakers
Dan Hopkins, Toxic Reduction Team Manager, U.S. EPA Region 5
The session was devoted to discussion of how EPA can improve its focus on emerging pollutants
and how researchers can put these issues on the Agency's radar screen and keep them there to
ensure that they are resolved. EPA's charge is to protect the environment and human health, so
it must respond to threats in a timely fashion. The session is intended to explore ways of
bringing good ideas to EPA decision-makers and making sure they are addressed. Questions
posed to the workshop participants included the following:
Question 1 - Processes for identifying chemicals for focus. Why is it important to address
emerging chemical issues?
Question 2 -Are there realistic opportunities to address the data gaps?
Question 3 -What would you suggest to improve the way we identify chemicals that might pose
threats?
Flip chart and discussion notes from this session can be found in Appendix D of this document.
Feedback From Environmental Journalist - An Outsider's Perceptions
Janet Raloff, Science News
Raloff is familiar with all of the topics that were discussed and has covered all of them except
for thallium. Asbestos is not an emerging pollutant, but a resurfacing one, she said. Pollutants
have been building up for decades, so Raloff would call them newly recognized concerns,
quietly coming up on the radar screen
Raloff commented that she likes to cover newly emerging issues, with risks that are still fairly
indeterminate, because she can extrapolate to everything else - can say the issue is a potential
problem for all of mankind and that it deserves everyone's attention. Once more data is
available, the issue becomes a lot more circumscribed.
She doesn't dwell on what we don't know. She focuses on the known and asks players in the
field to speculate on what new data might be and what concerns it might raise. Raloff says
science goes at a glacial pace. She can't write on scientists "mulling over possible findings." It
takes five years to get a paper out on new data, she added. Her readers want her to cut to the
chase, so she takes a snapshot of what's happening now. She uses lots of qualifiers, such as
"suggests," or "hints at." This allows her to avoid caveats.
News isn't what's expected. It's what's new, different, unexpected, or superlative. Most science
stories don't have this, so you have to find an angle for them. What is newsworthy to her is what
is newsworthy to politicians and bosses.
We worry about pollutants because they pose risk. You have to show why that is important.
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Raloff advised that to elevate managers' interest in issues, EPA staff must make thumbnail
descriptions or concerns to grab attention and compel action. Raloff had the following advice
on how one can compel people:
• Tell people what the risk is and say attention to the problem can't wait. "If you're on the
fence, no one will listen."
• Project authority and confidence to sell an idea. Say it's important with conviction.
Raloff said most federal agency people don't do this - they say they have data. She
wants - and other people want - information. Informed, knowledgeable analysis. Not
just data.
• Don't worry about data gaps. Focus on information with knowledge applied to gain
perspective and analysis.
• Be proactive by publishing a lot. This increases visibility and credibility. She advises
researchers to try to publish in first-tier, peer-reviewed journals that will be seen by the
right people.
• Contact the media to raise the issue. "We need to know about it before a paper comes
out. You can even do this for papers that aren't your own if you believe the media
should know about an issue."
• Tell reporters in one paragraph why it's important.
Raloff says she can give play and exposure to an issue in the 100 countries in which the magazine
circulates. Go to Newsweek and Time magazines, "because you are fighting against entrenched
bureaucrats for a share of money. Enlist grassroots support."
To raise concern about estrogenic effects in 1993, Theo Colborn pulled together all the research
on the topic and went on the lecture circuit. Then Theo Colborn, John Peterson Myers, and
Dianne Dumanoski wrote Our Stolen Future. This got the issue out to the public and the media.
This caused enough people to be worried that they wanted research done. EPA started throwing
money at the issue because pressure to do so came from Congress.
In less than eight years, the people who were championing this issue created a whole new area of
toxicology, even though they originally had no money. "It's a savvy approach to enlist the
media to carry an issue. You use people outside the Agency to affect the way things are done
inside the Agency," she said. Sometimes the new papers on emerging issues are coming only
from Europe.
"I can talk about the issues agency people have been told not to talk about," Raloff said. "I am
very disappointed in EPA in Washington, B.C. The gatekeepers try to keep us from talking with
researchers. It's not as big a problem outside Washington, but people are scared to talk with the
media."
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Endnotes
' T. S. Lin et al. 2001. "Thallium Concentration in Lake Trout from Lake Michigan." Bull. Environ. Contam.
Toxicology, 67, 921-925.
" James C. Ely et al. 2001. "Implications of Platinum-Group Element Accumulation along U.S. Roads from
Catalytic-Converter Attrition." Environ. Sci. Techno!., 35, 3816-3822
'" D. Cinti et al. 2002. "Platinum levels in natural and urban soils from Rome and Latium (italy): significance for
pollution by automobile catalytic converter." Sci. of the Total Env., 293, 47-57
" Ignza J. Buerge et al. 2003. "Caffeine, an anthropogenic marker of wastewater contamination of surface waters."
Environ. Sci. Technol, 37, 691-700
v Available at: http://ntp-server.niehs.nig.gov/htdocs/Chem H&S/NTP ChemS/RadianS8-08-2.html.
VI Available at: http://www.maripoinsoncenter.com/ctr/9411caffeine.html.
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APPENDIX A: AGENDA
DATE: AUGUST 11 - 14, 2003
LOCATION: REGION 5 OFFICES, CHICAGO, IL
Monday, August 11, 2003
10:00 am Registration Opens
1:00 pm Welcome: Bharat Mathur, Deputy Regional Administrator
U.S. EPA Region 5
ORD/Regional Workshops:
Paul Oilman, Assistant Administrator
Office of Research and Development
U.S. EPA Agency Science Advisor
1:20 pm Introduction to this Emerging Pollutants Workshop:
David Macarus, U.S. EPA Region 5
Regional Science Liaison to ORD
Chair, Workshop Planning Group
Moderator for the Day: Brad Schultz, U.S. EPA Region 5
1:30 pm Case Study - Triclosan: One Example of How Emerging Pollutants Come to Our
Attention: Steve Reimer, U.S. EPA Region 10
Perfluoro Octane Compounds in the Environment:
1:45 pm PFOS Toxicity Studies Christopher Lau, U.S. EPA/ORD/RTP
2:15 pm PFOA Toxicity Studies John Cicmanec, U.S. EPA/ORD/NRMRL- Cincinnati
2:40 pm Risk Information Update Jennifer Seed, U.S. EPA/OPPTS
2:55 pm Program Office Update Mary F. Dominiak, U.S. EPA/OPPTS
Questions from audience
3:10 pm Break
Toxic Chemicals Resulting From the Disposal of Electronic Equipment:
3:20 pm Potential to Leach Timothy Townsend, University of Florida
3:50 pm Combustion Issues Eric Stewart, ORD/NRMRL/RTP
4:20 pm Round Table: Timothy Townsend, Eric Stewart, Jason Swift
U.S. EPA, Region 5 RCRA Program
1. Risks quantifiable?
2. Research needs?
3. Risk management options?
4:40 pm Review of Tuesday's Program
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4:45 pm Adjourn for the day
Tuesday August 12, 2003
Brominated Flame Retardants:
8:30 am Welcome and Introduction:
Edwin (Ted) Smith, U.S. EPA/GLNPO
8:45 am Overview of BFRs:
Leif Magnuson, P2 Coordinator, U.S. EPA Region 9
Environmental Presence and Known Sources:
9:15 amHuman Health
Ron Kites, Indiana University
9:45 am Environmental
Mehran Alaee, Environment Canada
10:15 am Break
10:30 am Toxicology/Risk Analysis Status:
Linda Birnbaum, U.S. EPA/ORD/NHEERL
11:00 am Status of the VCCEP: Consultation re penta, octa, and decabromo diphenyl ethers:
Jennifer Seed, U.S. EPA/OPPT
11:05 am Introduction to Afternoon Roundtable Discussion:
Leif Magnuson, U.S. EPA Region 9
11:15 am Round Table Discussion with BFR Panel
12:15 pm Lunch
Afternoon Moderator: Michael Mikulka, U.S. EPA Region 5
1:30 pm Bisphenol A and Phthalate Esters: Potential Sources of Resin Compounds in the
Everyday Environments of Children:
Marsha Morgan, U.S. EPA/ORD/RTP/NERL
2:15 pm Radium in Oil and Gas Piping and Production Facilities:
Loren Setlow, U.S. EPA Office of Air and Radiation
2:45 pm Break
3:00 pm Exposures to Thallium and to Platinum Group Metals:
Frank Anscombe, U.S. EPA Region 5
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3:20 pm Break Out Groups Meet: Additional Suggestions on Where We Go From Here
Group A - PFOS/PFOA and BFRs
Group B - Bis-A and Phthalates
Group C - Electronics Disposal
Group D - Radium, Platinum, and Thallium
2:15pm Break Out Groups Report Out
4:45 pm Adjourn for the day
6:00 pm Meet at local restaurant for refreshments, dinner, networking & relaxed conversation.
Wednesday August 13, 2003
Moderator: Robert Pepin, U.S. EPA Region 5
8:30 am Asbestos and Related Durable Fibers: Too Ubiquitous, Too Persistent, Too Complex
to Put Health Risks to Rest?
Phillip Cook, U.S. EPA/ORD/NHEERL/Duluth, MN
9:30 am Pharmaceuticals and Personal Care Products in the Environment, Introduction and
Overview:
Christian Daughton, U.S. EPA/ORD/NERL/Las Vegas
10:15 am Break
10:30 am Environmental Monitoring for Chemicals in Waters:
Michael J. Focazio, U.S. Geological Survey
11:15 am Veterinary Pharmaceuticals: Potential Environmental Impact and Treatment
Strategies:
John Cicmanec, U.S. EPA/ORD/NRML/Cincinnati
12:00 pm Lunch
1:00 pm Assessing the Environmental Risk of Substances Under the US Food and Drug Act:
Charles Eirkson, U.S. FDA
Endocrine Disrupting Pollutants in Effluent Dominated Streams:
Moderator: Dennis Weslowski, U.S. EPA Region 5
1:45 pm A Regional Case Study of Alkyl Phenol and Ethoxylates:
Peter Howe, U.S. EPA Region 5
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2:10 pm Field Observations of the Contributions of Alkyl Phenols on Fish Endocrine
Disruption:
Cliff Rice, U.S. Department of Agriculture
Dr. Carys Mitchelmore, University of Maryland
2:40 pm Effects of Waste Water Treatment Effluents on Fish Endocrine Disruption:
Larry Barber, U.S. Geological Survey
3:10 pm Break
3:25 pm Aquatic Toxicity, Estrogenicity and Treatability of Nonyl Phenol and Ethoxylates in
Waste Water Effluents:
Charles Staples, Assessment Technologies, Inc.
3:45 pm Break Out Groups Meet:
A. Pharm and Personal Care Products
B. EDCs in streams
C. Asbestos, et. al
1. Is it reasonable to expect increased risks over time for human health and the
environment?
2. What knowledge gaps need to be filled to clarify the present and projected risks?
3. Pollution prevention/risk reduction options
4:30 pm Break Out Groups Report Out
4:45 pm Adjourn for the day — Prearranged entertainment/social event
Thursday August 14, 2003
8:30 am Objectives of the Final Session:
Dan Hopkins, Toxic Reduction Team Manager, U.S. EPA Region 5
8:40 am Biotechnology: The Promise, Potential Risks, and How Can We Find Out!
John Glaser, U.S. EPA/ORD/NRMRL - Cincinnati
9:25 am Environmental Futures: Nano Technology and Genomics Coming Over the
Horizon:
Gerardo (Pasky) Pascual, ORD/OSP Environmental Future Workgroup
10:10 am Break
10:25 am Wrap up Round Table of Speakers to Address:
Processes for identifying chemicals for focus
Are there realistic opportunities to address the data gaps?
Do we still need champions to move issues forward?
Are outside pressures necessary to move issues forward?
A-4
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop August 11-14, 2003
11:30 am Feed Back from Environmental Journalist:
Janet Raloff, Science News
How an outsider perceives these efforts:
This workshop
Action within the government agencies
A personal perspective
12:00 am Conference Closes
A-5
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop
August 11-14, 2003
APPENDIX B: LIST OF PARTICIPANTS
U.S. EPA Region/ORD Emerging Pollutants Workshop
August 11 -14, 2003
Chicago, IL
Carolyn Acheson
U.S. EPA, ORD
26 W. Martin Luther King Drive
Mail Code MS 420
Cincinnati, OH 45215
Phone: 513-821-2105
Email: Acheson.Caroly(5jepa.gov
Mehran Alaee
867 Lakeshore Road
P.O. Box 5050
Burlington, ONT CANADA L7R 4A6
Phone: 905-336-4752
Email: mehran.alaee@ec.gc.ca
Gilberto Alvarez
U.S. EPA, Region 5 OSEA
77 West Jackson Boulevard
Mail Code B-19J
Chicago, IL 60604
Phone: 312-886-6143
Email: alveraz.gilberto(5jepa.gov
Al Alwan
U.S. EPA, Region 5
77 West Jackson Boulevard
Chicago, IL 60604
Phone: 312-353-2004
Email: al.alwan(5jepa.gov
Ryan Bahr
U.S. EPA, Region 5, ARD
77 West Jackson Boulevard
Mail Code AR-18J
Chicago, IL 60604
Phone: 312-353-4366
Email: bahr.ryan(5jepa.gov
Larry Barber
U.S. Geological Survey
3215 Marine Street
Boulder, CO 80303
Phone: 303-541-3039
Email: lbbarber@usgs.gov
Jonathan Barney
U.S. EPA Region 5
77 West Jackson Boulevard
Chicago, IL 60604-3590
Phone: 312-886-6102
Email: barney.jonathan@epa.gov
Thomas Baugh
U.S. EPA Region 4
61 Forsyth Street, SW
Atlanta, GA 30303-8960
Phone: 404-562-8275
Email: Baugh.ThomasL@epa.gov
Linda Birnbaum
U.S. EPA, ORD
MD B143-01
109 T.W. Alexander Drive
Research Triangle Park, NC 27709
Phone: 919-541-2655
Email: birnbaum.linda@epa.gov
Sue Brauer
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code DW-8J
Chicago, IL 60604-3590
Phone: 312-353-6134
Email: brauer.sue@epa.gov
Bonnie Bush
U.S. EPA Region 5, ARD
77 West Jackson Boulevard
Chicago, IL 60604
Phone: 312 353-6684
Email: bush.bonnie@epa.gov
Gwen Christiansen
U.S. EPA Region 8
999 18th Street, Suite 300
8EPR-SA
Denver, CO 80211
Phone: 303-312-6463
Email: Christiansen.gwen@epa.gov
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop
August 11-14, 2003
John Cicmanec
U.S. EPA, ORD
26 W. Martin Luther King Drive
Mail Code G-75
Cincinnati, OH 45268
Phone: 513-569-7481
Email: cicmanec.john@epa.gov
Yamille Cirino
Great Lakes National Program Office, Region 5
77 West Jackson Boulevard
Chicago, IL 60604
Phone: 312-886-1437
Email: cirino.yamille@epa.gov
Stacey Coburn
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code AR-18J
Chicago, IL 60604
Phone: 312-886-2263
Email: coburn.stacey@epa.gov
Michelle Colledge
U.S. EPA Region 5
77 West Jackson Boulevard
Room 413
Chicago, IL 60626
Phone: 312-886-1462
Email: Colledge.Michelle@epa.gov
Yves Coulliard
Environment Canada
14th Floor, Place Vincent Massey
351 St. JosephB
Gatineau, QC, CANADA K1A OH3
Phone: 819-997-7588
Email: yves.coulliard@ec.gc.ca
Frances Dean
U.S. EPA Region 5
77 West Jackson Boulevard
Chicago, IL 60604
Phone: 312-886-5046
Email: Dean.frances@epa.gov
Charles Eirkson
U.S. FDA, CVM, HFV-103
7519 Standish Place
Rockville, MD 20855
Phone: 301-827-8561
Email: ceirkson@cvm.fda.gov
James Entzminger
Office of Chemical Emergency Preparedness &
Prevention
77 West Jackson Boulevard
Mail Code SC-6J
Chicago, IL 60604
Phone: 312-886-4062
Email: entzminger.james@epa.gov
Michael Focazio
U.S. Geological Survey, Office of Water Quality
12201 Sunrise Valley Drive
Reston, VA 20192
Phone: 703-648-6808
Email: mfocazio@usgs.gov
Kerry Gerard
U.S. EPA Region 5, WQB
77 West Jackson Boulevard
Mail Code WQ-16J
Chicago, IL 60604
Phone: 312-353-5791
Email: gerard.kerry@epa.gov
Stephen Goranson
U.S. EPA Region 5, OIS/RMD
77 West Jackson Boulevard
Mail Code MG-9J
Chicago, IL 60604-3507
Phone: 312-886-3445
Email: goranson.stephen@epa.gov
Neil Gray
AstraZeneca Canada Inc.
1004 Middlegate Road
Mississauga, ON L4Y1M4
Phone: 905-804-5831
Email: neil.gray@astrazeneca.com
Sandy Hellman
Great Lakes National Program Office
77 West Jackson Boulevard
Mail Code G-17J
Chicago, IL 60604
Phone: 312-353-5006
Email: hellman.sandra@epa.gov
Roland Hemmett
U.S. EPA Region 2
2890 Woodbridge Avenue
Edison, NJ 08837
Phone:732-332-6754
Email: hemmett.roland@epa.gov
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop
August 11-14, 2003
Steven Hentges
American Plastics Council
1300 Wilson Boulevard
Arlington, VA 22209
Phone:703-741-5588
Email: steve_hentges@plastics.org
Ronald Kites
Indiana University
School of Public and Environmental Affairs
SPEA410 H
Bloomington, IN 47405
Phone: 812-855-0193
Email: Hitesr@indiana.edu
Paul Horvatin
U.S. EPA, Great Lakes National Program Office
77 West Jackson Boulevard
MailCodeG-17J
Chicago, II 60604
Phone: 312-353-3612
Email: horvatin.paul@epa.gov
Melissa Hulling
U.S. EPA, Great Lakes National Program Office
77 West Jackson Boulevard
MailCodeG-17J
Chicago, II 60604
Phone: 312-886-2265
Email: hulting.melissa@epa.gov
Ariel Iglesias
U.S. EPA Region 2
2890 Woodbridge Avenue
Mail Code MS-215
Edison, NJ 08837
Phone: 732-452-6426
Email: iglesias.ariel@epa.gov
Bruce Kent
U.S. EPA, Region 8
999 18th Street, Suite 300
Denver, CO 80202
Phone: 303-312-6133
Email: kent.bruce@epa.gov
David Klauder
U.S. EPA, ORD
1200 Pennsylvania Avenue, N.W.
MailCode8104S
Washington, DC 20460
Phone: 202-564-6496
Email: klauder.david@epa.gov
Christopher Lambesis
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code DW-8J
Chicago, IL 60604
Phone: 312-886-3583
Email: lambesis.christopher@epa.gov
Edwina Lopes
Environment Canada
4905 Dufferin Street
Dowsview, ON CANADA M3H 5T4
Phone: 416 739-5863
Email: Edwina.Lopes@ec.gc.ca
Barbara Losey
Invited Stakeholder
600 Beacon Avenue
Beachwood, NJ 08722
Phone:732-557-5524
Email: blosey@regnet.com
Arthur Lubin
U.S. EPA, Region 5, OSEA
77 West Jackson Boulevard
Chicago, IL 60605
Phone: 312-886-6226
Email: lubin.Arthur@epa.gov
Dale Luecht
U.S. EPA Region 5, Water Division
77 West Jackson Boulevard
Mail Code WQ-16J
Chicago, IL 60604
Phone: 312-886-6098
Email: luecht.dale@epa.gov
David Macarus
U.S. EPA Region 5
77 West Jackson Boulevard
Chicago, IL 60604
Phone: 312-353-5814
Email: macarus.david@epa.gov
Leif Magnuson
U.S. EPA Region 9
75 Hawthorne Street
MailCodeWST-7
San Francisco, CA 94105
Phone:415-972-3286
Email: magnuson.leif@epa.gov
B-3
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop
August 11-14, 2003
Mario Mangino
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code DW-8J
Chicago, IL 60604
Phone: 312-886-2589
Email: mangino.mario@epa.gov
Simon Manoyan
U.S. EPA Region 5, Water Division
77 West Jackson Boulevard
Chicago, IL 60634
Phone: 312-353-2681
Email: manoyan.simon@epa.gov
Edward Master
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code DT-8J
Chicago, IL 60604
Phone: 312-353-5830
Email: master.edward@epa.gov
Barbara Mazur
U.S. EPA Region 5, ORD
77 West Jackson Boulevard
Chicago, IL 60137
Phone: 312-886-1491
Email: mazur.Barbara@epa.gov
Pat McCann
Minnesota Department of Health
121 East Seventh Place, Suite 220
PO Box 64975
St. Paul, MN 55164-0975
Phone: 651-215-0923
Email: patricia.mccann@health.state.mn.us
Michael Mikulka
U.S. EPA Region 5
77 West Jackson Boulevard
WPTD, ECAB, DE-9J
Chicago, IL 60604
Phone: 312-886-6760
Email: mikulka.michael@epa.gov
Marc Mills
U.S. EPA, ORD - NRMRL
26 W. Martin Luther King Drive
Cincinnati, OH 45268
Phone: 513-569-7322
Email: mills.marc@epa.gov
Susan Mooney
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code DW-8J
Chicago, IL 60604
Phone: 312-886-3585
Email: mooney.susan@epa.gov
Tammy Moore
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code DE-9J
Chicago, II 60604
Phone: 312 886 6181
Email: Moore.Tammy@epa.gov
Marsha Morgan
U.S. EPA Region 3
MD E205-04
Alexander Drive
Research Triangle Park, NC 27711
Phone: 919-541-2598
Email: morgan.marsha@epa.gov
Michael Murray
National Wildlife Federation
213 W. Liberty Street, Suite 200
Ann Arbor, MI 48104
Phone:734-769-3351
Email: murray@nwf.org
Erin Newman
U.S. EPA Region 5, ARD
77 West Jackson Boulevard
Mail Code AR-18J
Chicago, IL 60604
Phone: 312-886-4587
Email: newman.erin@epa.gov
Fardin Oliaei
Minnesota Pollution Control Agency
Environmental Outcomes Division, Lakes and Toxics
520 Lafayette Road North
St. Paul, MN 55127
Phone: 651-296-7967
Email: fardin.oliaei@pca.state.mn.us
Colleen Olsberg
U.S. EPA Region 5
77 West Jackson Boulevard
Chicago, IL 60604
Phone: 312-353-4686
Email: olsberg.colleen@epa.gov
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop
August 11-14, 2003
Neil Parke
Eli Lilly and Co.
Lilly Corporate Center
Indianapolis, IN 46285
Phone: 317-276-7201
Email: parke_neilj@lilly.com
Robert Pep in
U.S. EPA Region 5
77 West Jackson Boulevard
Chicago, IL 60604
Phone: 312-886-1505
Email: pepin.robert@epa.gov
David Petrovski
U.S. EPA Region 5, WPTD
77 West Jackson Boulevard
Mail Code DW-8J
Chicago, IL 60604
Phone: 312-886-0997
Email: petrovski.david@epa.gov
Dale Phenicie
Council of Great Lakes Industries
402 Lighthouse Lane
Peachree City, GA 30269
Phone: 770-487-7585
Email: dkphenicie@mindspring.com
Thomas Poleck
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code WQ-16J
Chicago, IL 60622
Phone: 312-886-0217
Email: poleck.thomas@epa.gov
Angela Preimesberger
Minnesota Pollution Control
520 Lafayette Road North
St. Paul, MN 55155-4194
Phone: 651-296-8723
Email: Angela.Preimesberger@state.mn.us
Pete Redmon
U.S. EPA Region 5, Water Division
77 West Jackson Boulevard
Mail Code WQ-16J
Chicago, IL 60604
Phone: 312-886-6110
Email: redmon.walter@epa.gov
Steve Reimer
U.S. EPA Region 10
7411 Beach Drive, East
Port Orchard, WA 98366
Phone: 360-871-8718
Email: reimer.steve@epa.gov
Clifford Rice
U.S. Dept. of Agriculture, Environmental Quality
Laboratory
Rm 219, Bldg. 001, BARC-W
10300 Baltimore Avenue
Beltsville, MD 20705
Phone: 301-504-6398
Email: ricec@ba.ars.usda.gov
Paul Ripple
Little River Band of Ottawa Indians
375 River Street
Manistee, MI 49660
Phone:231-723-1594
Email: pripple@lrboi.com
Vergel Santos
Great Lakes National Program Office
77 West Jackson Boulevard
Mail Code G-17J
Chicago, IL 60604
Phone: 312-353-5627
Email: santos.vergel@epa.gov
Gregory Sayles
U.S. EPA, ORD
26 W. Martin Luther King Drive
Cincinnati, OH 45268
Phone: 513-569-7607
Email: sayles.gregory@epa.gov
Brad Schultz
U.S. EPA, Region 5, OSEA
77 West Jackson Boulevard
Chicago, IL 60604
Phone: 312-353-9390
Email: schultz.brad@epa.gov
Jennifer Seed
U.S. EPA, OPPTS
1200 Pennsylvania Avenue, NW
Mail Code 7403M
Washington, DC 20460
Phone: 202-564-7634
Email: seed.jennifer@epa.gov
B-5
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop
August 11-14, 2003
Loren Setlow
U.S. EPA, Office of Radiation and Indoor Air
6608J
Washington, DC 20460
Phone: 202-564-9445
Email: setlow.loren@epa.gov
Verneta Simon
U.S. EPA Region 5
77 West Jackson Boulevard
Chicago, il 60604
Phone: 312-886-3601
Email: simon.verneta@epa.gov
Blaine Snyder
Tetra Tech, Inc.
10045 Red Run Boulevard
Suite 110
Owings Mills, MD 21117
Phone:410-356-8993
Email: Blaine.Snyder@tetratech.com
James Stahl
IDEM Office of Water Quality
P.O. Box 6015 (65-40-2jrs)
Shadeland Field Office
Indianapolis, IN 46206-6015
Phone: 317-308-3187
Email: jstahl@dem.state.in.us
Lucy Stan field
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code DW-8J
Chicago, IL 60604
Phone: 312-886-1121
Email: stanfield.lucy@epa.gov
Charles Staples
Assessment Technologies, Inc.
10201 Lee Highway, Suite 580
Fairfax, VA 22030
Phone: 703-273-2252
Email: castaple@ix.netcom.com
Jason Stow
Northern Contaminants Program, Indian &
Northern Affairs
10 Wellington Street
Gatineau, QC, CANADA K1A OH4
Phone: 819 997-0879
Email: stowj@inac.gc.ca
Maryann Suero
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code D-8J
Chicago, IL 60604
Phone: 312-886-9077
Email: suero.maryann@epa.gov
Bhooma Sundar
U.S. EPA Region 5
77 West Jackson Boulevard
Chicago, IL 60604
Phone: 312-886-1660
Email: sundar.bhooma@epa.gov
Jason Swift
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code DW-9J
Chicago, IL 60604
Phone: 312-886-0754
Email: swift.iason@epa.gov
Rae Trine
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code AE-17J
Chicago, IL 60604
Phone: 312-353-9228
Email: triae.rae@epa.gov
Robert Vashon
The Procter & Gamble Company
Sharon Woods Tech Center HB 2D45
11500 Reed Hartman Highway
Cincinnati, OH 45241
Phone: 513-626-1035
Email: vashon.rd@pg.com
Beth Walls
U.S. EPA Region 4
Sam Nunn Atlanta Federal Center
61 Forsyth Street
Atlanta, GA 30303-8960
Phone: 404-562-8309
Email: walls.beth@epa.gov
Michael Watson
U.S. EPA Region 10
1200 Sixth Avenue
OEA-095
Seattle, WA 98101
Phone:206-553-1072
Email: watson.michael@epa.gov
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop August 11-14, 2003
Michelle Walters
U.S. EPA Region 5, ATSDR
77 West Jackson Boulevard
Room 413 (ATSD-4J)
Chicago, IL 60604
Phone: 312-886-7476
Email: waiters.michellefajepa.gov
Dennis Wesolowski
U.S. EPA Region 5
536 South Clark Street
Chicago, IL 60605
Phone: 312-353-9084
Email: wesolowski.dennis(5jepa.gov
Wayne Whippie
U.S. EPA Region 5
536 South Clark Street
Mail Code ML-IOC
Chicago, IL 60605
Phone: 312-543-0661
Email: whipple.waynefaiepa.gov
Mary White
U.S. EPA Region 5
77 West Jackson Boulevard
Mailstop B-19J
Chicago, IL 60604
Phone: 312-353-5878
Email: White.mary (5jepa.gov
Daniel Wilson
The Dow Chemical Company
1803 Building
Midland, MI 48674
Phone: 989-636-0712
Email: ddwilsonfajdow.com
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop
August 11-14,2003
ADDENDUM
F.R. Anscombe
U.S. EPA
77 West Jackson Boulevard
MailCodeG-17J
Chicago, IL 60604
Phone: 312-353-0201
Email: anscombe.frank@epa.gov
Dale Bates
U.S. EPA Region 7
Regional Science and Technology Center
901 North 5th Street
Kansas City, KS 66101
Phone: 913-551-5091
Email: bates.dale@epa.gov
Mark Burrows
IJC-Great Lakes Regional Office
P.O. Box 32869
Phone: 313-226-2170
Email: burrowsm@windsor.ijc.org
Alva Daniels
U.S. EPA, ORD
26 W. Martin Luther King Drive
Cincinnati, OH 45268
Phone: 513-569-7693
Email: daniels.alva@epa.gov
Jon Dettling
Great Lakes Commission
2805 S. Industrial Highway, Suite 100
Ann Arbor, MI 48104
Phone:734-971-9135
Email: dettling@glc.org
Wayne Garfinkel
U.S. EPA Region 4
61 Forsyth Street
Atlanta, GA 30303
Phone: 404-562-8982
Email: Garfinkel.Wayne@epa.gov
Roger Gauthier
Great Lakes Commission
2805 S. Industrial Highway, Suite 100
Ann Arbor, MI 48104
Phone:734-971-9135
Email: gauthier@glc.org
Christopher Lau
U.S. EPA, ORD/NHEERL
Mail Drop 67
Research Triangle Park, NC 27711
Phone: 919-541-5097
Email: lau.christopher@epa.gov
John Morris
U.S. EPA Region 5, CRL
536 South Clark Street
Chicago, IL 60605-1509
Phone: 312-353-3594
Email: morris.iohn@epa.gov
Christopher Newman
U.S. EPA Region 5
77 West Jackson Boulevard
Mail Code DW-8J
Chicago, IL 60604
Phone: 312-353-9402
Email: newman.christopher@epa.gov
Kimberly Null
U.S. EPA Central Regional Laboratory
536 South Clark Street
Chicago, IL 60605
Phone: 312-353-8362
Email: Null.Kimberly@epamail.epa.gov
Edward Nowak
Johnson & Johnson Pharmaceutical
Research and Development
1000 Rout 202 South
RoomOMPE109M
Raritan, NH 08869
Phone: 908-927-3235
Email: enowak@prdus.inj.com
Peter Philbrook
U.S. EPA Region 1
11 Technology Drive
North Chelmsford, MA 01863
Phone: 617-918-8602
Email: philbrook.peter@epa.gov
E. Marie Phillips
U.S. EPA Region 5 GLNPO
77 West Jackson Boulevard
Chicago, IL 60604
Phone: 312-886-6034
Email: phillips.emarie@epa.gov
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop August 11-14, 2003
Phil Sayre
OA Science Advisory Board
(Mail Code 1400A), Suite 6450-R
1200 Pennsylvania Avenue, NW
Washington, DC 20460
Phone: 202-564-7673
Email: sayre.philfajepa.gov
Ted Smith
Great Lakes National Program Office
77 West Jackson Boulevard
MailCodeG-17J
Chicago, IL 60604
Phone: 312-353-6571
Email: smith, edwinfajepa.go v
Hilary Snook
U.S. EPA Region 1
11 Technology Drive
North Chelmsford, MA 01863
Phone: 617-978-8670
Email: snook.hilaryfaiepa.gov
Noel Vargas
U.S. EPA Region 5, Air and Radiation
77 West Jackson Boulevard
Mail Code AE-17J
Chicago, IL 60625
Phone: 312-353-3575
Email: vargas.noelffljepa.gov
Els Weeg-Aerssens
The Health & Environmental Safety
Alliance, Inc.
442 Oliver Road
Cincinnati, OH 45215
Phone: 513-821-0518
Email: eweegfajcinci.rr.com
Kevin Yam
Great Lakes Commission
2805 S. Industrial Highway, Suite 100
Ann Arbor, MI 48104
Phone:734-971-9135
Email: kyam@glc.org
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop
August 11 -14, 2003
APPENDIX C: SLIDES FROM PRESENTATIONS
These slides can be found at: www.epa.gov/osp/regions/emerpoll.htm
Triclosan: One Example of How Emerging Pollutants
Come to Our Attention
Perfluoro Octane Compounds in the Environment
PFOS Toxicity Studies
Studies of Human and Animal Toxicity
Risk Information Update: Overview of Assessment and
Activities of PFOS and PFOA
PFOS and PFOA Program Office Update
Toxic Chemicals Resulting From the Disposal of Electronic Equipment
Examining the Pollution Potential of Discarded Electronic
Equipment Disposal
Emissions from the Incineration of Electronics Industry
Waste
Toxic Chemicals Resulting From the Disposal of Electronic
Equipment
Brominated Flame Retardants
Overview of Brominated Flame Retardants
Polybrominated Diphenyl Ethers in People
Brominated Flame Retardants in the Environment
Brominated Flame Retardants: Toxicology and Risk
Bisphenol A and Phthalate Esters: Potential Sources of
Resin Components in the Everyday Environments of
Preschool Children
Radium in Oil and Gas Piping and Production Facilities
Balanced Perspectives Regarding Environmental
Levels of Thallium and Platinum Group Metals
Asbestos and Related Durable Fibers: Too Ubiquitous,
Too Persistent, Too Complex to Put Health Risks to Rest?
Steve Reimer
Christopher Lau
John Cicmanec
Jennifer Seed
Mary F. Dominiak
Timothy Townsend
Eric Stewart
Jason Swift
Leif Magnuson
Ron Kites
Mehran Alaee
Linda Birnbaum
Marsha Morgan
Loren Setlow
Frank Anscombe
Phillip Cook
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop
August 11 -14, 2003
Pharmaceuticals and Personal Care Products in the Environment
Pharmaceuticals and Personal Care Products as Environmental
Pollutants: Pollution from Personal Actions
Veterinary Pharmaceuticals: Potential Environmental
Impact and Treatment Strategies
Environmental Assessments - Human and Animal Drugs
Endocrine Disrupting Pollutants in Effluent Dominated Streams
A Regional Case Study of Alkylphenol and Ethoxylates
Field Observations of the Contributions of Alkyphenols on
Fish Endocrine Disruption
Effects of Waste Water Treatment Effluents on
Fish Endocrine Disruption
Aquatic Toxicity, Estrogenicity, and Treatability of
Nonyl Phenol and Ethoxylates in Waste Water Effluents
Biotechnology: A New Frontier
The Promise, Potential Risks, and How Can We Find Out?
Environmental Futures: Nano Technology and Genomics
Coming Over the Horizon
Christian Daughton
John Cicmanec
Charles E. Eirkson III
Peter Howe
Cliff Rice
Carys Mitchelmore
Larry Barber
Charles Staples
John A. Glaser
Gerardo (Pasky) Pascual
C-2
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop August 11 - 14, 2003
APPENDIX D: FLIP CHART NOTES
The following information reflects two types of information developed during breakout sessions: flip
chart notes - which, in some cases, were rather abbreviated; and other points made by discussion
participants regarding the topics in question.
As a general matter, the breakout group participants were tasked with answering the following questions
about each emerging pollutant/issue being discussed:
1. Is it reasonable to expect increased risks over time for human health and the environment?
2. What knowledge gaps need to be filled to clarify the present and projected risks?
3. Are there pollution prevention/risk reduction options?
Break Out Sessions - Tuesday, August 12
BFRs and Electronic Equipment
Participants of this break out session gave a run down on how they would apportion $100 if this amount
were to be spent on researching these two topic areas:
Responses
SOURCES
Where the chemical is manufactured $7
FATE
Where it is found in the environment $ 11
TRANSPORT
How it is getting from the manufacturer, $13
products and wastes to the environment
and, movement through the environment
EXPOSURE PATHWAYS
How it is getting from product or the $23
environment into the biota
EFFECTS
What are the effects on humans, animals $30
RISK MANAGEMENT
How to prevent release and exposure $15
Other comments:
The above priorities from the Regions will help the Agency begin setting agendas for research, if not
specific funding levels. It is important also that EPA not do all the research or fund all of it, but the
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Region/ORD Emerging Pollutants Workshop August 11 - 14, 2003
Agency should know Regional priorities. Regions represented at the workshop include Regions 2, 4, 5,
and 9.
Regions can get involved in the ORD process and help raise ORD 's voice. However, dollars for research
at U.S. EPA will have to be taken from other programs as there is little new money available. A number
of channels already exist for possible funding for research on BFRs and electronic devices:
• RARE program funded at $200,000/year for each region or a total of $2 million annually
• STAR program funded at $5 million/year
• NHANES-Add BFRs by December 2004
• Pollution Prevention Programs alternatives analysis, funded at $140,000/year per region
• GLNPO emerging issues program funded at $150,000/year
• GLAD (ARD R5) funded at $1.2 million/year for air deposition studies
• Program Offices funding and priorities
• Office of Solid Waste product stewardship for electronics
• Office of Children's Health programs
• Champions in program areas like TSCA under OPPT (BFRs not listed as PBT or BNS substance)
• Water Division's IRIS program
• Research Coordination Teams: Endocrine Disruption Team, Multimedia Team, B. Walls R4
Paper
• ORD Multi-Year Plans (for 2006 budget cycle); recognize regional priorities
• Agency Strategic Plan - all regions work together to identify top three common research
priorities
• "Short-Circuit" Process: Get priorities to Deputy Regional Administrator level, then to Oilman
• Health Canada 2-gen study
• Partner with CDC, OSHA, NIHS, other outside agencies
• USDA dietary surveys; market basket surveys to get data on food other than fish.
More research is needed on indoor air quality in houses and house dust. The VCCEP documents food
and dust, but there is no consideration of effects. There are people with high-end concentrations, but an
exposure study is needed to determine why; perhaps the source is fatty animal food.
BFR composition in foam is 1-10%, but it is not known if the BFRs crumble out of the foam. Research is
needed on the BFR content in foam and how much is released. There isn't much released from chemical
manufacturers, but what about foam and furniture manufacturers? Priorities must be expressed to the
Deputy Regional Administrator. Non-governmental organizations are good allies.
States need to know what to communicate to the public about this issue as a health risk. Is BFR in fish
the number one route of exposure? States need to move forward and look at BFR prevalence and what
risk that may pose to the population. However, it is hard to assess risks without much information. There
are no human studies, only animal studies to date.
States also would like to have fish advisories for BFRs. If states push their needs, EPA might fund the
research. Analytical methods for emerging pollutants must be standardized and cost-effectiveness
examined. Health Canada is screening 23,000 substances, including BFRs.
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Region/ORD Emerging Pollutants Workshop August 11 - 14, 2003
Radium, Thallium, Platinum, and Other Metals
Question 1 - Is it reasonable to expect increased risks over time for human health and the environment?
Yes. We expect the risk from TENORM to go up because of the recycling of property and materials and
making new products out of materials that have radium in them (e.g., coal ash used to make wall board).
Also, as oil wells age, they have lower yields of oil and more water is generated. This can produce more
radium in the pipe scale. In regard to platinum, because its use is increasing, there may be more human
and environmental exposures - though we don't know the effects. Unsure as to whether thallium will
pose more of a risk - but we wonder if some concerns about mercury poisoning actually involve thallium.
Additionally, there are new metals being developed through nanotechnology involving combining rare
earth metals with organic molecules, some of which can cross the blood-brain barrier. This could lead to
additional risk. More research is needed to better quantify future risk.
Question 2 - What knowledge gaps need to be filled to clarify the present and projected risks?
Need to know more about "legacy" TENORM sites.
What is the fate of the radium in oil when descaling products are used? Is it simply moving the
TENORM problem down the pipe to the refineries?
What is the chronic toxicity of some of these metals?
Also need to work on method development for laboratories. The levels of thallium and platinum are so
low good laboratory analysis needs to be done.
Question 3 - Pollution prevention/risk reduction options?
In regard to TENORM, have to get information out to EPA people who are working at legacy sites (on-
site people), on how you measure it and what you need to do if you find it.
Get information out to "ma and pa" oil and natural gas businesses to make them aware of the TENORM
problem. Put information on radium in oil in the Oil Pollution Act of 1990 web site so that others in the
industry will also know about it (including the Coast Guard).
Develop a GIS of legacy sites so that developers can be made aware of potential problems before they
build houses on old, contaminated sites.
PFOS/PFOA
Question 1 - Is it reasonable to expect increased risks over time for human health and the environment?
We know that PFOS/PFOA is in the blood, so there is a concern about risk. We also know it is in
children, and that it lasts in the body for a long time. But since PFOS is no longer being made in the U.S.,
don't know about future risk.
Question 2 - What knowledge gaps need to be filled to clarify the present and projected risks?
Need to figure out how the timing of the dose may determines effects. What is the mechanism that makes
it lethal?
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Need to look more closely at the effects data so they can extrapolate better.
Because effects on the lungs of mice were seen, is there a link between PFOS exposure and childhood
asthma?
Have CDC include PFOS/PFOA in NHANES to monitor what is happening with this chemical.
Question 3 - Pollution prevention/risk reduction options?
More research to understand mechanisms by which it causes effects.
Bisphenol A and Phthalate Esters
Check current data on web site - synthesize data to find data gaps.
After review of data, determine chronic and acute toxicity.
Emerging data.
CDC review.
Recommend further study on exposure of humans and the environment and on endocrine disruption.
Break Out Sessions - Wednesday August 13
EDC and Effluent Dominated Streams
Question 1 - Is it reasonable to expect increased risks over time for human health and the environment?
Looked at NP and hormones. Is risk increasing? APEs production is stable and/or is being phased out.
Also looked at whether WWTP performance will increase or decrease in effectiveness over time. Believe
that removals will be going down as excess capacity is removed, because the water will be retained for
shorter periods of time. Additionally, a large number of modern plants are 20 to 30 years old and are
coming to the end of their lives.
Question 2 - What knowledge gaps need to be filled to clarify the present and projected risks?
APEs and hormones - need to understand fate of hormones when they leave WWTP. Are effects
significant?
Some hormones enter WWTPs as conjugated, others do not. When they are deconjugated, they become
biologically active. What happens?
What happens to NP and carboxylated compounds when they degrade? Do carboxylated compounds go
into anaerobic zones where they can become NP?
Need to understand the effects of combined sewage overflows on effluent dominated streams.
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What is the long-term fate of NPs and hormones in the sediments near WWTP outfalls?
Did not address pollution prevention for this topic.
Asbestos and Durable Fibers
Question 1 - Is it reasonable to expect increased risks over time for human health and the environment?
Scope of what is asbestos and asbestos-like fibers?
Risk could increase because:
Long latency period. Disease doesn't appear until 30, 40, or 50 years after exposure.
Incidence of disease is increasing.
What exposures are going on now?
Products are still out there.
Natural asbestos in the soils means that exposure to the general population may increase.
Risk may not increase because:
In the 40s, working conditions were different. Different products, vacuums, etc. Great reductions of
exposure in occupational settings.
Other observations:
Different analytical schemes for Libby, Montana and the World Trade Center.
Do not rule out certain fiber sizes. Short, thin fibers are strongly connected to tumors. Will not agree that
different types of fibers are different in regard to effects.
Question 2 - What knowledge gaps need to be filled to clarify the present and projected risks?
Premise of risk - where risk comes from. Ideas about asbestos are based on old data. Need to reassess
the role of fiber size.
Measure relative potency of different sizes and times. Refine methods for evaluating different fibers
(relative potency factor).
Model what a person would accumulate in the lungs and then base evaluation on that.
Exposures are always a mixture.
Question 3 - Pollution prevention/risk reduction options?
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What characteristics of fibers make them hazardous? We don't want to replicate the hazard of asbestos
with other materials. Use our knowledge of which fibers cause disease to point out sizes and shapes that
would not mimic asbestos.
Nanofibers are not into full-scale production yet. This is the optimum chance to prevent production of
nanofibers than could be harmful.
Where we have mineral fiber dust that bears similarities to asbestos fibers, we should be very careful.
Pha rm aceuticals
These contaminants could be broken up into categories: hormonal, antibiotics, and highly chemically
reactive for discussion purposes. However, audience members decided that their answers to all three
questions applied equally to all three categories.
Question 1 - Is it reasonable to expect increased risks over time for human health and the environment?
Yes, risks will increase due to the aging population's needs for medications, and perhaps to the growing
uses of growth hormones in children. There are no controls on disposal for existing drugs. People are
told to flush old medications down the toilet. Doctors and pharmacists must be educated and regulations
established to prohibit this practice, which immediately transports myriad compounds to wastewater
treatment plants.
Other choices for disposal include solid waste landfills, incineration, or recycling. Health care workers,
industry, and the public must also be made aware of disposal concerns. The FDA does not regulate
Pharmaceuticals after their manufacture, but they do perform environmental impact analysis for animal
drugs.
Question 2 - What knowledge gaps need to be filled to clarify the present and projected risks?
There are many gaps in data and knowledge for pharmaceuticals. Researchers need to determine what the
degradation products are, and all of them must be part of any analysis. It must be determined whether
there are additive compounds being formed, and the risk of all possible chemical interactions must be
assessed. There is a data gap in regard to exposure data, i.e., what are the relevant exposures?
There is a need to define what constitutes a harmful amount of each compound as well as for all of them
together. Detailed information on product constituents is needed. Some components of products may not
be "inert" as listed on product labels. All applications of a product must be determined as well as whether
anti-microbial resistance in the field translates to humans.
Personal Care Products
Time was limited for this discussion. Researchers have hardly begun to address the problem.
Terminology can be a problem. Personal care products are those that are placed in contact with or on the
human body, according to industry representatives. Lotions, cosmetics, and perfumes fit into this
category. Home care products include soaps and detergents.
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Effects of personal care products may be greater because they are placed directly on the body. Some are
meant to be chemically interactive. There is a chemical ingredient review process by the FDA under the
Food, Drug and Cosmetics Act, which regulates products. A toxics profile is produced by the FDA. For
fragrances there is a toxics profile developed by RIFM, an industry group, with the FDA having
oversight.
Final Group Discussion - Thursday August 14
This final group discussion was held at the end of the scientific presentations. The following information
was recorded on flip charts and through other note-taking of participants' comments. Questions posed to
participants were as follows:
1. Processes for identifying chemicals for focus. Why is it important to address emerging
chemical issues?
2. Are there realistic opportunities to address the data gaps?
3. What would you suggest to improve the way we identify chemicals that might pose threats?
Question 1 - Processes for identifying chemicals for focus. Why is it important to address emerging
chemical issues?
There is always competition for the interest and resources necessary to get emerging issues addressed.
Preventive action is important to prevent human and environmental impact and is always better than
contingent action. It is faster, cheaper, and smarter. Unfortunately, it often takes a crisis to generate the
political will to dedicate resources to a problem.
The Agency's future lies in getting ahead of problems rather than merely reacting to them.
Rachel Carson's Silent Spring proposed alternatives to pesticides. This is important- you don't just want
to criticize. EPA needs to also pose alternatives. Several of the presentations that were given during the
workshop mentioned alternatives. This is good.
Agrees that it is important to be proactive. The radium issue is already spreading and the levels are the
highest seen in 20 years. This is a big problem. The Superfund group does inspections and was asked to
come to the workshop, but no one attended.
Asbestos is an example of an issue we thought was closed, but it isn't. It was addressed when the issue
was hot, and then EPA moved on to other things. It's still an issue.
Nanotechnology brings a ray of hope as a model for preventive action. We need to look at asbestos and
make sure that with nanotechnology, we are creating products that will prevent the problems we've had
with asbestos. Legacy pollutants have a long latency period and are problems for decades. You want to
prevent them.
EPA's futures group has only five staff members. More are needed to raise emerging pollutant issues.
We also need to look at more networking and look to ORD to help with future issues. Extrapolate from
other information to move issues forward. Policy staff should be linked with research staff.
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Scientists don't want to be too speculative, but they need to do something to be able to exchange
information on things they have found that need to be looked at further, without looking like alarmists.
ORD should be proactive in helping EPA staff network and share ideas and solutions. A cross-
department committee could assist in looking at possibilities without seeming alarmist.
An issue that is frustrating is the reluctance of EPA to apply the "precautionary principle" appropriately.
Don't just ban chemicals when little is known about them, but if you do know something and it's negative
- maybe this is a road we don't want to go down. Look at the signals. Europe and Canada have moved
ahead of the U.S. in this regard. If we look at a chemical and see it's persistent, then maybe this should
be a warning. We aren't listening to the signals.
We haven't applied what we've learned. Issues aren't resolved. PCBs, asbestos, mercury - we haven't
completed these things. We need a straight-forward approach that carries through to an endpoint. We
found that when we began looking for PCBs and mercury that they were all over the place. We need to
push the knowledge forward, finish projects, and get the information out.
Smart people have to stay on jobs and finish them. We should not get distracted with the "crisis
chemical" of the moment. Research was done on asbestos in the 1980s and preserved on magnetic tape,
but then abandoned and never used. If we have to address something else in the short term, "park" the
data and come back to it. Don't just abandon it.
There is a need to have a structure for addressing emerging pollutants. Europe and Canada both have
structures. They looked cumbersome initially, but they work. They set priorities, achieve their goals, and
move on. There are a lot of stakeholders involved in Canada and Europe.
The Europeans are six years ahead of us in regard to brominated flame retardants.
Partner with Europe and Canada to combine processes. This would put us much further down the road.
There is a need to link the policy folks with the research folks. Need to enlist OPPT in this.
EPA should function as one Agency, not groups of individuals competing with each other for money.
We had a national lake study going on and we looked at sites that we thought were important, but the
studies were designed by people who didn't know about the work and included testing for pollutants we
decided weren't there. OPPT required that we test for these things that they knew weren't there. We
didn't take advantage of the knowledge we have.
Researchers need to know ecological thresholds and whether pollutants are heading toward concentrations
that would cause an ecological collapse and not just rely on old linear trends.
Care must be taken when talking about thresholds so people won't think that there is a point below which
there is no problem. Lead in humans is a classic example. We have to look at distributions within
populations, not just thresholds.
An internal EPA forum or seminar could be designed to engage outside researchers and industry
representatives to broaden the knowledge base. They would not have the burden of program ownership
and could take information to EPA managers who aren't involved in specific programs.
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U.S. Environmental Protection Agency
Region/ORD Emerging Pollutants Workshop August 11 - 14, 2003
Enlisting assistance and information from outsiders is important, but care must be taken not to
disenfranchise EPA staff who need to be empowered, supported, and involved.
(Comment by an industry representative) When working on an issue with EPA, she ends up talking with
people in the agency about others in the Agency who may have information they didn't know about.
EPA needs a network of some sort for passing information around internally.
Question 2: Are there realistic opportunities to address the data gaps?
There may be realistic authorities and programs that could be tapped for resources to do research, such as
the following:
• TSCA Section 5: Chemicals to be introduced into commerce.
• TSCA Section 8: Chemicals already in commerce, but industry must notice a problem
• HPVC Program: High production volume chemicals - screening data.
• VCCEP: Chemicals that may pose risk to children - 35 companies, 10 consortia sponsor 20
chemicals.
• Monitoring Programs: State and federal levels.
• Academic Studies
• Other Federal Agency/Department Efforts
How can EPA start looking ahead to identify emerging areas of pollution and science and then get them
to "stick" to the radar screen so they don't fall off?
Start a valid, objective, well-defined monitoring program and devote about 15% of the Agency's budget
to it. EPA has been driven out of monitoring by politicians so we don't know what some conditions
really are.
Cut back on spending time researching pollutants we already know are there. Look for unidentified peaks
in analytical results and put more effort into identifying emerging pollution.
Labs should be involved from the beginning when developing testing programs. We need to have
methodologies and know what we are looking for and how to quantify the results. The chemists need to
be involved so they know what methods need to be developed.
Have tried to put together an emerging pollutants monitoring program, but haven't had any luck.
Have had the experience of finding negative data that weren't used.
TSCA can be used to ban chemicals, but some chemicals, such as dioxins, aren't manufactured as a
product. They are by-products.
Have any chemicals gone through TSCA and been approved, then found later to be harmful, or was most
of the bad stuff we are concerned with made before TSCA?
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Believes that TSCA has cut down on the manufacture of harmful chemicals because companies know
they will never be allowed under TSCA, so they don't develop them further.
Under section 8 of TSCA, EPA has gone after certain chemicals. At that time, they didn't realize that
BFRs were an environmental problem.
There is a trend away from Section 8 to voluntary actions. Industry likes to work in dialogue groups and
work with the Agency so research is done, but industry provides funds to accomplish it.
Question 3 - What would you suggest to improve the way we identify chemicals that might pose threats?
Champions may need to promote issues to gain EPA attention, but that may not be the most proactive role
for the Agency to identify concerns.
The multimedia pollution prevention forum is one way to bring an emerging issue to management's
attention, but they tried to do this with BFRs and the managers weren't interested.
OEI could catalogue information management issues, but may need outside people in an ombudsman role
to assure the Agency that there is a constituency that cares about an issue. Bosses often want to know
"who cares?" Have people from outside come in with issues and show why there is interest.
OEI could help develop a computer list serve in the Agency to help scientists and policy makers share
information on emerging issues. Every six months or so, OEI could ask participants what they believe the
priorities should be. This will help get around some of the isolation of researchers so they can see that
others may be working on similar projects.
"Who cares" is an important issue. Multimedia issues are a problem because the program offices have
louder voices. The Regions can have a lot of issues but they don't bubble up to ORD planning. We need
to get more people involved from the Regions in planning. At this point, only one representative from the
Regions participates, so not all interests can possibly be represented.
(Comment from an Environment Canada participant) NAFTA may provide a mechanism for dialogue that
EPA could use.
The International Transport of Air Pollutants (ITAP) gets top management to call people together on
issues.
Someone needs to develop a structure that can be used to raise issues. Challenges anyone who has good
ideas to put them out there and get others involved. Get support and get it going.
Interest generated across the Agency will generate funding.
Some emerging issues are not associated with chemicals, e.g., wetlands quality or legal issues. We're not
just dealing with scientific issues.
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Region/ORD Emerging Pollutants Workshop August 11 -14, 2003
APPENDIX E: PARTICIPANT EVALUATION SUMMARY
Twenty-one written workshop evaluation forms were received at the close of the workshop, containing
variable amounts of feedback. Meeting participants agreed that the Emerging Pollutants Workshop was a
valuable opportunity to gain new information and insights about emerging issues, make valuable contacts,
and exchange perspectives.
All responding participants rated the workshop either as "good" or "excellent" and most offered similar
ratings for the major workshop components (Opening Welcome, Roundtable Discussions, and Closing
Session), though about half (9 of 20) rated the Breakout Sessions as only "fair" and two rated them
"poor." Accompanying written comments suggested that more structure (e.g., a designated moderator)
and a more precise discussion question would have improved the effectiveness of these sessions. Five
participants similarly rated the Roundtable Discussions either as "fair" or "poor." Regarding workshop
accommodations and logistics, responding participants rated all categories (Meeting Materials,
Registration Process, Hotel Accommodations, Helpfulness of Meeting Staff, and Meeting Room) as
"good" or "excellent" with the exception of three individual "fair"ratings. Ratings were generally split
fairly evenly between "good" and "excellent" for all five categories. Comments suggested that a more
moderate room temperature and more legible handouts would improve the quality of future workshops.
Substantively, the information provided on brominated flame retardants (BFRs) was viewed by many (9
of 21) participants as the most valuable, and anumber of respondents stated that EPA needs to develop a
strategy for addressing concerns raised by BFR production and use. Several others made favorable
comments about the value provided by the presentation on asbestos. Many other topics were singled out
as being of particular value by individual workshop participants. Some respondents made particular note
of the value provided by being able to better understand the state of existing Agency science regarding
emerging pollutant issues, and the process by which specific issues are elevated within EPA. Others
expressed the view that emerging pollutants should be a top Agency priority, and be examined on a
continuing basis.
Many participants expressed appreciation for the opportunity to engage in dialog with Agency peers and
counterparts on important emerging pollutant issues, and numerous suggestions were offered that this
type of dialog be either continued or even instituted as a formal ORD process. Several respondents also
appreciated the participation of people from outside EPA, and suggested that external stakeholders be
included in future Agency dialog on emerging pollutant issues. Many respondents also suggested one or
more mechanisms by which ongoing communication could/should be fostered among workshop
participants and their respective organizations. Specific examples included the following: annual or semi-
annual conferences and/or teleconferences, maintaining list-serves, publishing a newsletter, and
supporting various approaches to less formal networking.
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