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Ro b e r t A . Bil o t t (513) 357-9638
bilott@taftlaw.com
February 3,2003
TELECOPY AND CERTIFIED MAIL
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7002 0860 0006 6119 4507 Dr. Charles M. Auer Chemical Control Division Office of Prevention, Pesticides and Toxic Substances U.S. Environmental Protection Agency 1201 Constitution Avenue, N.W. Mail Code 7405M Washington, DC 20004
7002 0860 0006 6119 4514
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Oscar Hernandez
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Director, Risk Assessment Division
Office of Prevention, Pesticides and Toxic
Substances
U.S. Environmental Protection Agency
1201 Constitution Avenue, N.W.
Mail Code 7405M
Washington, DC 20004
7002 0860 0006 6119 4521 Jennifer Seed U.S. Environmental Protection Agency 410 M Street, S.W. Washington, DC 20460
7002 0860 0006 6119 4552 John Wheeler, Ph.D. (3WC11) U.S. Environmental Protection Agency 1650 Arch Street Philadelphia, PA 19103-2029
7002 0860 0006 6119 4545 Christopher Jones, Esq. Director Ohio Environmental Protection Agency 122 South Front Street Columbus, OH 43215
7002 0860 0006 6119 4583 Thomas V. Skinner Regional Administrator U.S. Environmental Protection Agency 77 West Jackson Blvd. Chicago, IL 60604
7002 0860 0006 6119 4576 Donald S. Welsh Regional Administrator U.S. Environmental Protection Agency Region III 1650 Arch Street Philadelphia, PA 19103-2029
Re: Notification Of Human Health Threat Arising From Releases Of PFOA/APFO/C-8 In West Virginia And Ohio_______________
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February 3, 2003 Page 2
Ladies and Gentlemen:
Our law firm serves as class counsel for all persons whose drinking water is or has been contaminated with ammonium perfluorooctanoate (PFOA/APFO/C-8) attributable to releases from E.I. duPont de Nemours and Company's ("DuPont's") Washington Works Plant in Wood County, West Virginia. Based upon data collected to date by both DuPont and the State of West Virginia's Department for Environmental Protection ("WVDEP"), we understand that there are currently tens of thousands of individuals living in both Ohio and West Virginia whose drinking water is contaminated with C-8 from DuPont's Washington Works Plant. We write on behalf of that Class to bring to your attention what we believe may be an imminent and substantial threat to the health of the Class members arising from their past, current, and on-going exposure to such C-8 in their air, drinking water, and possibly other media.
We understand that USEPA requested in September of 2002 a priority review of the human health risks associated with C-8 exposure, after reviewing the results of recent C-8 toxicology studies and human blood data from industry. More specifically, we understand that, upon review of blood sampling data indicating the presence of PFOA in blood of the general U.S. population at an average level of approximately 3 parts per billion and the results of a 6-month primate study and 2-generation rat reproduction study recently completed by industry, USEPA concluded that "toxicological studies in rodents and primates have shown that exposure to PFOA can result in a variety of effects including developmental/reproductive toxicity, liver toxicity and cancer," that "blood monitoring data suggested widespread exposure to the general population, albeit at low levels," and that "human blood monitoring data, coupled with what is currently understood about the hazards of PFOA is sufficient from EPA's perspective to generate concern about potential PFOA risks." In response, USEPA's OPPT ordered a "priority review . . . to determine the significance of the risks presented by PFOA and its salts" because of the "possibility that PFOA might meet the criteria for action under Section 4(f) of the Toxic Substances Control Act." {Id.) Section 4(f) of TSCA is the section that authorizes USEPA to undertake a risk review when the Agency receives information "which indicates . . . that there may be a reasonable basis to conclude that a chemical or substance or mixture presents or will present a significant risk of serious or widespread harm to human beings from cancer, gene mutations, or birth defects." 15 U.S.C. 2603(f). In addition, we understand that the Science Advisory Board is to perform a peer review of a draft risk assessment for PFOA prepared but not yet released by USEPA. Thus, we understand that USEPA's interpretation of the existing human exposure and toxicological data for PFOA was sufficient to raise concerns with respect to the potential health risks posed to the general U.S. population that may have PFOA in their blood at an average level of approximately 3 parts per billion.
With these health risk issues in mind, we believe that we have a responsibility to bring to your attention information we reviewed from DuPont relating to the level of PFOA exposure in the communities surrounding DuPont's Washington Works Plant that, according to DuPont's
X
February 3, 2003 Page 3
data, may be approximately a thousand times higher than the general population exposure levels that initially triggered USEPA's concerns.
More specifically, we understand that DuPont performed internal PFOA kinetics/pharmicokinetics research that resulted in the development of a model during the Summer of 2000 to relate C-8 exposure levels to human blood levels. {See Exhibit A (DuPont Abstract # 19) - DuPont continued working with that data to generate by October of 2001, a draft, simple "compartmental model" to relate C-8 exposures through air and drinking water to estimates of perfluorooctanoate (PFO) concentrations in human blood. (See Exhibit B) The creation of that model enabled DuPont to develop a table from which estimated PFO levels in human blood can be determined from known C-8 exposure levels in air and drinking water. {See id (Table 1))
Sampling and modeling performed to date by both DuPont and WVDEP confirm levels of C-8 over 4 ppb in the drinking water provided to at least one of the communities (with approximately 12,000 water customers) adjacent to DuPont's Washington Works Plant, and confirm annual average levels of C-8 in community air (based on DuPont's Year 2000 emissions) as high as 1 ug/m3. (Exhibits C and D) The Ohio Environmental Protection Agency recently confirmed that its own air modeling and analysis revealed predicted eight-hour ambient concentration of C-8 "well above the ACGUT health based work place standard [of 10 ug/m3] at multiple receptors in Ohio" that "raise our level of concern with regards to short term exposures to workers and sensitive populations." (Exhibit E) According to DuPont's PFOA blood model and related exposure table, such exposure levels would be expected to result in concentrations of PFO in the blood of those exposed at several thousand parts per billion. In fact, we understand that, according to DuPont's own PFOA blood model, some of the communities receiving the highest levels of C-8 in their drinking water and air would be expected to have levels of C-8 in their blood in concentrations that are approximately double the average levels of C-8 found in the DuPont employees working directly with C-8 at the Washington Works Plant (reported by DuPont to be an average of 1530 ppb in 2000). {See Exhibit F) As indicated in the attached report from David Gray, Ph.D., of Sciences International, such levels of exposure are of particular concern, given that the C-8 exposure in these communities is estimated by DuPont's model to result in C-8 blood concentrations well above the C-8 blood levels that caused renal and developmental toxicity in female rats. {See Exhibit I) Moreover, these affected local
- As a defendant in a class action lawsuit pending against DuPont in a West Virginia State Court, DuPont has the right to mark documents produced in that case as "confidential" under the terms of a Stipulated Protective Order that allows parties to limit distribution of documents, if they qualify as documents for which "confidential business information" (CBI), protection would be available under, among other provisions, 40 C.F.R. Part 2, Subpart B. DuPont did not mark the attached documents from its files as "confidential" under the terms of the Stipulated Protective Order.
February 3, 2003 Page 4
communities include numerous sensitive sub-populations, such as the elderly, pregnant women, and infants that are not found among the DuPont "healthy," predominantly adult male workers.
To put this exposure data into perspective, it should be noted that, as far back as 1987, DuPont told its own employees at the Washington Works plant that an "acceptable level" of C-8 in blood was 500 ppb and that employees with more than 50% of this "acceptable level" (250 ppb) should be removed from further exposure. (See Exhibits G and H) Although DuPont's modeling indicates that the local community is likely to have C-8 in their blood at levels more than 8-16 times higher than DuPont's 250 ppb "acceptable" level, we are unaware of any steps having been taken by DuPont to remove any members of the community from their exposure to the Washington Work's ongoing C-8 emissions. Moreover, although DuPont's Washington Works employees exposed to C-8 are provided special personal protective equipment, bottled water at the Plant, and routine medical surveillance, DuPont does not provide such benefits to the communities surrounding its Washington Works Plant. In addition, DuPont continues to discharge C-8 into the environment from its Washington Works Plant. As of today's date, we are unaware of any steps having been taken by WVDEP to even acknowledge excessive exposures among the local communities, let alone address such exposures.
In summary, DuPont's own modeling data, including kinetic models prepared by DuPont several years ago, indicate that residents living in the communities surrounding DuPont's Washington Works Plant in Wood County, West Virginia have been and are continuing to be exposed to levels of PFOA that are possibly a thousand times higher than the low levels of exposure among the general U.S. population that triggered USEPA's recent "priority" review of the human health risks associated with such exposures. There is no indication that WVDEP intends to address this issue. We request, therefore, that USEPA and Ohio EPA take those steps necessary to respond to this situation and that ATSDR consider the exposure of the specific communities actually impacted by DuPont's C-8 emissions (as opposed to broad County-wide statistics) in connection with any investigation of the impact of C-8 exposures in the communities surrounding DuPont's Washington Works Plant. Thank you.
A. Bilott RAB/mdm Enclosures (Exhibits A-I) cc: R. Edison Hill, Esq. (w/o ends.)
Larry A. Winter, Esq. (w/o ends.) Gerald J. Rapien, Esq. (w/o ends.) Lillian Pinzon, Esq. (USEPA, Region 5) (w/ ends.) Janet Sharke, Esq. (USEPA, Region 3) (w/ ends.) Mary Dominiak, (USEPA, OPPT) (for inclusion in AR-226) (w/ ends.) Michael Baker (Ohio EPA, DDAGW) (w/ ends.)
A S'
From: Paul M Hinderliter on 08/29/2000 10:17 AM To: Gary W Jepson/AE/DuPont@DuPont cc: Subject: Hinderliter SOT 2001 d< Jepson SOT 2001.do
EID277489
DEVELOPMENT OF A BIOLOGICALLY BASED MODEL TO DESCRIBE PERFLUOROOCTANOIC ACID (PFOA) KINETICS. P M Hinderliter, and G W Jepson, Haskell Laboratory, DuPont, Newark, DE Perfluorooctanoic acid is a fluoroorganic surfactant used in the production of a variety of fluoropolymers. Questions about general fluororganic surfactant biodistribution and persistence have been generated as a result of a recent decision to remove a widely used fluoroorganic fabric treatment from the marketplace. In order to better understand the biodistribution and biopersistence potential of PFOA in humans, a biologically based kinetic (BBK) human model was developed. A physiologically-based pharmacokinetic model (PBPK) using Advanced Continuous Simulation Language (ACSL) was first developed and validated using available rodent and primate data. This model was then scaled up to humans. Both dermal and oral routes of exposure were included in the model as these routes account for nearly all human exposure to PFOA. The resulting BBK model for PFOA had explicit descriptions of liver, gut, lung, fat, kidney, and skin as well as general descriptions for compartments with kinetically similar behavior. Binding equations were included to account for the interaction between PFOA and tissue and plasma proteins. The resulting model successfully described the plasma and tissue kinetics of PFOA in rats exposed via repeated oral dosing. Additionally, comparison o f human model simulations with human PFOA blood data demonstrated the utility of the BBK model in assessing the behavior of PFOA in humans exposed to PFOA.
EID277490
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COMPARISON OF PERFLUOROOCTANOIC ACID (PFOA) AND PERFLUOROOCTANYL SULFONATE (PFOS) BLOOD KINETICS IN RATS FOLLOWING REPEATED ORAL DOSING. G W Jepson, P M Hinderliter, J Stadler, C Finlay, Haskell Laboratory, DuPont, Newark, DE
Perfluorooctanoic acid is a fluoroorganic surfactant that has been used for decades to produce a variety of fluoropolymers. Considerable focus has been placed on determining the biopersistence potential PFOA because of a recent decision to remove another fluoroorganic compound, perfluorooctanyl sulfonate, from the marketplace. In order to compare the biopersistence potential o f PFOA and PFOS, male rats were dosed once per day for 10 days and followed for 94 days. Blood was drawn and analyzed for total fluoride on days 1, 5, 10, 13, 24, 52 and 94. Noncompartmental analysis of the blood data was conducted using a WinNonlin mathematical software package. There was considerable difference in PFOA and PFOS blood kinetics as determined by peak blood concentrations and total exposure as determined by area under the curve (AUC) for doses normalized to 0.1 mmoles/Kg body weight. The maximum concentration (Cmax) in blood was 518 and 990 uM equivalents for PFOA and PFOS, respectively. The PFOS AUC in blood was 8 times higher than the PFOA AUC in blood at a normalized dose of 0.1 mmoles/Kg and the terminal half-life in blood was 40.5 days for PFOS as compared to 8.3 days for PFOA. While PFOA and PFOS are both fluoroorganic materials, comparison of PFOA and PFOS blood kinetics following repeated oral dosing illustrates that PFOA and PFOS are kinetically different in the rat. In the male rat, PFOS attains higher concentrations in the blood and persists in the blood longer than does PFOA.
EI0277491
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A Simple, Conservative Compartmental Model to Relate Ammonium Perfluorooctanoate (APFO) Exposure to Estimates of Perfluorooctanoate (PFO) Blood Levels in Humans
Paul M. Hinderliter, Ph.D. Gary W. Jepson, Ph.D. Biochemical Toxicology
DuPont Haskell Laboratory for Health and Environmental Sciences
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10 October, 2001
IO
Page 1 o f 10
EID166599 GKO 0 4 7 9 7
Abstract
A simple and conservative compartmental model was developed to relate ammonium perfluorooctanoate (APFO) exposures to estimates of periluorooctanoate (PFO) concentrations in human blood. The model was based on kinetic principles, but it did not include mechanistic or physiological descriptions. Further, the model was not intended to replace the need for more robust models that include mechanistic and appropriate physiological descriptions. The model included zero-order mathematical descriptions of oral and inhalation input and a first order elimination description. Standard estimates of the volumes of daily water consumption and air breathed were used to relate daily intake of APFO to concentrations of APFO in air and drinking water. The model was exercised under a variety of exposure conditions and used to create a table relating APFO intake via drinking water and/or air to PFO blood concentrations. The simplicity and utility of this model provide decision-makers with an easily applied tool to relate APFO exposures to estimates of resulting PFO concentrations in human blood.
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EID166600
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Introduction
A simple compartmental model was developed and used to estimate the concentration of perfluorooctanoate (PFO) in blood following inhalation or ingestion of ammonium perfluorooctanoate (APFO). The model presented is intended to complement various consequence analysis and planning activities and is not intended to be a substitute for a robust, mechanism based physiological model. It order to realize both the strengths and limitations of the model, it is important to carefully consider the assumptions and caveats relevant to the model development and application.
Approach
Model Development:
The model developed for this application was a two-compartment open model with one compartment defined as the blood compartment and the other as the body compartment. While the model is constructed as a two-compartment model, transfer of PFO is confined to only one compartment (blood compartment) in order to provide a conservative estimate of PFO concentrations in blood following APFO exposure. Functionally, this reduces to a one-compartment open model with two zero-order-input processes and one first-order elimination process. In other words, PFO is confined to the blood compartment and the PFO concentration in blood cannot be reduced by the distribution of PFO into other body tissues. In order to contribute to the conservative estimates produced by this model, any APFO that is ingested or inhaled is not subject to diffusional resistance and is assumed to be completely and instantly absorbed into the blood compartment. Since PFO is not metabolized, elimination from the blood is via renal excretion. In this model the elimination is described as a pseudo first-order process. A schematic of the model is shown in Figure 1.
Figure 1. Schematic of PFO Compartmental Model.
In Figure I, KACC is the distribution coefficient for transfer of PFO between the blood and body compartments. It has the units of day'1, but as discussed earlier, it is set to zero
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in order to create a conservative one-compartment model. KUPO is a zero-order term to describe PFO input into the blood compartment (ug/day) via the oral route. KUPI is a zero-order term to describe PFO input into the blood compartment (ug/day) via tne inhalation route. KFT TM is a pseudo first-order elimination coefficient (day1) that describes removal of PFO from the blood compartment via renal excretion. Differential rate equations were developed from the schematic in Figure 1 and the equations were solved using Advanced Continuous Simulation Language (ACSL, Aegis Corp.). The mathematical equations used to describe the concentration of PFO in the blood compartment (CBLOOD) are shown in the series of equations below.
-- = KUPO + KUPI - KEUM * CBLOOD * VOL - RAF dt
dAB = (KUPO + KUPI - KEUM * CBLOOD *VOL - RAF)dt
P* dAB = [` {KUPO + KUPI - KEUM * CBLOOD * VOL - RAF)di
Jab*o
Jt=a
^
AB = [^{KUPO + KUPI - KEUM * CBLOOD *VOL - RAF)it
CBLOOD = AB! VOL
( 1) (2)
(4) (5)
In the equations above, AB is the amount (ug) of PFO in blood, t is time (days), VOL is the volume (ml) of the blood compartment and RAF (ug/day) is the rate of PFO movement between the blood and body compartments (RAF=0 in this model). The ACSL coding of the above equations is given immediately below and in Appendix 1. The corresponding ACSL command file is provided in Appendix 2.
RA=KUPO + KUPI - KELIM*CBLOOD*VOL - RAF CBLOOD=INTEG(RA,0.)/VOL
Model Input Assumptions/Descriptions:
(6) (7)
Blood Compartment Volume: The blood volume of 3.5 L used in the model was that of a 50-Kg human (average human female weight). The female weight was selected to maintain the conservative approach desired for this model. Obviously, blood volume is a function of body weight so larger body weights will equate to larger blood volumes. PFO concentrations in blood will therefore decrease for a given APFO exposure as body weights increase.
Elimination Rate Constant: The elimination rate constant, KELIM, was assigned a value of 0.0019/day. This was derived assuming a PFO half-life (ti/2) in humans of 365 days and that first order kinetics apply. While current human half-life estimates are placed in the 200-300 day range, the 365-day half-life is a conservative value for initial model conditions. The actual value for KELIM was derived using the relationship between the half-life and the elimination rate constant where first order kinetics are obeyed.
( 8)
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13
EID166602 G K 004800
Input of APFO via Drinking Water: Drinking water concentrations of APFO were converted to micrograms (ug) of APFO ingested per day using the assumption that approximately 2L of the water are consumed per day. An example follows where drinking water containing 1 part per billion (ppb) APFO was consumed:
lug ^ 2L _ 2ug L day day
(9)
Input of APFO via Inhalation: Inhaled concentrations of APFO were converted to micrograms of APFO absorbed into the blood using the assumption that approximately 20 m3of air are breathed per day. An example follows where air containing 1 ug/m3 APFO was inhaled.
lug 20m3 _ 20wg m 3 day day
( 10)
General Assumptions:
The simple model described here is designed to be conservative and is not intended to be a substitute for a more robust, mechanism based physiological model. Consistent with the design of this model, several general assumptions have been made.
kL c (1) The PFO is distributed only in the human blood compartment.
^ S rf(2 ) There is no metabolism of PFO. (3) No binding or mechanistic descriptions are included in the model. ^
^
actually displays biphasic elimination with an initial rapid elimination phase followed by a slower or terminal phase elimination. In order to be consistent with the conservative nature of the model, only the slow (terminal) phase elimination is included in the model.
absorbed into the blood compartment. Va** d f o * ^ (6) APFO exposures occur every day throughout the exposure period modeled.
Results
The simulated PFO levels in human blood resulting from repeated ingestion of 6 ug/day APFO are shown in Figure 2. As would be expected based on the estimated half-life of PFO in the human body, the simulation illustrates that steady-state PFO blood levels are reached only after repeated exposure for over 6 years. Figure 3 is a simulation of the elimination of PFO from the blood once PFO levels are at steady state and PFO exposure is terminated.
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Page 5 of 10
Figure 2. Simulated PFO Concentration in Human Blood Following Continuous Intake of 6 ug/day
0 300 1000 1300 2000 2300 1000 1300 4000 f
Time (days)
Figure 3. Simulated PFO Concentration in Human Blood During and After 2600 Days of Exposure to 6 ug/day APFO
PFO Concentration in Blood (ppm)
0 500 1000 1300 2000 2500 3000 1M0 00
Time (days)
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EID166604 G K 004802
A series of model simulations were run to estimate the steady-state human PFO blood levels resulting from drinking water containing APFO, breathing air containing APFO or combinations of the two. The resulting estimates of PFO concentrations in human blood are shown in Table 1. Table 1 can be used under the conditions described in the text, to assign a PFO blood concentration to a particular exposure. Example 1: If drinking water containing 1 ppb APFO was consumed and no APFO was present in the inhaled air, the resulting steady-state PFO concentration estimate in human blood would be 0.30 ppm. Example 2: If no APFO was present in the drinking water and 0.05 ug/m3APFO was in the inhaled air, the resulting steady-state PFO concentration estimate in human blood would be 0.15 ppm. Example 3: If APFO was present in the drinking water at lppb and in the air at 0.3 ug/m3, the resulting steady-state PFO concentration estimate in human blood would be 1.20 ppm.
Table 1. Estima ted human steady-state PFO blood levels (ppm) following exposure to APFO via air and/or drinking water.
Parts per billion APFO in drinkine water
PFO Blood levels less than or equal to 5 ppm PFO Blood levels greater than 5 ppm but less than or equal to 10 ppm
* Use of this table requires careful consideration of assumptions and limitations described in the text.
Discussion
A relatively simple and conservative compartmental model was developed and exercised to create an estimate of the PFO concentration in human blood following exposure to APFO in drinking water and/or inhaled air. The model was then used to create a table relating APFO exposures to estimates of steady-state PFO blood concentrations. Within the constraints of the assumptions and descriptions provided in this report, a variety of
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EID1 6 6 6 0 5 G K 004803
exposure combinations could be evaluated using the model. Given a specific PFO concentration in blood, the model could also be used to create a plausible exposure scenario that could produce the observed PFO blood level. For example, if one had a hypothetical steady-state PFO concentration of 5 ppb in blood, the corresponding APFO exposure estimate using the model would be approximately 16 parts per trillion (ppt).
The model and approach presented in this report may be valuable for consequence analysis or planning activities, however, it should not serve as a substitute for more robust mechanistic, physiologically based models as they become available. The model presented here is based on sound compartmental analysis principles and is exclusive of mechanistic or physiological descriptions. As discussed earlier, this model is based on conservative assumptions and therefore is likely to provide high estimates of PFO concentrations in blood following ingestion or inhalation of PFO. Nevertheless, the simplicity and utility of this modei provide decision-makers an easily applied tool to relate APFO exposures to estimates of resulting PFO concentrations in human blood.
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EID16 6 6 0 6 G K 004804
/7
Appendix 1: ACSL Model Code
PROGRAM MODEL TO SIMULATE PFO BLOOD LEVELS FOLLOWING ORAL AND !INHALATION OF APFO VARIABLE TIME
INITIAL
'CONSTANTS CAN BE GIVEN VALUES TO SIMULATE EXPOSURE AND SYSTEM OF INTEREST
CONST.ANT KUPI CONSTANT KUPO CONSTANT KELIM CONST .ANT KACC CONSTANT VOL CONSTANT VF
= 0. ZERO ORDER INHALATION UPTAKE (ug/day) = 0. ZERO ORDER ORAL UPTAKE (ug/day) = 0. FIRST-ORDER ELIMINATION (/day) = 0. FIRST-ORDER DISTRIBUTION TO BODY (/day) = I. BLOOD VOLUME (ml) = 1. BODY VOLUME (ml)
TIMING COMMANDS
CONSTANT TSTOP CONSTANT POINTS CONSTANT TOFF
=3650. =3650. =3650.
'.LENGTH OF EXPOSURE (days) NO. OF POINTS IN PLOT END OF EXPOSURE TIME (DAYS)
CINT=TSTOP/POINTS END
COMMUNICATION INTERVAL END INITIAL
DYNAMIC
ALGORITHM 1ALG=2
DERIVATIVE IF (TIME GT. TOFF) THEN KUPI = 0. KUPO=0.
END
IF TERMT(TIME.GE.TSTOP)
CONCENTRATION OF PFO IN THE BLOOD COMPARTMENT (ug/day) RA=KUPO + KUPI - KELIM*CBLOOD*VOL - RAF CBLOOD=INTEG(RA,0. VVOL
CONCENTRATION OF PFO IN THE BODY RAF = KACC*(CBLOOD*VOL-CF*VF) CF = INTEG(RAF,0.0)/VF
END END END
END DERIVATIVE END DYNAMIC
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EID166607 G K 004805
Appendix 2: ACSL Command File for Assigning Appropriate Parameter Values
TSTOP= 10*365; POINTS=50; TOFF=TSTOP+1; VOL=3500;
KACC=0.; KELIM=0.0019; KUPO=2; KUPI=6;
keyboard figure; !START line(_time, _cblood, @linestyle="+"); _cblood(POtNTS)
xlabel(Time (Days)5); ylabelfConc. in blood (ug/mL)1); titleCBLOOD CONCENTRATION');
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EID166608 G K 004806
o?0
DuPont Engineering
November 20, 2002
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DuPoni Engmeei iii'j Earley Mill Plaza - Slily. 21 Lancaster PiLa rue/!-i i Wilmington, 06 15803
David P. Watkins West Virginia Department of Environmental Protection Division of Water Resources 1201 Greenbrier Street Charleston, West Virginia 25311-1088
3Q02 anc^4'%>2 Public W ater Supply Results, W est Virginia and Ohio rliu P o n t W ashington W orks, W ashington, WV
Dear Mr. Watkins:
%
Sampling of public water supplies along the Ohio River to determine C-8 concentrations began in December 2001 as required by the Consent Order (Order No. GWR-2001-019). Public water supplies located as far as three and a half miles upstream of the DuPont Washington Works facility and 53 miles downstream have been included in the sampling events. Based on the very low C-8 concentrations measured at the various public water supplies, the number and frequency of sampling events at the public water supplies was reduced by the Groundwater Investigation Steering Team in May 2002. Currently, three public water supplies, Lubeck (West Virginia), Tuppers Plains (Ohio) and Little Hocking (Ohio), are sampled on a quarterly basis.
The finalized C-8 results for the 3Q02 and 4Q02 sampling events conducted at Lubeck (West Virginia), Tuppers Plains (Ohio) and Little Hocking (Ohio) are presented in Table 1. For the public water supplies that have been sampled more than once, results are presented with the most recent sampling event listed last. Figure 1 shows the locations of all the public water supplies sampled along the Ohio River.
The next sampling event at these Public Water Supply Wells is scheduled for 1Q2003. Please contact me at (302) 992-6820 if you have any questions.
Sincerely,
Andrew S. Hartten Project Director cc: GIST Members Attachments
E I du Pont de Memour: and Company
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OEPA 2548
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Table 1. Summary of C-8 in Groundwater Public W ater Supplies, West Virginia and Ohio Dupont Washington Works, Washington W V
Parkersburg, WV Belpre, OH
Blennerhassett Island, WV Little Hocking, OH
k g e m m w sm o PPSDPT PPSDAT PPSDAT
PPSDRANY1 PPSDRANY1 PPSDRANY1 PPSDRANY2 PPSDRANY3 PPSDRANY4 PPSDRANY5
BELPSDAT BELPSDAT BELPSDAT BELPSPW1 BELPSDPW1 BELPSDPW2 BELPSDPW2 BELPSDPW2 BELPSDPW3 BELPSDPW3 BELPSDPW4 BELPSDPW4 BELPSDPW4 BELPSDPW5 BELPSDPW5 BELPSDPW5 BELPSDPW5
BLENI TWO BLENI TW7 BLENI W19A BLENISLEPS1
LHPSD1 LHPSD1 LHPSD1 LHPSD1 LHPSD1 LHPSD1 LHPSD1 LHPSD2 LHPSD2 LHPSD2 LHPSD2 LHPSD2 LHPSD2 LHPSD2 LHPSD2 LHPSD2 LHPSD3 LHPSD3 LHPSD3 LHPSD3 LHPSD3
T jlM B ifc tS J g /l --
3/6/2002
NQ (<0.050)
3/6/2002
NQ (<0.050)
4/25/2002
NQ (<0.050)
3/6/2002
0.0693
3/6/2002
0.0686
4/25/2002 3/6/2002
0.0746 ND (<0.010)
3/6/2002
ND (<0.010)
3/6/2002 3/6/2002
ND (<0.010) ND (<0.010)
2/7/2002
0.0818
3/25/2002
0.113
4/23/2002
0.12
2/7/2002
0.0995
3/25/2002
0.13
2/7/2002
NQ (<0.050)
2/7/2002
NQ (<0.05Q)
3/25/2002
NQ (0 .0 5 0 )
3/25/2002
0.141
4/23/2002
0.12
2/712002
0.101
3/25/2002
0.133
4/23/2002
0.114
2/7/2002
0.107
3/25/2002
0.103
4/23/2002
0.107
4/23/2002
0.111
2/21/2002
ND (0 .0 1 0 )
2/21/2002
NQ (0 .0 5 0 )
2/21/2002
0.316
1/30/2002
0.165
12/20/2001
1.82
1/21/2002
1.72
2/22/2002
2.37
3/26/2002
2.99
4/23/2002
2.02
8/21/2002
3.65
10/16/2002
3.41
12/20/2001
3.72
12/20/2001
3.52
1/21/2002
2.97
2/22/2002
2.03
2/22/2002
2.07
3/26/2002
3.31
4/23/2002
3.4
8/21/2002
4.26
10/16/2002
3.98
12/20/2001
0.844
1/21/2002
0.744
2/22/2002 3/26/2002 4/23/2002
0.42 0.827 0.783
M W IP " O T T --
l
Before Treatment Sample
After Treatment Sample)
After Treatment Sample Production Well
duplicate Production Well
Production Weil
Production Well
Production Well
Production Well
After Treatment Sample
After Treatment Sample
After Treatment Sample
Production Well
Production Well
Production Well
duplicate
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
duplicate
Test well
Test well
Test well
Drinking Supply Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Weil
Production Well
duplicate
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
Production Well
11/12/2002
Page 1 of 5
OEPA 2549
3Q4Q02PWS.xls
m m mwmm wm Little Hocking, OH (cont.)
General Electric, WV
Table 1. Summary of C-8 in Groundwater Public Water Supplies, W est Virginia and Ohio Dupont Washington Works, Washington W V
LHPSD3 LHPSD3 LHPSD3 LHPSD5 LHPSD5 LHPSD5 LHPSD5 LHPSD5 LHPSD5 LHPSD5 LHPSD5 LHPSDEP001 LHPSDEP001 LHPSDEP001 LHPSDEP001 LHPSDTW1 LHPSDTW1 LHPSDTW10 LHPSDTW10 LHPSDTW11 LHPSDTW11 LHPSDTW12 LHPSDTW12 LHPSDTW2 LHPSDTW2 LHPSDTW3 LHPSDTW3 LHPSDTW4 LHPSDTW4 LHPSDTW4 LHPSDTW4 LHPSDTW4 LHPSDTW5 LHPSDTW6 LHPSDTW6 LHPSOTW6 LHPSDTW9 LHPSDTW9 LHTORCHBS BARTLETTCC 339B STA GE WELL 3 GE WELL 3 GE WELL 3 GE WELL 3
M ^ H r c A o g /i H K C o n m U fR s lB IM B lI
8/21/2002 10/16/2002 10/16/2002 12/20/2001
1/21/2002 1/21/2002 2/22/2002 3/26/2002 4/23/2002 8/21/2002 10/16/2002 1/22/2002 3/26/2002 4/23/2002 10/16/2002
0.952 0.495 0.434
7.66 6.22 6.14 5.69 6.57 6.11 8.09 8.58 1.69 2.62 1.93 4.29
Production Well Production Well
duplicate Production Well Production Well
duplicate Production Well Production Well Production Well Production Well Production Well Water System Point Water System Point Water System Point Water System Point
1/22/2002 8/21/2002 1/21/2002 8/21/2002 1/21/2002 8/21/2002 1/21/2002
2.16 0.81
1.9 1.1 1.41 1.73 0.758
Test well Test well Test well Test well Test well Test well Test well
8/21/2002
0.824
Test well
1/22/2002
0.103
Test well
8/21/2002
0.081
Test well
1/22/2002
4.48
Test well
8/21/2002 1/22/2002
4.17 37.1
Test well Test well
3/26/2002 4/23/2002
33.3 28.7
Test well Test well
8/21/2002 10/16/2002
12.3 14.5
Test well Test well
8/21/2002 1/22/2002
6.26 1.79
Test well Test well
8/21/2002
1.15
Test well
8/21/2002 1/22/2002
1.23 0.364
duplicate Test well
8/21/2002
0.812
Test well
1/22/2002
1.85 Water System Point
1/22/2002
1.94 Water System Point
1/22/2002
1.81 Water System Point
1/3/2002 1/3/2002
1.78 1.87
Production Well duplicate
2/21/2002
1.75
Production Well
4/26/2002
1.84
Production Well
11/12/2002
Page 2 of 5
-S3
OEPA 2550
3Q4Q02PWS .xls
Table 1. Summary of C-8 in Groundwater Public W ater Supplies, West Virginia and Ohio Dupont Washington Works, Washington W V
w tm m x m m m m m iflN H M H B S a irS fftP i iilii i i M f g s s n
Lubeck, WV
LPSDAT LPSDAT LPSDAT LPSDAT
3/28/2002 4/26/2002 6/24/2002 10/15/2002
0.69 0.652
0.6 0.653
LPSD WELL A
1/3/2002
0.764
LPSD WELL A
2/21/2002
0.683
LPSD WELL A
3/28/2002
0.796
LPSD WELL A
4/26/2002
0.938
LPSD WELL A
7/24/2002
0.753
LPSD WELL A
10/15/2002
0.856
LPSD WELL B
2/21/2002
0.61
LPSD WELL B
3/28/2002
0.551
LPSD WELL B
4/26/2002
0.532
LPSD WELL B
7/24/2002
0.443
LPSD WELL B
10/15/2002
0.537
LPSD WELL C
1/3/2002
0.592
LPSD WELLC
2/21/2002
0.479
LPSD WELL C
3/28/2002
0.491
LPSD WELL C
4/26/2002
0.471
LPSD WELL C
7/24/2002
0.398
LPSD WELL C
10/15/2002
0.504
LPSD WELL D
1/3/2002
0.758
LPSD WELL D
2/21/2002
0.725
LPSD WELL D
3/28/2002
0.692
LPSD WELL D
4/26/2002
0.506
LPSD WELL D
7/24/2002
0.444
LPSD WELL D
10/15/2002
0.517
LPSD WELL E
1/3/2002
0.332
LPSD WELL E
2/21/2002
1
LPSD WELL E
3/28/2002
1.09
LPSD WELL E
4/26/2002
1.11
LPSD WELL E
7/24/2002
1.02
LPSD WELL E
10/15/2002
1.21
LPSD WELL F
1/3/2002
1.04
LPSD WELL F
2/21/2002
0.313
LPSD WELL F
3/28/2002
0.358
LPSD WELL F
3/28/2002
0.352
LPSD WELL F
4/26/2002
0.332
LPSD WELL F
7/24/2002
0.284
LPSD WELL F
7/24/2002
0.283
LPSD WELL F
10/15/2002
0.355
Belleville Hydra Plant WV
BELLEVILLELD
1/29/2002
NQ (0 .0 5 0 )
Tuppers Plains PSD, OH
TPPSDPT
2/6/2002
0.372
TPPSDPT
3/25/2002
0.347
TPPSDPT
7/23/2002
0.24
TPPSDPT
10/15/2002
0.226
TPPSDAT
2/6/2002
0.361
TPPSDAT
3/25/2002
0.358
TPPSDAT
4/24/2002
0.363
TPPSDAT
7/23/2002
0.246
TPPSDAT
10/15/2002
0.268
TPPSDPW1
2/6/2002
0.726
TPPSDPW1
3/25/2002
0.705
M i ~i-- n r w i i i i -
After Treatment Sample After Treatment Sample After Treatment Sample After Treatment Sample
Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well
duplicate Production Well Production Well
duplicate Production Well Miscellaneous Use
Before Treatment Sample Before Treatment Sample Before Treatment Sample Before Treatment Sample
After Treatment Sample After Treatment Sample After Treatment Sample After Treatment Sample After Treatment Sample
Production Well Production Well
11/12/2002
Page 3 of 5
OEPA2551
3Q4Q02PWS.xls
Tuppers Plains PSD, OH (cont.)
Ravenswood Municipal, WV Mason County PSD, WV
Racine Locks and Dam, WV Village of Racine, OH
New Haven Water Dept, WV
11/12/2002
Table 1. Summary of C-8 in Groundwater Public W ater Supplies, W est Virginia and Ohio Dupont Washington Works. Washington W V
B a m p B 'D irK M M M e v n s n
TPPSDPW1 TPPSDPW1 TPPSDPW1 TPPSDPW2
4/24/2002 7/23/2002 10/15/2002
2/6/2002
0.702 0.588 0.486 0.417
TPPSDPW2
3/25/2002
0.327
TPPSDPW2
4/24/2002
0.371
TPPSDPW2
7/23/2002
0.235
TPPSDPW2
10/15/2002
0.255
TPPSDPW3
2/6/2002
NQ (<0.050)
TPPSDPW3
3/25/2002
NQ (<0.050)
TPPSDPW3
7/23/2002
ND (<0.010)
TPPSDPW3 TPPSDPW4 TPPSDPW4
10/15/2002 2/6/2002
3/25/2002
ND (0 .0 1 0 ) 0.0734 0.07
TPPSDPW4
7/23/2002
0.052
TPPSDPW4 TPPSDPW5
10/15/2002 2/6/2002
0.076 0.201
TPPSDPW5
3/25/2002
0.201
TPPSDPW5
7/23/2002
0.216
TPPSDPW5 TPPSDPW6
10/15/2002 2/6/2002
0.229 0.649
TPPSDPW6
3/25/2002
0.634
TPPSDPW6
4/24/2002
0.62
TPPSDPW6
7/23/2002
0.62
TPPSDPW6
10/15/2002
0.433
COR ASIN
3/27/2002
ND (0 .0 1 0 )
COR ASOUT
3/27/2002
NQ (0 .0 5 0 )
COR BLEND AT
3/27/2002
ND (0 .0 1 0 )
COR WELL1
3/27/2002
ND (0 .0 1 0 )
COR WELL 2
3/27/2002
ND (0 .0 1 0 )
COR WELL3
3/27/2002
ND (0 .0 1 0 )
COR WELL 4 COR WELL 5
3/27/2002 3/27/2002
ND (0 .0 1 0 ) ND (0 .0 1 0 )
MASONCPSD1
1/29/2002
NQ (0 .0 5 0 )
MASONCPSD1
3/27/2002
NQ (0 .0 5 0 )
MASONCPSD1
4/25/2002
NQ (0 .0 5 0 )
MASONCPSD2
1/29/2002
0.0618
MASONCPSD2
3/27/2002
0.0838
MASONCPSD2
4/25/2002
0.0714
MASONCPSD3 MASONCPSD3 MASONCPSD3
1/29/2002 3/27/2002 4/25/2002
0.0707 0.102 0.063
RACINELD
1/4/2002
0.518
VORAT
3/26/2002
ND (0 .0 1 0 )
VORRV3 VORWELL1 VORWELL2
3/26/2002 3/26/2002 3/26/2002
ND (0 .0 1 0 ) ND (0 .0 1 0 ) ND (0 .0 1 0 )
NHPSDAT NHPSDPW1 NHPSDPW1
4/10/2002 4/10/2002 4/10/2002
ND (0 .0 1 0 ) NQ (0 .0 5 0 ) NQ (0 .0 5 0 )
Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well
Air Stripper In Air Stripper Out Blend After Treatment Production Well Production Well Production Well Production Well Production Well
Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Production Well Miscellaneous Use After Treatment Sample Production Well Production Well Production Well
After Treatment Sample Production Well duplicate
Page 4 of 5
OEPA 2552 r
3Q4Q02PWS.xls
Table 1. Summary of C-8 in Groundwater Public W ater Supplies, West Virginia and Ohio Dupont Washington Works, Washington W V
- .. .- - Location ' Village of Syracuse, OH
Village of Pomeroy, OH
Sample ID
VOSAT VOSAT VOS NORTH 2 VOS NORTH 2 VOS SOUTH R3 VOS SOUTH R3 VOPAT VOPAT VOPWELL1 VOPWELL2 VOPWELL2 VOPWELL4 VOPWELL4
Sample Date
3/29/2002 4/24/2002 3/29/2002 4/24/2002 3/26/2002 4/24/2002 3/26/2002 4/24/2002 4/24/2002 3/26/2002 4/24/2002 3/26/2002 4/24/2002
? ' C -8 ug/l
NQ (<0.050) ND (*=0.010) NQ (<0.050)
0.491 0.208 ND (0 .0 1 0 ) 0.0659 0.0628 ND (0 .0 1 0 ) 0.0689 ND (0 .0 1 0 ) 0.0851 0.0712
NO = Not Detected at or above the limit of detection (LOO). The listed LOD is approximate and varies by instrument and over time.
NQ = Not Quantifiable. Detected at a level above the LOO and below the limit of quantification (LOQ).
All C-8 results are reported in ug/l. Mlsc. = Miscellaneous water use is not used for drinking.
Comments . After Treatment Sample After Treatment Sample
Production Well Production Well Production Well Production Well After Treatment Sample After Treatment Sample Production Well Production Well Production Well Production Well Production Well
11/ 12/2002
Page 5 of 5
OEPA 2553
3Q4Q02PWS.xls
,L a w O f f ic e s
Spilman Thomas & Battle PLLC
Since 1864
990 ELMER PRINCE DRIVE, SUITE 205 MORGANTOWN. WEST VIRGINIA 26505
TELEPHONE (304) 599-8175
417 GRAND PARK DRIVE, SUITE 203 PARKERSBURG, WEST VIRGINIA 26101
TELEPHONE (304) 422-6700
SPILMAN CENTER 300 KANAWHA BOULEVARD, EAST
POST OFFICE BOX 273 CHARLESTON, WEST VIRGINIA 25321-0273
TELEPHONE (304) 340-3800 FACSIMILE (304) 340-3801
333 PENCO ROAD, SUITE A WEIRTON, WEST VIRGINIA 26062
TELEPHONE (304) 723-6980
W RITER'S DIRECT DIAL NO. (304) 340-3882
e-mail: abrad1ey@spilmanlaw.com
June 13,2002
Mr. Armando Benincasa Dr. Dee Ann Staats West Virginia Department of Environmental Protection 1356 Hansford Street Charleston, W*V 25301
Dear Dr. Staats and Mr. Benincasa:
tM'' *
Enclosed is the final report of the air dispersion modeling for year 2000 actual emissions. Please contact me if you have any questions regarding this matter.
Very truly yours,
Enclosure
cc: 1/
Christopher Negley, Esq. Mr. Michael Baker, Ohio EPA Mr. John Benedict, DAQ Mr. Jesse Hanshaw, DAQ
WVDEP 14300
ISC Modeling Methodology and Results
Emission Source Information
The ISC3 model was used to calculate ambient ground-level air concentrations and deposition rates for year 2000 actual C8 emissions from the Washington Works site. Table 1 shows the stack parameters used in the model for each emission point. Table 2 shows the emission rates used. The stack parameters and emission rates used are those that were submitted pursuant to Consent Order GWR-2001-019. In addition, two additional emission points have been added to the model beyond what was submitted pursuant to the Consent Order. Since the C8 emissions are partitioned between the vapor and particle phases, deposition runs were completed by modeling each phase separately. (Modeling nans to determine ground-level concentrations were based on the total emissions.)
Deposition modeling requires paiticle size distribution information and scavenging coefficients for each phase of emissions (vapor and particle). The size distribution information used in the modeling for the particle phase was obtained from testing at the Washington Works site. The scavenging coefficients used for the particle phase were obtained from Figure 1-11 o f the EPA ISC3 User's Guide. The vapor phase scavenging coefficients used were based on calculations by DuPont which were submitted under the Consent Order. This data shows the calculated vapor scavenging coefficient based on rain intensity. Since only one value of the scavenging coefficient can be entered into the ISC3 model, the largest scavenging coefficient was chosen to ensure that the model predictions were conservative. Table 3 shows the gas and particle data used in the model and, additionally, shows the basis for the vapor scavenging coefficient used in the model.
Modeling Methodology
Dispersion and deposition modeling was performed using the Industrial Source Complex 3 Model (ISC3), version 00101, provided by Lakes Environmental. All modeling was done in accordance with the procedures in EPA's Guideline on Air Quality Models (40 CFR Part 51, Appendix W). The EPA regulatory default options and rural dispersion coefficients were used in the model.
The C8 emission sources were evaluated for downwash effects from surrounding buildings. The Lakes Environmental BPIP View model was used to provide wind direction specific building parameters. All buildings on the site were evaluated to determine if they could potentially impact the stack by causing building downwash effects. A plot plan showing the location of buildings included in the model is shown in Figure 1. (The buildings included in the model are identical to the list submitted under Consent Order GWR-2001-019).
A 100-meter grid extending out 4,000 meters from the source was used. In addition, discrete receptors with 100-meter spacing were placed on the plant property line. Terrain elevations were imported from electronic files obtained from the U.S. Geological Survey using the "highest" method to assign an elevation to each receptor.
WVDEP 14301
6/7/02
An additional receptor grid was used to determine deposition to the watershed for the Little Hocking Water Association well field. A USGS topographical map was used to identify the general area of the watershed (Figure 2), and a receptor grid with 100 meter spacing was placed within this watershed (Figure 3).
One year of on-site meteorological data (1996) was analyzed. The data was processed by Trinity consultants, using Wilmington, Ohio for the upper air data. The precipitation data used is from the Parkersburg, West Virginia airport. Missing data and measured wind speeds of less than 1 m/s were treated consistent with the recommendations made in EPA's On-site Meteorological Program Guidance for Regulatory Modeling. An anemometer height of 10 meters was used for the modeling.
Modeling Results
An averaging time of one year was used to determine the annual average vapor concentrations and annual deposition rates over the entire receptor grid. A contour plot of the annual average vapor concentrations is shown in Figure 4. Contour plots of the total deposition rates for the particle and vapor phases are shown in Figures 5 and 6. The maximum off-site values predicted by the model were:
n
Maximum Annual Average Ground-Level Concentration = 2.675 pg/m3
Particle Phase: Maximum Dry Deposition Rate = 0.1347 g/m2/yr Maximum Wet Deposition Rate = 0.0456 g/m2/yr Maximum Total Deposition Rate = 0.1803 g/nr/yr
Vapor Phase: Maximum Wet Deposition Rate = 0.0085 g/m2/yr
The maximum ground-level concentration and all of the maximum deposition rates were predicted to occur at the same receptor (442135.47E, 4346899N), which is located on the plant fenceline north of the plant. The maximum annual ground-level concentration predicted to occur in areas where people may reside in the community is approximately 0.8 pg/m3.
Additionally, a smaller receptor grid was used to determine the annual deposition rate to the Little Hocldng well watershed. The model was run to calculate vapor and particle phase deposition rates for each receptor, which rates were then imported into a spreadsheet. An average deposition rate was calculated for all of the receptors and multiplied by the receptor grid area (2.57 km2) to get a total deposition per year over the entire watershed. The deposition amounts calculated were:
Particle Phase: Vapor Phase:
Total Dry Deposition * 6,732 g/yr (14.8 lb/yr) Total Wet Deposition = 12,608 g/yr (27.8 lb/yr) Total Deposition = 19,340 g/yr (42.6 lb/yr) Total Wet Deposition = 1,644 g/yr (3.6 lb/yr)
WVDEP 14302
JO
Table 1 Stack Parameters
6/7/02
1823A 815D 815D
1353A Pre-Existing
614A 614A 781 1953 2365A 2365A 2365A Semiworks Application Semiworks Application Semiworks Application Semiworks Application
T7LME T6IFCE T6IZCE
164-5E 164-2E 163-E-26 163-E-ll 163-E-33
242 C1FSE C1FKE C1CAE R022EEF6 R022EEF86 R022EEF87 R022EEF89
662 644 699
652 658 231 232 216 242 274 268 205
442025 442084 442091
441920 441923 441952 441953 441960 441954 441787 441774 442310 442086 442069 442058 442063
4346847 4346835 4346836
150 59 63
4346767 70 4346756 68 4346776 93 4346766 81 4346788 60 4346741 114.5 4346744 110 4346753 72.5 4346800 6.66 4346624 47 4346627 49 4346634 49 4346635 ___ 41_9_____
1.33 1.5 18-1 ft
1.96 1.63 0.67 0.67 1.3 0.5 0.69 0.27 0.5 2.5 2.0 2.0 2.0
3,349 18,000 18000"
9,800 2,800 500 600 2,750 1,250 1,000 100 1,000 8836 7540 1885 3770
"Vent ID T61ZCE consists of 18 one-foot diameter vents. The flow rate given is the total for all 18 vents. bThe velocity listed is the velocity calculated for one individual vent.
40.2 169.8 21.2b
54.1 22.4 23.6 28.4 34.5 106.1 44.6 29.1 84.9 30.0 40.0 10.0 20.0
172 111 111
200 300 130 130 158 200 255 110 70 80 80 80 80
31
t
WVDEP 14303
6/7/02
Table 2 Emission Information
U.itrwi' ' r'1 1
T7IME T6IFCE T6IZCE 164-5E 164-2E 163-E-26 163-E-ll 163-E-33
242 C1FSE C1FKE C1CAE R022EEF6 R022EEF86 R022EEF87 R022EEF89
1i\ :
662 644 699 652 658 231 232 216 242 274 268 205
'whKS' : :i i t i ,)"!
i , f * ifitibSiiO .iH '
r a. j !i*)fl1
ils' 't:\
....... m m
! ip *ftUr !.% !s1c V
;|
y,# jsllilKh'liO'.iji.-. ,
, _ Lnjii.itsaiy 0 i.feyt j
' F'j:*-
u `:>
`
0 0.54 0.9 0.9 0.9 0.11 i 0.09
0 0.9 0.03 1 1 1 1 1 1
1 0.46 0.1 0.1 0.1 0.89 0.91
1 0.1 0.97 0 0 0 0 0 0
0 13,977
0 33 79 3,541 4,680 0 3,510 5,414 107 0 12 0.3 3 0.6
0 0.2010
0 0.0005 0.0011 0.0509 0.0673
0 0.0505 0.0779 0.0015
0 1.73E-04 4.32E-06 4.32E-05 8.63E-06
0 0.1086
0 4.27E-04 0.00102 0.00560 0.00606
0 0.0454 0.00234 0.0015
0 1.73E-04 4.32E-06 4.32E-05 8.63E-06
0 0.0925
0 4.75E-05 1.14E-04 0.0453 0.0613
0 0.00505 0.0755
0 0 0 0 0 0
WVDEP 14304
4\
Table 3 Gas & Particle Data
Particle Phase:
Particle Diameter (microns)
0.2 0.4 0.75 2.0 4.0
Mass Fraction
0.538 0.267 0.035 0.127 0.033
Particle Density (g/cm3)
2.2 2.2 2.2 2.2 2.2
Scavengin; ; Coefficients
Liquid
Frozen
Precipitation Precipitation
(s'Vmm-h'1) (s'Vmm-h'1)
1.2X10"4
4x1 O'5
5x10'5
1.67x1O'5
143xx110Q'54
1.33x10 4.33x10
2.8xl04
9.33x10
Vapor Phase:
Liquid Scavenging Coefficient (s'Vmm-h'1) = 6.4x10 Frozen Scavenging Coefficient (s'Vmm-h'1) = 6.4x10"6
Calculations of Vapor Scavenging Coefficient: - vapor scavenging coefficients are presented in the consent order submittal as a list of values for
different rainfall intensities - the vapor scavenging coefficient that is entered into the ISC model is in units of s'Vmm-h'1,
therefore the scavenging coefficients shown in the consent order must be adjusted to the proper
units and then divided by the rainfall intensity - to ensure that model predictions would be conservative, the scavenging coefficient based on a 1
mm/hr rain intensity was used, as this gives the largest value for input into the model
2.31
6.4x10"6
= 6.4x1O'6-- ------r
h r 3600r 1m m
s mm
mm hr
5 WVDEP 14305
WVDEP 14306
43469004346800434670043466004346500-
441600
6/7/02
---- ------------------------------- 1
441800
441900
i
442000
i
442100
Figure 1 - Building Plot Plan
2
f
442200
i
WVDEP 14308
!
4348500-1 43480004347500434700043465004346000H--
441000
6/7/02
+++ ++ ++ ++ ++ + +++ ++++ +++ + + + + + + + + + + + + +* + -t- + + +- + + + + ++++++++++++++ +++++++ + + + + + + + + + + + + + + + + + + + + + 4+ + + + + + + + + + + + + + + + + + + + >+ + + + + + + + + + + + + + + + + + + + + _ll_ "r 4- + 4- + + + + + + + + + ' + + + + + + + + + + + + + + + + 4- + + + +++++++++ +++++++++++++++ +++ +++ +++++++++++++++++++ +++ ++++++ ++ ++ ++ ++++++ + -1- + + + + -I- + + + + + + + + + + + + + + + +
Figure 3 Little H ocking W ell W atershed Receptors M odeled
36 9I
445000
43490"
U'3964Jm S T ~ .................... ...........
443899 1
E
/fP
uarv* Q^vamnwtntCanw
22 S. ftBfrt S frM t
iunMn, OH 4321VK99
S ta u o f O k u Ia -rfa u M M *U l Y u c d m Acacy
mstu]Fu4oao mx: (u>a* . i.; ,;.'\L!vy'
IW ;
_________ mmiwtOOTCUi
P .O .lo x IOmUI CoHjm bua.OH 49216-1049
January 7, 2003
Mr. Paul Bossert E.l. Du Pont da Nemours and Company Washington Works P.O.Box 1217 Parkersburg, West Virginia 26102
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Re: Ammonium Perfluorooctanoate (C8)%itpaets in Little Hocking, Ohio
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Dear Mr. Bessert
I am writing to express Ohio EPA's concerns with respect to air impacts in Ohio due to emissions of C8. from your Washington Works facility. We have been following the progress on the evaluation and review ofambient Impacts due to this facility, as well as the evaluation of ambient screening levels for both the air and water pathways developed by the C8 Assessment ofToxicityTeam (CATT). We are also aware ofadditional evaluations in progress by U.S. EPA and the Science Advisory board for reassessing the toxicity and possible carcinogenic effects of C8.
In addition, we have been contacted by a citizens group expressing concern over ambient levels of C8, as predicted by air quality modeling of year 2000 actual emissions. Short [ term levels used to assessworkplace exposures were identified as health based levels not fully considered by the CAT team in the development of ah air screening level for C8.
My staff has assessed the modeled ambient Impacts resulting fromthe year2000 emission levels. Among the averaging times evaluated, my staff has Identified predicted eight-hour concentrations well above the ACGIH health based work place standard at multiple receptors In Ohio. While these ambient concentrations may not be directly comparable to
workplace exposures, these predicted concentrations raise our level of concern with regards to short term exposures to workers and sensitive populations.
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Du Pont has indicated that future production levels, modifications to a scrubber, a taller stack on a major source, as wall as agreements with U.S. EPA to reduce releases to all
media will limit future impacts In the area. You presented information that future impacts .would be below those associated with year 2000 actual Impacts. And. the year 2000 \ emissions are the basis of your agreement with West Virginia to limit future air emission . levels. However, we do not believe that there is enough certainty in the assumptions to insure that future ambient air impacts will be significantly below 2000 levels.
Pm iadaM aoiM Ft0M
M e r a n O 'Connor. U w O ra n t d o w n o r Chriatephar Ja m a . Diractar
Page 2 \ Mr. Paul Bossert .. January 3!, 2003 W e are requesting that you work with the State of West Virginia to adopt enforceable permit restrictions that will reduce ambient impacts below the workplace exposure limits at all receptors beyond the plant fence line. We believe that this is a prudent interim step until the potential effects of C8 are fully evaluated. Oncethese evaluations are complete, future acceptable emission levels can be determined. If you have any questions with respect to our concerns, please feel free to contact Bob *-+iodanbosc of the Division of Air Pollution Control at 614-644-2270.
i ce Bnard J. Reilly Esq., E.I. Du Pont de Nemours and Company, Legal Dpt
John Benedict, WV Department of Environmental Protection
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January 22, 200t
Dr. Charles M. Auer. Director
U S. Environmental Protecuon Agency
Office of Pollution Prevention and Toxics
Chemical Control Division
410 M Street NW Room a03 Washington. D C. 20460
o o M R w r aA N m zEo
Dear Dr. Auer
In my June 23. 2000 letter that transmitted DuPont's Voluntary Use and Exposure Information Profile i,L"E!Pi for .Ammonium Perfluorooctanoate (APFO. CAS#3825-26I ). I noted that, as part or me ongoing surveillance of workers potentially exposed to APFO. a senes of blood samples were taken in year 2000 from workers and that DuPont would voiuntaniy submit a summary or the results when they became available.
The results of the blood serum tests am now available. A summary of this year's results for workers with identified .APFO exposure potential is below.
Year j ; i
i 2000
* of Samples
*2
Minimum Concentrauon
ppm) 0 02
1 Maximum
! Concentrauon comi
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1 Mean Concentrauon pom) '. 3
1 '
Note the following concerning the aoove data.
> Five samples, ail from worsen n one particular ;ob. tested greater than 5 0 ppm. Among he ,obs wiui potential APFO exposure. Jus ;ob should have me least exposure cotenuai. We are investigating me cause of these elevated results m this group of women. Eliminating he five ia u points from these worken gives i maximum concentration of * 4 ppm and a mean concentration of 1.16 ppm.
> Some employees not routinely wonting with a?FO provided blood samples. APFO levels h his group of people are ccnistemly .ess than 0.2 ppm.
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January 23. 2001 Dr. Charles M. Auer
> Blood serum APFO concentration seems to be a function of length of time in assignments with potential APFO exposure. Due to variances in length of service among workers .n assignments with potential .APFO exposure, average values may be influenced not only by exposure potential but also by average length of service of ihe volunteer group.
Additional groundwater and surface water measurements have been reported and some older data has been located. These additional data are reported on pages S and 6 of a revised Voluntary UEIP. Please replace the previous submission with the attached version. Noui that there s a public copy and a copy containing Confidential Business [nforiiiauot..
[f you wish to discuss the information contained m this document, please contact Robert F. Pinchot at (3021999-M374 or e-mail at RabenF Pincnm-aimJunonLrnm or me ax (30213665239.
Very truly yours.
Attachments
Gerald L. Kennedy Director. Applied Toxicology and Health
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An acceptable level for ammonium p e r f l u o r o o c - a n o a t e (C-8) in the blood of workers would be 0.5 p p m . This v a l _ e n a s b een calculated using the average daily C-8 accumulation rate observed
in new e m p l o y e e s who w e r e e x p o s e d to a i r b o r n e c o n c e r t r a t i o n s of 0 . 0 0 8 mg/nr (memo, 0. G. L o s c h i a v o to R. J. Z i p f e l , 7 , ' 2 9 / 8 2 ) .
From this data, a steady-state concentration of 0 . 5 i opm, which represents the dynamics of exposure and elimination, was e s t i m a t e d (M e m o , T. P. P a s t o o r to 0. G. L o s c h i a v o , ' 2 5 / 8 2 ) . These estimates appear consistent with most of the r e s o r t e d human dat a but the d a t a b a s e is not too e x t e n s i v e . In a d d i t i o n , in rat inhalation experiments, no signs of toxicity were d e f e c t e d
following exposure to 1 mg/m , an atmospheric c o n c e r z r at ion corresponding to a blood level in the male rat of 12 oon. Extrapolation of the data relating the concentratior cf C-8 in the air to blood levels in the rat suggests that i n r s l a t i o n of
0.01 mg/nr would result in blood level of approx i m a t e - y 1 ppm (equation is blood level a 12 ^ a i r concentracin).
An acceptable level for community drinking w a r e r . w o u l d be
5 p p b . This value has been arrived at as follows:
"
1. T h e - A E L ( 8 - h r TWA) is 0.0 1 m g / m ^ j a w o r k e r b r e a t h i n g 1 0 m / d a y would take in 0.1 mg. Assume 10 C 3 a b s o r p t i o n .
2. D a i l y i n g e s t i o n b y m a n o f 2 L o f w a t e r / d a y : 0 . 1 m g / 2 L (assume 1003 absorption) s 50 ppb (a c o n c e n t r a t i o n in water) .
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3. H o w e v e r , c o m m u n i t y p o p u l a t i o n s a re n ot e q u i v a l e n t to worker populations. Therefore, factor in a 10X reduction - 5 ppb (concentration in water).
This doesn't take into account the time factor (porker exposed 8 hours, n o t - e x p o s e d 16 hours, etc. whereas drinking water intake could be anytime during 16 hours, off 8 hours, etc.). However, the long half-life of this chemical in the blood might make this consideration less important.
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I h o p e t h a t t h e s e s u g g e s t e d g u i d e l i n e s w i l l bfe u s e f u l . Please call if you have any questions.^ GLK:ms
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G. R. Alms/S. V. Gangal J. G. Loschiavo - 012022-3 J. E. Crua D. H. Flcnsborg G. L. Herridge J. F. Kline TRfn>.'Tanyon t w. A. Ott J. L. Post D. A. Schneider W. M. Stewart
July 7, 1987
TO: C. A. DYKES J. A. SCHMID
FROM: R. J. ZIPFEL
C -8 CONTROL PROGRAM
My review on this issue with Or. Bruce Karrh on June 11, 1967, vent very well with little change required to our present control prograa. Or. Karrh was most interested in the presence of C-8 outside the plant boundaries. He stated that we need to place the highest priority on these environaental issues. Dr. Karrh also accepted the position that our eaployees will continue to have C-8 in their blood. My charts and the specific coaaents made during the review are attached.
The following is a restatement of the specific prograa iteas in our C-8 control plan with the necessary action steps indicated.
I. ADMINISTRATIVE CONTROLS
A. EQUIPMENT DESIGN
1. IMPLEMENT AN IMPROVED FINE POWDER DRYER GASKET DESIGN (RESP - KU N E )
B. PROTECTIVE EQUIPMENT
1. AUDIT WASHINGTON WORKS C-8 IN BLOOD AND C-8 IN AIR DATA TO DETERMINE IF CURRENT PROTECTIVE EQUIPMENT (AND OPERATING PROCEDURES) ARE THE OPTIMUM AVAILABLE (RESP - LOSCHIAVO)
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C. A. UIJUS / J. A. awu*/ C-8 CONTROL PROGRAM PAGE 2 JULY 7, 1987
C. C-8 MONITORING 1. REDUCE EMPLOYEE BLOOD TESTING TO ONLY THE FOLLOWING JOBS: RAW DISPERSION AUTOCLAVE OPERATOR DISPERSION OPERATOR
FINE POWDER DRYER OPERATOR ENVIRONMENTAL OPERATOR (SUMP)
DISPERSION PACKOUT OPERATOR
GRANULAR POLYKETTLE OPERATOR FINE POWDER PACKOUT OPERATOR , m FEP POLYKETTLE OPERATOR FEP WET FINISHING OPERATOR FEP DISPERSION OPERATOR
FIRST LINE SUPERVISION OF ABOVE PERSONNEL
(RESP - LANYON) NOTE: BEFORE WE CHANGE OUR BLOOD SAMPLING PROGRAM, WE WILL WANT TO
HAVE AN INTERNAL BTO COMMUNICATION (RESP - ZIPFEL) 2. PERSONAL C-8 IN AIR SAMPLING - MONTHLY SAMPLES SHOULD BE REQUIRED OF
THE FOLLOWING JOBS: RAW DISPERSION AUTOCLAVE OPERATOR
GRANULAR POLYKETTLE OPERATOR FINE POWDER DRYER OPERATOR DISPERSION OPERATOR FEP POLYKETTLE OPERATOR FEP WET FINISHING OPERATOR
FEP DISPERSION OPERATOR (RESP - POLYMERS - OTT
COPOLYMERS - POST)
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C. A. DIKES / J. A. SCHMID 0-8 CONTROL PROGRAM PAGE 3 JULY 7, 1987
3. AREA C-8 IN AIR MONITORING - AS NEEDED BY AREA AROUND CRITICAL EQUIPMENT (e.g., FINE POVDER DRYERS) AND TO RESPOND TO HIGH LEVELS NOTED WITH PERSONAL SAMPLES (RESP - POLYMERS - OTT COPOLYMERS - POST)
NOTE: IN GENERAL, VE ARE TAKING FAR TOO MANY AREA SAMPLES AND NOT ENOUGH PERSONAL SAMPLES
4. DOCUMENTATION - EXPLANATIONS OF REASONS AND ACTION RESPONSE FOR AIR LEVELS (PERSONAL SAMPLES ONLY) ABOVE SOX OF THE AEL (0.S6 MPB) REQUIRE IMPROVEMENT IN THE DIVISION'S ENVIRONMENTAL SAMPLING BOOKS (RESP - POLYMERS - OTT COPOLYMERS - POST)
D. C-8 CONTROL LEVELS
1. ESTABLISH MAXIMUM SAFE C-8 IN BLOOD AND C-8 IN DRINKING VATER LEVELS (RESP - G. L. KENNEDY - HASKELL)
NOTE: ONCE A SAFE LEVEL IS ESTABLISHED, THOSE PERSONNEL EXCEEDING 50X OP THIS LEVEL WILL BB REQUIRED TO BE REMOVED FROM THE BXPOSURB AREA
II. PROCESS CHANGES
A. IMPLEMENT USE OF PURCHASED LIQUID C-8 AS IS'BEING DONE AT DORDRECHT AND CHAMBERS VORKS (RESP - POLYMERS - CRUM COPOLYMERS - HERRIDGE)
B. NEV SURFACTANTS
1. TBSA IN FEP - REDUCE PRIORITY ON THIS PROGRAM TO THE POINT VHERE BUSINESS NEEDS JUSTIFY FURTHER USE (QUALITY AND COST) (RESP HERRIDGE)
2. C-9, C-10, C-12 - NO ENVIRONMENTAL LIMITS ARE PLACED ON THE USE OF NEV SURFACTANTS
C. C-8 RECOVERY
1. FINE POVDER DRYER VENT - DEVELOP BASIC DATA TO IDENTIFY RECOVERY PROCESS BY 4087 (RESP - SCHNEIDER)
2. FEP AQUEOUS STREAMS - APPLY ABOVE TECHNOLOGY IF ECONOMICAL (RESP SCHNEIDER)
D. LUBECK VATER DISTRICT CONTAMINATION
1. ELIMINATE SUFERNATB PONDS - GOAL 15 NOVEMBER 1587 (RESP - FLENSBORG)
2. DETERMINE MODE OF CONTAMINATION (RESP - STEVART)
Attachments
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EID079684
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January 31, 2003
PFOA Pharmacokinetics Review David Gray, Ph.D.
Sciences International Inc.
1
A considerable amount of data on PFOA distribution and kinetics has been generated in studies on laboratory animals (Biegel, 1997; Goldenthal, 1978a,b; York, 2002; Thomford, 2001). These data reveal a complex relationship between dose, body-burden, and toxic effect.
Serum PFOA concentrations have been determined at various time intervals during repeated oral or inhalation dosing or after a single dose. Urine and fecal PFOA concentrations have also be obtained in some studies. Test species include rats, mice, hamsters, monkeys, and dogs. The data indicate that renal and developmental toxicity occurs in the female rat with PFOA serum levels of approximately 1 part-per-million (ppm). The currently-available compartmental PFOA kinetic model for humans indicates that a PFOA blood level of 1 ppm would be reached in exposed human populations if their only source of PFOA exposure was the consumption of drinking water at something less than 3 parts-per-billion (ppb). If human populations were additionally exposed to PFOA in air, the model indicates that it would take significantly less PFOA in drinking water to reach the 1 ppm blood level that results in toxicity to the female rat. The details of this analysis follow below.
[The data on the partitioning o fPFOA between serum and red blood cells indicates that, although there is a difference between serum concentration and blood concentration for PFOA, it is not large since most, but not all, blood PFOA is in the serumfraction. Therefore, serum levels and blood levels will be considered comparable without adjustment in the present report to simplify the presentation.]
1. Gender differences in sensitivity to the effects of PFOA exposure
Much attention has been given to the early observation that the male rat is much less efficient in clearing PFOA than the female rat (Hanhijarvi et al., 1982). Urinary, and to a lesser extent fecal
January 31, 2003
excretion, are the primary clearance processes for PFOA. PFOA is not thought to be metabolized and is excreted as the intact molecule.
2
A number of studies have reported that the active secretory mechanism responsible for the rapid urinary excretion of PFOA in the female rat is inhibited by testosterone in the male rat (Ylinen et al., 1989; Vanden Heuvel et al., 1992; Kudo et al., 2002). Consequently, the elimination half-life is much longer in the male rat (9 days) than in the female (4 hours) (Vanden Heuvel et al., 1991). This allows serum PFOA levels in male rats to reach much higher levels than in an equivalently dosed female. Other species also exhibit a considerable gender difference in the elimination of PFOA, e.g. the male hamster is more efficient than the female. Rhesus monkeys did not demonstrate a large sex-linked elimination difference (Goldenthal 1978b).
The greater accumulation of PFOA in a repeatedly dosed male rat results in the male exhibiting much greater toxicity than the female at the same dose level. This difference in apparent sensitivity has led investigators to consider the male rat to be the more susceptible gender and to base PFOA risk analysis on the male rat. However, if one considers differences in body-burden, the female rat is the more sensitive sex.
For most compounds, serum concentration is a reflection of total body-burden once steady-state is reached during a repeated dosing experiment or during chronic exposure to human populations. This is true whether or not a compound binds to serum proteins, such as has been reported for PFOA. In a recent 2 generation reproduction study in rats, York (2002), the high dose parental females exhibited toxicity (absolute and relative kidney weights and FI pup body weight) at a PFOA serum level of about 1 ppm. The parental males demonstrated more pronounced toxicity, but the average serum level in the equivalent high-dose group was very much higher at 45 ppm.
In an earlier 90-day study by Goldenthal et al. (1978a), serum PFOA levels showed an even greater difference between male and female rats. This study reported liver hypertrophy, pigmentation, and necrosis that was more pronounced in males than females. However, hepatocellular necrosis and diffuse sinusoidal hepatic congestion was reported in females at
January 31, 2003
3
doses o f 2.5, 18, 25, and 80 mg/kg/d. Serum PFOA levels in the 2.5 mg/kg/d female group averaged 0.15 ppm. Serum PFOA levels in the 2.5 mg/kg/day male rat group average 34 ppm. While the effects in males were more pronounced, their body-burden was over 200 fold greater than that of female rats at the same dose level. Again, these data suggest that female rats may actually be more sensitive to the effects of PFOA than males. A direct comparison of male and female rats at the same or similar serum PFOA levels in the same study is difficult because the range o f doses in any of the studies is not great enough to provide an overlap in serum levels.
If one considers nonhuman primates, the same magnitude of gender difference in elimination efficiency has not been reported. Goldenthal et al. (1978b) conducted a PFOA study in Rhesus monkeys. In this study, female monkeys had slightly higher serum PFOA levels than did males from the same dose group, indicating there is not a major gender difference in elimination. This study indicates that the large gender difference in PFOA elimination that has been demonstrated in rats is not present in Rhesus monkeys and may not occur in humans.
In summary, the available distribution and kinetic data for PFOA indicates that the female rat is likely the more sensitive sex when body-burden rather than administered dose is used as a dose metric.
2. The very long PFOA half-life in humans
The current estimate of the elimination half-life in humans is 4 years, much longer than any other species. This long half-life indicates that humans excrete PFOA much more slowly than other species. For long-term human exposures, PFOA would be expected to accumulate to high bodyburdens over very long periods (~ 20 years) before leveling out. Low-level environmental exposures to PFOA, accumulated over a long period, could eventually result in significant bodyburdens. The inability of humans to efficiently excrete PFOA potentially makes the chronicallyexposed human uniquely susceptible to PFOA toxicity. This long period of accumulation to high body-burdens in the human has not been directly factored into any risk estimation to date.
January 31, 2003 3. Risk estimation based on pharmacokinetic models
4
Based on available kinetic data, body-burden and the long elimination half-life of PFOA in humans are critical in estimating the risk resulting from human exposure to environmental PFOA concentrations. These considerations can be incorporated into quantitative estimates of human health risk through the development of a physiologically-based pharmacokinetic (PBPK) model. Although efforts are underway to develop such a model for PFOA in the rat and human, no such models have been published.
A simplified approach to obtaining the exposure/blood concentration relationship has been taken in the development of a compartmental model for PFOA based on kinetic principles without mechanistic and limited physiological descriptions (Hinderliter and Jepson, 2001). The stated purpose of the model was to provide decision-makers with an easily applied tool to relate PFOA exposure to concentrations in human blood. The model assumes that all PFOA is absorbed immediately and is eliminated from the body with a half-life of 1 year. The utility of using a model such as this is that takes into account the very long half-life of PFOA in humans.
The model is exercised over an exposure period of 6 years, which purportedly allows steadystate to be achieved and for blood concentrations to level out. Yet recent data indicates the PFOA half-life in humans is over 4 years. Thus, by assuming a half-life of one year, the model will substantially underestimate the steady-state blood level. A higher blood level is reached with the longer half-life because steady-state is not attained until around 24 years of accumulation rather than 6 years. The simplified model also assumes that there is no tissue distribution and that all PFOA is contained in the blood.
The model was exercised with various assumptions regarding input of PFOA via inhalation and/or ingestion of drinking water. The output of these calculations was presented as a matrix of blood levels resulting from combinations of air and water PFOA concentrations. As indicated above, the blood level in a female rat that results in renal and developmental toxicity is about 1 ppm. Using the simplified model, one can easily calculate the drinking water concentration that would result in a human blood level of 1 ppm PFOA. The simple model predicts a blood level of
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January 31, 2003
5
approximately 1 ppm would result from consuming 3 parts-per-billion (ppb) of PFOA in drinking water over a period of 6 years, assuming no PFOA exposure through air or other media. If the model were adjusted to incorporate the more recent estimate of human half-life of 4 years, a substantially lower level of PFOA in drinking water would be needed to reach the 1 ppm in blood level that produced toxicity in the female rat.
In summary, a simplified compartment model exists to estimate the relationship between PFOA drinking water and air concentrations and blood levels in human populations. The model indicates that a level of PFOA in human blood corresponding to level of PFOA in blood that caused renal and developmental toxicity in the female rat would result from the human consumption of water containing less than 3 ppb PFOA.
References
Biegel, L.B. 1997. Hazard characterization for human health C8 exposure CAS Registry No. 3825-26-1. DuPont Haskell Laboratory.
Goldenthal, E.I. 1978a. Ninety day subacute rat toxicity study. Final report prepared for 3M, St Paul, Minnesota, by International Research and Development Corporation, St. Paul, Minnesota, November 6, 1978.
Goldenthal, E.I. 1978b. Ninety day subacute Rhesus monkey toxicity study. Final report prepared for 3M, St Paul, Minnesota, by International Research and Development Corporation, St. Paul, Minnesota, November 10, 1978.
Hanhijarvi, H., Ophaug, R.H., and Singer, L. 1982. The sex-related difference in perfluorooctanoate excretion in the rat. Proc. Soc. Exp. Biol. Med. 171:50-55.
Hinderliter, P.M. and Jepson, G.W. 2001. A simple, conservative compartmental model to relate ammonium perfluorooctanoate (APFO) exposure to estimates of perfluorooctanoate (PFO) blood levels in humans. DuPont Haskell Laboratory for Health and Environmental Sciences.
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Kudo, N., Katakura, M., Sato, Y., Kawashima, Y. 2002. Sex hormone-regulated renal transport of perfluorooctanoic acid. Chem. Biol. Interact. 139: 301-316.
Thomford, P.J. 2001. 26-week capsule toxicity study with ammonium perfluorooctanoate (APFO) in Cynomolgus monkeys. Study performed by Covance Laboratories Inc., Madison
Vanden Heuvel, J.P., Kuslikis, B.I., and Peterson, R.E. 1991. Covalent binding of perfluorinated fatty acids to proteins in the plasma, liver and testes of rats. Chem.-Biol. Interact. 82:317-328.
Vanden Heuvel, J.P., David, J.W., Sommers, R., and Peterson, R.E. 1992. Renal excretion of perfluorooctanoic acid in male rats: Inhibitory effect of testosterone. J.Biochem. Toxicol. 7(1 ):31-36.
Wisconsin 53704-2592 for APME ad-hoc APFO Toxicology Working Group. Study No. Covance 6329-230, completion date December 18, 2001,159 pp.
Ylinen, M., Hanhijarvi, H., Jaakonaho, I., and Peura, P. 1989. Stimulation by estradiol of the urinary excretion of perfluorooctanoic acid in the male rat. Pharmacol. Toxicol. 65:274-277.
York, R.G. 2002. Oral (gavage) two-generation (one litter per generation) reproduction study of ammonium perfluorooctanoic (APFO) in rats. Argus Research Laboratories, Inc. Protocol Number: 418-020, Sponsor Study Number: T-6889.6, March 26, 2002.
