EPA Region 5 Records Ctr. Timothy Drexler/R5/USEP/VUS 02/08/2008 01:49 PM 290480 To [email protected]cc Joan Tanaka/R5/USEPA/US@EPA, Wendy Carney/R5/USEP/VUS@EPA, [email protected], [email protected], Mark Johnson/R5/USEPA/US@EPA, [email protected], Clayton Koher/r5/usepa/us@EPA, [email protected], [email protected], [email protected], [email protected], [email protected], [email protected], [email protected], [email protected], [email protected], [email protected], David Brauner/R5/USEPA/US@EPA, [email protected], [email protected], [email protected], Jane Neumann/R5/USEP/VUS@EPA, Barbara Wester/R5/USEPA/US@EPA, Thomas Turner/R5/USEPA/US@EPA, Monesh Chabria/R5/USEPA/US@EPA, Ed Fairbanks/R5/USEP/\/US@EPA, Don Debiasio/R5/USEP/\/US@EPA bcc Subject U.S. EPA on HH and Eco Risk Assessment: St. Regis Paper Co., Superfund Site Hi Tom: Attached are our comments on the Sept. 28, 2007 revised St. Regis Risk Assessment. A cover letter is also attached. Hard copies will follow. Please call me if you have any questions. Tim Drexler Remedial Project IVIanager Superfund Division United States Environmental Protection Agency 77 W. Jackson Blvd., SR-6J Chicago, Illinois 60604-3590 phone: 312.353.4367 fax: 312.886.4071 EPA_wPartnerCommentsJinal.doc EPA com final cover.doc
44
Embed
EPA Region 5 Records Ctr. · EPA Region 5 Records Ctr. Timothy ... Turner/R5/USEPA/US@EPA, ... Section 4.4.2 presents citations that are extremely selective.
This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
Subject U.S. EPA on HH and Eco Risk Assessment: St. Regis Paper Co., Superfund Site
Hi Tom:
Attached are our comments on the Sept. 28, 2007 revised St. Regis Risk Assessment. A cover letter is also attached. Hard copies will follow. Please call me if you have any questions.
Tim Drexler Remedial Project IVIanager Superfund Division United States Environmental Protection Agency 77 W. Jackson Blvd., SR-6J Chicago, Illinois 60604-3590
phone: 312.353.4367 fax: 312.886.4071
EPA_wPartnerCommentsJinal.doc EPA com final cover.doc
February 8, 2008 SR-6J Mr. Thomas C. Richardson Project Manager Environment, Health, & Safety Services Intemational Paper 6400 Poplar Avenue Memphis, Tennessee 38197
Re: U.S. EPA Comments on Revised Human Health and Ecological Risk Assessment for the St. Regis Paper Company Site, Cass Lake, MN: UAO Docket No. V-W-04-C-796
Dear Mr. Richardson:
Attached please find the U.S. EPA and agency partner comments on the revised version of the Human Health and Ecological Risk Assessment submitted on September 28, 2007. A complete revision of the document is not necessary. U.S. EPA will consider that an addendum which adequately responds to these comments is sufficient to satisfy the requirements of the Order for the Risk Assessment.
U.S. EPA will expect the addendum 30-days from the receipt of this letter. After you have had an opportunity to review these comments, please contact me at (312) 353-4367 or at drexler;[email protected] if you have any questions.
Thank you for your attention. 1 look forward to the successful close-out of this Order in the near future.
Sincerely,
Tim Drexler Remedial Project Manager
cc: S. Nordrum, LLBO S. Johnson, MPCA R. Messing, MDH M. Johnson, ATSDR K. Peters, City of Cass Lake T. Ross. IP
CuiTent Future (Area A) and future (Area B) Reasonable maximum exposure Not applicable
Hazards (no fish or rice) from Table 4-17 Risks (no fish or rice) fi-om Table 4-20 Risks and hazards for fish and rice from Table 4-21
The development of medium-specific data sets is a critical element of any human health risk
assessment (HHRA) because these data sets form the basis of other risk assessment
calculations such as chemical- and exposure pathway-specific exposures. Tables 2-1 through
2-7 present medium-specific data evaluations. Because the fish tissue data set for St. Regis is
very complicated and potential exposures through ingestion offish tissue are relatively large
compared to exposures to other media, Table 2-7 was reviewed as an example to evaluate
whether medium-specific data evaluations were accurate and adequately documented. EPA
identified a number of issues in the review of Table 2-7; these are summarized below along
with a statement of necessary revisions.
The data selection decisions (that is, the selection of sample-specific analytical results for each analyte group) were evaluated against the decision mles presented in Section 2.2.3. One case was identified in which the data support selection of different results from those specified in Table 2-7, as discussed below.
Regarding sample SL-T-0404-E (2004 LLB-F), Table 2-7 indicates that dioxin/furan results from the ETL laboratory were selected because of "more detected values." However, the decision mles (Section 2.2.3) do not mention number of detections, and Table 2-7 does not report any bias for the data. The CAS laboratory results are the preferred investigative results, and the detection limits (DL) from the CAS laboratory are lower than those for the ETL laboratory as reported in Table 2-7. Therefore, dioxin/furan results from the CAS laboratory should be selected.
The selection of one data set over another for PAHs, PCBs (Aroclor), and PCBs (total) are not documented in the comments section in a variety of cases (see, for example, the selection of the PCBs [Aroclor] data set for CL-S-15 and the selection of the PAHs data set for BSL-S-0403-E). The selection of PAHs, PCBs (Aroclor), and PCBs (total) data sets should be documented in Table 2-7.
In three cases, analytical results for several IP samples collected as part of the 2001 IP sampling event are attributed to the LXX laboratory; however. Table 2-7a in the 2005 risk assessment attributed these results to the CAS laboratory (see samples CL-WH-52, PB-W-31, and PB-WH-33). The source of these analytical results should be verified and corrected as necessary.
Table 2-7 does not include the National Lake Fish Tissue Study (NLFTS) samples used in the background comparisons. Table 2-7 should be revised to either add the NLFTS samples or provide a note directing the reader to the appropriate tables in Appendix C where the NLFTS results are presented.
Table 2-7 and the other medium-specific data evaluation tables should be closely reviewed to
ensure accuracy, documentation, and adherence to the selection criteria discussed in
Section 2.2.3.
4. Tim Drexler, the EPA Remedial Project Manager, sent a letter to IP regarding usability of
laboratory data in support of the St. Regis Paper Company Superfimd Site, Cass Lake,
Minnesota; the letter is dated July 10, 2007. Under the heading "ETL Fish Tissue Data
(2001, 2002)" the letter specified that initial analyses for fish tissue samples CL-WH-14 and
CL-S-29 should be rejected and "the average [toxic equivalents] TEQs from the replicate
analyses of these two samples must be used." However, Table 2-7 states that dioxin and PCB
resuhs from Alta (CL-WH-14R) and Paradigm (CL-S-29) should be used based on lower
detection limits.
An e-mail dated October 26, 2007, from Eric Morton, Tetra Tech EM Inc., to Bill Locke,
Integral Consulting, requested additional documentation to determine whether averaging had
taken place as requested by EPA. In an e-mail response dated November 5, 2007, Integral
Consulting reiterated that the Alta (CL-WH-14R) and Paradigm (CL-S-29) results had been
used instead of the ETL replicate results for the reasons stated in Table 2-7, and "in
accordance with the data selection mles laid out in Section 2.2.3 of the risk assessment."
A misunderstanding appears to have occurred. EPA's directive that "average TEQs from
replicate analyses will be used" for CL-WH-14 and CL-S-29 reflects a resolution of unique,
sample-specific circumstances that supersedes the general data selection rules laid out in
Section 2.2.3 of the risk assessment. If EPA had desired that the initial analyses for CL-WH-
14 and CL-S-29 be rejected and the replicate analyses considered in accordance with the data
selection mles, this sentiment would have been spelled out. Instead, EPA clearly indicated
that the initial analyses be rejected and "the average TEQs from the replicate analyses of the
two samples must be used." Therefore, Table 2-7 specifically, and the remainder of the
HHRA (in particular, Appendix C and fish tissue-specific exposures, risks, and hazards),
should be revised accordingly.
5. The complexity of the technical assessments and size of the risk assessment report make it
difficult for reviewers to independently reproduce a number of the findings and, therefore,
corroborate the main conclusions of the study. In particular, some instances lack
transparency in the manner in which data are presented and results of calculations and
individual analyses are summarized in tables and figures. It is suggested that some revision is
needed to increase the overall accessibility of the data and results of analyses used to support
the risk assessments, and to allow more efficient navigation through the various sections of
the report. The following are examples of changes that could be incorporated to make the
findings more transparent and to aid readers in accessing key data and results:
• The supplemental Excel files provided by IP (through Integral) on November 30, 2007, to document the calculation of media-specific exposure point concentrations (EPC) should be re-formatted in a manner appropriate for inclusion in the report. In particular, location or sample identifiers should be presented alongside individual results used in each EPC calculation to allow for easier cross-referencing with the flat files. Totals that represent the sum of multiple constituents should include columns to indicate the total number of constituents and number of nondetect constituents used in the calculation of each location- or sample-specific total.
• The recommendation in the bullet above should be extended to all tables presenting summary results for multiple-constituent totals, especially when the purpose is to evaluate the impact of using different simple-substitution approaches (e.g., zero versus one-half DL) for nondetects. Also, in cases where results are summarized for individual exposure areas, sample sizes should be included in each table (e.g.. Table 4-25).
• For all of the site versus background or reference comparisons in Appendix A, B, and C, it would be usefiil to provide a side-by-side presentation of the results of tests of central tendency and upper quantiles, along with general summary information for the site and background populations. That is, in order to fiilly evaluate the conclusions drawn for each of these comparisons, readers need to consult one or more tables to obtain the sample size and detection frequency for each population, and two additional tables for the results comparing central tendency and upper quantiles. Having all of this information on a single table would be a more effective complement to the box-plot figures, and would allow independent reviewers an opportunity to judge the strength of conclusions drawn strictly from application of statistical tests. This is especially important in cases where sample sizes and/or detection frequencies are low, and basing decisions on qualitative assessments of the data might be pmdent.
6. Tables 2-8 through 2-20 summarize media-specific nondetect results that were excluded from
analyses because they exceeded the maximum detected datum (i.e., referenced as "biasing
non-detects"). It is not clear from the footnotes in these tables, or the text in Section 2.2.2.1,
exactly how these high nondetect results were identified. It is acknowledged that nondetect
results that exceed the maximum detected datum provide no useful information for
calculating UCL-based EPCs for single constituents. However, in cases where EPC
calculations are performed for an individual medium and exposure area, identification of
biased nondetects logically would be based on the maximum detected datum in each medium-
specific exposure area. This appears to be what the authors have done, at least in selected
cases (e.g., Appendix A, page A-4, last paragraph and Appendix B, page B-4, third
paragraph). In these cases, please include a colunm in each table that summarizes excluded
non-detects, and to list the maximum detected datum in each exposure area that was used to
screen out biasing nondetects. A short statement should also be inserted in Section 2.2.2.1 of
the main text in order to more clearly explain exceptions to how biasing non-detects were
handled in different analyses.
Less straightforward are identification and removal of these high nondetects in cases where
multiple constituents are summed at individual locations to calculate a total. In this context,
individual constituents are no longer evaluated as a population of results (i.e., all media-
specific results are not being pooled to calculate an EPC for each constituent), so comparison
to the maximum media-specific detected concentration does not seem appropriate. In these
cases, it seems more appropriate to include all nondetect constituents in the calculation of
each total, using each of the simple-substitution options. It is not clear if biasing non-detects
were treated any differently for estimates of totals,please provide additional text to the main
report and appendices, where appropriate, to explain how nondetects were treated under this
scenario.
Again, please provide additional text and/or footnotes to clarify how biasing nondetects were
treated in both the single- and multiple-constituent cases described above.
7. The primary cumulative exposures considered in the risk assessment reflect potential
residential and recreational exposures by the same receptor. Additional cumulative
exposures, unique to or more likely to occur in a small community such as Cass Lake
(including the Leech Lake Indian Reservation), also occur and should be considered in the
risk assessment. EPA recently became aware that a public works employee (site worker)
lives near the site. It is not unreasonable that a similar individual may also perform
constmction/utility work at the site. Therefore, the risk assessment should be revised to
identify and discuss such additional cumulative exposures; evaluate potential cumulative
exposures, risks, and hazards (based on potential residential, recreational, site work, and site
construction/utility work); and discuss any potential uncertainties associated with estimating
such a cumulative exposure (for example, potential double-counting).
8. Several potential exposure pathways are only briefly identified and dismissed in the risk
assessment. Exposures, risks, and hazards are not quantified for these exposure pathways.
However, these exposure pathways (ingestion of aboveground produce and fish eggs) are
well known to the local community and, in the case of the ingestion of aboveground produce,
have been evaluated as part of other risk assessments in Minnesota and throughout Region 5.
The risk assessment discusses the potential for contamination of aboveground produce
through root uptake of chemicals. However, aboveground produce may also become
contaminated through the deposition of fugitive dusts. The risk assessment (including the
uncertainty analysis [Section 4.6]) should be revised to discuss the potential for aboveground
produce to become contaminated through deposition of fugitive dust and the potential for
receptors to become exposed to chemicals through ingestion of aboveground produce
contaminated in such a manner.
Also, the risk assessment briefly discusses the potential for exposure through ingestion of fish
eggs, and dismisses this exposure pathway because the contribution to total exposure via
ingestion offish eggs is very small as compared to the contribution assumed through
ingestion of fish tissue. However, the risk assessment does not discuss the fact that chemical
concentrations (particularly for lipophilic compounds) are often higher in fish eggs than in
fish tissue. The risk assessment (including the uncertainty analyses [Sections 4.6 and 5.5])
should be revised to discuss the impacts of not considering potential ingestion of fish eggs.
The discussion should consider not only the relative mass of fish eggs ingested as compared
to other fish tissue, but also the relative chemical concentrations in fish eggs as compared to
those other tissues, especially with regard to bolus dosing of fish eggs by residents during fish
spawning season.
9. It is recognized that the calculations involved in a HHRA of this magnitude are necessarily
complex. However, many of the Excel files and worksheets within the files were difficult to
navigate and hard for the user to follow. It would be helpful if the calculations and individual
Excel worksheets were more transparent for the user.
For example, with all 14 of the Risk Calculation spreadsheets open at one time, some of the
actual links are to files not included on the compact discs (CD), but located elsewhere. For
example, one link apparently is not to the actual Parameter_Risk.xls file that is grouped on
the CD. Instead, the spreadsheet references this same file as part ofa series of files under the
header "Sarah Scott." However, the calculations were determined mathematically correct
when the information presented in the "Parameter_Risk.xls" file on the CD was used in the
equations even though the "Parameter_Risk.xls" file wasn't directly referenced. Please limit
references to files on the CDs submitted with the HHRA.
10. The risk characterization discussion in Section 4.5 periodically refers to Appendix D4 as the
general location of receptor-, exposure pathway-, and chemical of potential concem (COPC)-
specific exposure, risks, and hazard results. However, Appendix D4 contains a large number
of tables (over 500 pages). Please include references to specific tables when calling out
particular results such as maximum hazards and risks. For example, in Section 4.5.1.1, the
text states "Future CTE and RME hazard indices for a child resident at the second highest
location (RES-8) with soil mixing are 0.4 and 0.8, respectively (Appendix D4). It is very
difficult to go to Appendix D4 as a whole and verify that (1) RES-8 is the second highest
location and (2) the identified CTE and RME hazard indices are correct. Section 4.5 should
be revised to include references to specific tables in Appendix D4 to support the
identification and discussion of particular risk and hazard results in the text.
11. The results of the ongoing non-aqueous phase liquid (NAPL) investigation could affect
conclusions about ecological risks at the site. Therefore, the text should (1) mention the
ongoing NAPL investigation, (2) indicate that the ecological risk assessment (ERA) did not
evaluate the groundwater-to-surface water pathway, (3) explain that conclusions about
ecological risk are independent of possible risks associated with NAPL releases to habitats at
the site, and (4) state that the ecological risk assessment may be updated after evaluation of
the results of the NAPL investigation.
12. A variety of editorial inconsistencies, omissions, and errors regarding referencing, acronyms,
and abbreviations throughout the text are suinmarized as follows:
• Referencing - incorrect references are cited in text (e.g., USEPA 2002e for National Functional Guidelines [pg 2-2] and USEPA 1992c for EPC guidance). Also, references cited in text are not listed in Section 6 (References) (e.g., Van Wijnen et al. 1990 [pg 4-60]). Finally, duplicate references are in Section 6 (e.g.. Sample and Arenal 1999; Wild and Jones 1992).
• Acronyms and abbreviations ~ acronyms and abbreviations used in the text are missing from the acronyms and abbreviations list (for example, NPDES [pp 1 -
10
12] and numerous others including many units of measure). Various acronyms and abbreviations in the text are not defined on first use (for example, 2,4-D, DDx, and TEQ). At least one acronym is defined in two different ways (RAL is defined as "response action level" in the acronym and abbreviation list and in the text [see page 3-9], but also as "removal action level" in the text [see page 1-10].
The entire risk assessment should be closely reviewed and revised as necessary to eliminate
editorial inconsistencies, omissions, and errors regarding referencing and acronyms and
abbreviations. The specific instances identified in the two bulleted items above are examples
only, and do not encompass all editorial inconsistencies, omissions, and errors that require
correction or clarification.
11
HUMAN HEALTH RISK ASSESSMENT SPECIFIC COMMENTS
1. Section 1.1. Pages 1-1 and 1-2. Section 1.1 presents a summary of the human health risk
assessment. This section states that there are no site-related noncancer risks to current
residents. As noted in Specific Comment 6, the interim remedial measures consisting of the
placement of clean topsoil at residences cannot be considered final and cannot be assumed to
provide long-term effectiveness without additional efforts to eliminate further transport of
contaminated site soils onto nearby residences and to continue maintenance of clean topsoil at
nearby residences. Therefore, Section 1.1 should be revised as specified in Specific
Comments 7 and 8, and to indicate that adverse noncarcinogenic risks may exist at specific
residences under current conditions.
Also, as stated in General Comment 1, the HHRA should be revised to incorporate risks and
hazards associated with ingestion offish into receptor-specific total risks and hazards.
Receptor-specific risks and hazards based on fish ingestion alone, and total risks and hazards
including fish ingestion results, exceed EPA's risk range (see the tribal receptor) and a hazard
index of 1 for both general population and tribal child receptors. Section 1.1 should be
revised to incorporate risks and hazards based on fish ingestion.
2. Section 1.4, Pages 1-4 through 1-6. Section 1.4 discusses the site setting and history. There
is no mention that the site, as currently defined, lies entirely within the Leech Lake Indian
Reservation. Section 1.4 and associated figures (for example, Figures 1-1 and 1-2) should be
revised to clearly state and show that the site lies within the Leech Lake Indian Reservation.
3. Section 1.4.1. Page 1-7. Paragraph 1 and Section 1.4.2. Page 1-7, Paragraph 5. The text
states that at both locations, sludge from the wood-treating operations was reportedly
transported "to a pit at the city dump and periodically bumed by the City." The only
reference for these statements is a personal communication with a former St. Regis Company
employee. No further documentation of direct involvement by the City of Cass Lake in the
buming of sludge from wood-treating operations is provided. The City of Cass Lake has
denied directing or participating in the buming of such sludge at the city dump. Both sections
should be revised to tmncate the statements at the phrase "periodically bumed," provide more
direct evidence of the City's involvement, or clarify that the City denies any direct
participation in the buming of wood-treatment sludge at the city dump.
12
4. Section 1.4.4. Pages 1-9 through 1-11. Section 1.4.4 discusses the site regulatory history.
Nowhere in the discussion is the Leech Lake Tribal Govemment mentioned, despite the
Band's important role in the Site's regulatory process. Section 1.4.4 should be revised to
summarize the Band's role in the Site's regulatory process.
5. Section 1.4.4. Page 1-11. Paragraph 1. This paragraph refers to a removal action on city
property. WTdle soil was removed from City property, clean fill was not placed over the
excavated area. The placement of clean fill over any excavated area will help to minimize
dust issues for neighboring residences. Therefore, Paragraph 1 should be revised to add the
following clause after the first sentence of Paragraph 1: "Soil was removed, but clean soil
was not placed on top of the excavation site."
6. Section 1.4.5. Page 1-14, Paragraph 1. In part, the text states "fieldwork was performed
from June to October 2004, with final restoration being completed in June 2005." It should
be stated that IP's planting of vegetation and grading to address the slope and mnoff issues
that had been created during the initial excavation is considered a final restoration only for
the purposes of the time-critical removal action ordered by U.S. EPA and does not preclude
to calculate medium-specific EPCs. The text states "EPCs for each medium in each exposure
21
unit and descriptive statistics are presented in Appendix D-2. The data points included in the
EPC calculations are also shown in Appendix D-2." Several elements of this statement are
incorrect and should be corrected, as discussed below.
Appendix D2 does present medium-specific EPCs. However, the results are presented
without any documentation. Specifically, contrary to the statement in the text, Appendix D-2
does not present (1) descriptive statistics or (2) the data points used in the EPC calculations.
Without this information, it is not possible to verify the medium-specific EPCs presented in
Appendix D-2 and used in the exposure calculations. Appendix D-2 should be revised to
include descriptive statistics and the data points used for each medium-specific EPC
calculation. Because EPA's ProUCL software was used to calculate many (if not the
majority) of the medium-specific EPCs, Appendix A-2 should also be revised to include the
outputs from each ProUCL calculation. (Note: the requested information was provided to
EPA as part of an electronic mail message from Bill Locke of Integral to Eric Morton of
Tetra Tech, dated November 30, 2007. Based on review of the information provided, EPA
feels that this information, along with additional documentation, is required to increase the
transparency and verifiability of the EPC calculations as discussed in General Comment 4).
34. Section 4.3.3.3. Page 4-44. Paragraph 2. This paragraph states that a trench depth of 4 and
6 feet below ground surface (bgs) was assumed for Areas A and B, respectively, based on
depth to groundwater. Given the depth of frost in northem Minnesota, many utilities are
buried 6 feet deep. Presumably, pumping could be performed to allow excavation below the
water table. Section 4.3.3.3 and other relevant portions of the risk assessment should be
revised to evaluate the impact on trench modeling results if the trench depth in both Areas A
and B is increased to 6 feet or more (a trench would likely need to be excavated deeper than 6
feet to repair a utility installed at a depth of 6 feet). For example, a lower air changes (ACH)
value would be appropriate if worker's heads would not extend out of the trench.
35. Section 4.3.4.2, Page 4-53. Paragraph 4. This paragraph presents the assumption that
exposure to outdoor soil occurs only during "the seven warmer months when snow is not
covering the ground." This assumption is valid only if there is snow cover, however. Over
the past four years, snow cover in the site area has not been complete during the assumed
five-month period. Therefore, the risk assessment should be revised to indicate that this
22
assumption may lead to an underestimation of potential exposure to outdoor soil to the extent
that snow cover is absent during the assumed five-month period.
36. Section 4.3.5.2. Pages 4-63 through 4-65. This paragraph discusses the use of a relative
bioavailability (RBA) factor in exposure estimates related to exposure to soil and house dust.
The same RBA factors were used for both soil and house dust. However, the smaller dust
particle size and increased digestible organic content found in dust may result in an increased
bioavailability. Section 4.3.5.2 and the uncertainty analysis (Section 4.6) should be revised to
discuss the uncertainty introduced by assuming the same RBA factors for both soil and house
dust.
37. Section 4.3.5.2. Page 4-65. Paragraph 1. The text indicates a RBA value of 0.9 was used
for pentachlorophenol (PCP). However, Table 4-11 indicates that a value of 1 was used.
This discrepancy should be resolved.
38. Section 4.3.6.3. Page 4-74. Paragraph 1. The text states "It is unlikely that loadings of Fox
Creek and channel area sediments on skin would reach the monolayer coverage required to
attain the adherence factors found in the Shaof et.al. studies." No explanation or
documentation is provided for this statement. Section 4.3.6.3 should be revised to include
adequate explanation and documentation to support the statement regarding reaching
monolayer coverage.
39. Section 4.3.8.2. Page 4-87. Paragraph 4. The risk assessment narrowly defines the utility
worker, limiting possible groundwater exposure to utility/constmction workers excavating
trenches. However, the groundwater is very shallow at the site, especially at the former
operational area where high levels of contamination are present. There could be potential
exposure to workers engaged with any type of constmction that involves grading or
disturbing soil in this area. Also, any type of general constmction work in this area might
require groundwater dewatering because of the shallow water table, which is about 5 feet bgs.
Therefore, the risk assessment should be revised to indicate that potential exposure to
groundwater may not be limited to only utility/constmction workers digging trenches, and
that any type of general constmction work at the site may require dewatering because of the
shallow groundwater table.
23
40. Sections 4.4.1.3 and 4.4.2, Pages 4-105 through 4-120. These secfions discuss the toxicity
assessment of mixtures and present a dose response assessment for mixtures of dioxins,
furans, and dioxin-like coplanar PCBs. Section 4.4.2 presents citations that are extremely
selective and, in many instances, lack references. In particular, use actual references rather
than referencing communications with Tim Drexler of EPA. Also, when stating that "EPA's
cancer-based approach ., .is counter to the risk assessment approach conducted by several
other health agencies..." state what your references are and what agencies you are discussing.
This section must be rewritten to include references for cited information and must present a
more balanced discussion that incorporates and evaluates the following additional
information.
• Toxicity assessment of mixtures - EPA has its own guidance. One important thing to understand about mixtures is that interactions are usually a high dose phenomenon.
• For mixtures of PCDDs/Fs/Bs - the reader should immediately be referred to the WnO results. These are NOT drafts. The fiill publications from the 1993, 1997, and 2005 meetings are all published (Ahlborg, 1994; Vandenberg, 1998, 2006) and are used internationally. These were essentially updates from the original 1987 and 1989 EPA TEFs for PCCDs/Fs and the 1988 NATO values. For inclusion in the TEQ approach, compounds must be stmcturally related, have a common mechanism of action, cause a common spectmm of responses, and be biologically persistent. Persistence is a KEY requirement.
• This document focuses ONLY on the negative comments made in the SAB and NAS reviews, which overall were extremely complimentary and positive. In fact, the 2000 SAB stressed that they did NOT need to see a revised document and wanted EPA to just "get it out". The NAS also asked for some clarification and transparency, but said that the document should also be rapidly finalized and released, with several of the issues they raised really research projects.
• While cancer is often the focus of the discussion of dioxins, there has been growing concem for the non-cancer effects. If the EPA's analyses are correct, and the upper bound for cancer could result in 1/1000 excess risk, this would not be seen in the general population where 1/3 get cancer anyway. The effects can only be seen in large population-based studies. The entire issue of dioxin being a "known human carcinogen" was extensively debated at the 1997 lARC meeting as well as by DHHS - all concluding that dioxin is a known human carcinogen. The general consensus in the scientific community is that dioxin is a human carcinogen - where most of the discussion centers is the dose issue. lAR fully discussed the issue of increase in all cancers and concluded that while unusual, it was possible for dioxin, because of its ability to promote tumors in multiple tissues. There is also evidence for respiratory-tract cancers and breast cancer in humans, among other sites. Some of the data from Seveso, where peak dioxin concentrations were measured - not extrapolated - support the human carcinogenicity.
24
•
While the traditional approach for non-cancer risk assessment assumes a threshold, the extensive modeling done in the dioxin reassessment (see Chapter 8 of the dioxin reassessment) clearly showed that while many responses were best fit by a non-linear model, a nearly equivalent number were best fit by a linear model. These results are also part of the 1998 WTIO assessment of the TDI for dioxins.
EPA made a policy decision not to develop an RfD for dioxin. The SAB asked EPA to do so both in 1994 and 2000. EPA preferred to use a MOE approach.
The underlying data for both cancer and non-cancer risk assessments used by many intemational organizations were all based on the 1998 WHO analysis. The same data were used by EPA in the document reviewed by the SAB in 2000. It is important to remember that the NAS did NOT review the entire dioxin reassessment, but only the executive summary, with some attention to the dose/response modeling chapter (8) and the TEF chapter (9). The vast amount of supporting information was in all of the background chapters. In fact, in the dose-response modeling chapter, the results for both linear and non-linear models for both cancer and non-cancer responses were given. In fact, essentially all of the animal cancer responses were modeled. One reason that the Kociba data was carried forward into the executive summary and the linear model used was that the CSF from this model was almost identical to that determined from several human occupational cohorts. And the fact that a linear model best fit the human data was published by Kenny Cmmp in 2003, as well as work by Kyle Steenland.
The TDI established by WHO in 1998 was 1-4 pg TEQ/kg/d. This was a tolerable - not a "safe" - level. The group did NOT want to declare much of the world's food supply at the time "contaminated."
There are multiple problems with the ATSDR MRLs for dioxin. They did NOT account for pharmacokinetic differences between animals and humans. If they had done so, their MRL would be 10 to 100-fold lower.
The "history" is selective. For example, the charge to the NAS was quoted selectively (as are the recommendations). The 1984 dioxin risk assessment CSF is still used throughout EPA. In addition, the comments of the SAB and NAS are selectively cited.
The pharmacokinetic issues are not as simple as stated. There is growing consensus that the elimination of dioxins is dependent upon dose and body composition: at high doses, elimination is more rapid; at low doses, body fat content increases the half-life. This has been elegantly described, with the consequences, by the PBPK modeling work of Emond et al (2005, 2006). Aylward has used a classical modeling approach and come to similar conclusions (note: citing Aylward, 1996 is NOT the right citation - her work is in 2005 and 2006). EPA would agree that we may be underestimating the peak exposure concentration by simple back extrapolation. But we do not know if the key issue, especially for cancer, is peak or lifetime exposure.
Both the 2000 SAB and the 2006 NAS panel members were split on some of the conclusions. All members wanted more transparency and clarity.
Smoking was accounted for in most of the cancer studies. For many of the occupational studies, the exposure was predominately to TCDD. For those in which there was
25
•
•
•
substantial TEQ< that was modeled too. There is more data today, supporting the carcinogenicity of dioxins, from Seveso and from the Vietnam experience - Ranch Hand, Korean, and New Zealand vet studies.
In environmental epidemiology, small increases in relative risk or odds ratio is the best that can be expected. Also, the NRC's criticism that EPA should have modeled all of the animal tumor data indicates that they missed what was done in chapter 8.
We know of no credible scientists who do not believe that the mechanism of actions involves persistent activation of the Ah receptor. This is no different than the acceptance of the mechanism of action of estrogens involving activation of the estrogen receptor. It is the necessary step to initiate the process. The AhR has been shown to function siinilarly throughout the vertebrates. Dioxin causes multiple effects in multiple species at multiple developmental stages in both sexes. A given species can be an outlier for a given response - but we have no evidence that any species studied is an outlier for everything. Even the "resistant to die" adult hamster readily succombs to developmental toxicity. The issue of sublinear responses at low doses is also not tme when dealing with additivity to background issues. The AhR is a key regulatory protein; dioxin interferes with essential pathways. There is a growing body of evidence that the AhR is a tumor suppressor - dioxin treatment thus allows tumors to be expressed. The data coming from studies with both constitutively expressed AhR mice (paralleling dioxin treatment) and AliR-knockout mice is extremely infonnative.
Tumor promotion is often thought to be reversible - up to a point. The reversibility of dioxin tumors was examined in a stop-study conducted by the NTP (work by Nigel Walker and others). They found that when they stopped dosing, some of the tumors regressed but others grew even bigger. Bottom line - the animals still had malignant tumors.
The liver tumors in the Kociba study were NOT all associated with hepatotoxicity. In several cases, there were tumors in animals with no liver toxicity at all.
This document cites criticisms of EPA's 2000 SAB version when it suits the author, even though some of these issues were addressed in the revised 2003 draft. For example, modeling of the human cancer epi data was included in the 2003 version - and matched the Kociba liver tumor models. Citing repeatedly the Pohl, 2002 criticisms is inappropriate.
Despite the NAS comments, in the 2003 draft, EPA did use both linear and non-linear models for cancer and non-cancer. They are all in chapter 8.
A misunderstanding (?) of linearity is that it has to go through "zero". That is not what linear means. If there is a background level of response, which there is for most biological processes, extrapolation should NOT go through zero.
The wide range in ED levels is a function of differentially susceptibility for different responses. That is NOT an uncertainty, but a biological reality.
The discussion of TEFs is poor. There is intemafional consensus to use the "new" 2005 WHO TEFs. The re-evaluation was planned by WTIO from its 1997 meeting, it was
26
NOT driven by issues with the data base. Improvements in the quality of the data base were always wanted. In fact, the TEF values are only slightly different from the 1997 TEF values: in part the changes were driven by the decision to go to a logarithmic scale (1, .3, .1, .03....) from the ordinal scale (1, .5, .1, .05...). Other changes were based on new data. It is a mistake to over-value the new excellent NTP data - it is still one study in one sex of one strain of one species. In general, however, for the congeners examined, the NTP comparative potency values are very close to the WHO TEFs. Among issues stressed by the 2005 WHO committee was that the TEFs are based on intake - not intemal doses; and certainly not soil/sediment/air values for which an approach using fate and transport modeling should be developed in the fiiture. Also, the group pointed out the need for development of TEFs for other classes of compounds which meet the criteria of the TEQ approach - especially the brominated dioxins and fiirans.
• The issue of non-additive effects when dealing with the TEFs is incorrect. There is NO evidence for anything other than additivity when dealing with the 29 dioxin-like PCDDs/Fs/Bs. The non-additivity can occur in the presence of NON-dioxinlike compounds, such as some of the PCBs. But such interactions can be either synergistic or antagonistic, depending on the dose and the response. In fact, at low doses, there is little evidence for anything other than simple additivity.
• A limited number of the 29 congeners which have TEF values drive the total TEQ in people: TCDD, 1,2,3,7,8-PeCDD; 2,3,4,7,8-PeCDF, and PCB 126 account for over 70 percent or more of the TEQ in people. There is extensive experimental data to derive TEFs for these congeners.
• The WnO committee, as well as the SAB and the NAS, all concluded that while the TEFs are not perfect, they are a reasonable approach and work. The revisions of the TEF values result in a 10 to 25 percent decrease in the total TEQ in several data sets - depends on the "Matrix" and the exposure sources.
41. Sections 4.5.1.1 and 4.5.1.3. Sections 4.5.1.1 and 4.5.1.3 discuss noncancer health hazards
for Areas A and B, respectively. The text discusses hazards that exceed 1. However, the
COPCs driving hazards greater than or equal to 1 are not identified. Sections 4.5.1.1 and
4.5.1.3 should be revised to identify hazard drivers.
42. Section 4.5.1.2. Page 4-130. Paragraph 2. The results presented in this paragraph are very
difficult to follow and are not at all transparent. For example, the text states "For both
children and adults, the current hazard index at the location with minimum pre-IRM soil
concentrations (RES-05) is 30 percent of the pre-IRM value (Table 4-16)." However,
Table 4-16 does not clearly support this statement; ratios of current HI to past HI range from
0.1 to 4.1 for potential exposures to soil and indoor dust. Section 4.5.1.2 (and Table 4-16)
should be revised to provide clear documentation and explanation for all results presented so
that these results may be more easily understood and verified. As discussed in General
Comments 4 and 5, the overall transparency of the risk assessment must be improved
27
(consistent with EPA guidance and policy) to allow risk managers and the general public to
better follow, understand, and verify the exposure, risk, and hazard results presented and
for Area B. The text indicates that cancer risk estimates do not include ingestion offish.
29
Potential exposure through ingestion of fish tissue is evaluated separately from other
pathways and not included in totals because "concentrations of dioxins/furans (as TCDD
TEQdf) and PAHs (as BaPE) in fish . . . from Cass Lake and Pike Bay are not higher than
concentrations of these chemicals in fish . . . from background reference lakes." As discussed
in General Comment 1, based on the overall equivocal statistical results, it is appropriate and
consistent with a health-protective mandate to conservatively conclude that concentrations of
dioxins/furans and coplanar, dioxin-like PCB congeners (as TEQdfp), and Aroclor 1260 may
be higher in fish from Cass Lake and Pike Bay than in fish from background reference lakes.
Therefore, exposure and risk results associated with potential ingestion offish should be
included in the body of the text and considered as part of total exposures and risks (see
illustrative examples in General Comment 1).
49. Section 4.6.2.5. Page 4-164. Paragraph 3. Section 4.6.2.5 discusses the sensitivity of the
risk and hazard results to changes in the dermal absorption factor. The text discusses the
impact of decreasing the dermal absorption factor for all chemicals by a factor of 10. No
basis is provided for selecting a factor of 10. Section 4.6.2.5 should be revised to provide a
basis for the selection ofa factor of 10 in the dermal absorption factor.
50. Section 6. Section 6 presents the references cited in the HHRA. Most listed references were
cited in the text. However, the following errors or omissions were identified and should be
corrected:
• The reference Bomschein (1994) is apparently not cited in the text.
• The reference identified as "FWP" should be revised to add the year of publication to the reference immediately after the source of the reference.
• The reference identified by the acronym "OEHHA" should be revised to spell out this acronym.
• The reference identified as "Sample and Arenal. 1999a" is presented twice; the duplicate reference should be removed and the date changed from 1999a to 1999 on the remaining reference.
• The references "St. Regis Paper Company. 2007" and "USEPA. 2004a" were apparently not cited in the text.
• The reference identified as "Wild and Jones. 1992a" is included twice; the duplicate reference should be removed and the date changed from 1992a to 1992 on the remaining reference.
30
51. Table 2-1. Table 2-1 presents the soil data evaluated for use in the risk assessment. In
several cases, data were excluded for unacceptable reasons. These reasons are summarized
below:
• "Samples of stained material in roadway collected at unknown depth." It is acknowledged that roadways do not fall into any of the exposure areas considered quantitatively in the risk assessment. Nonetheless, various receptors may be exposed directly or indirectly (for example, generation of fugitive dusts) to soils from roadways.
• "Excluded: Topsoil used to backfill excavated areas on the Allen property during the removal." Receptors may still be exposed to contaminants present in the topsoil. For example, the concentrations of contaminants in the 4 inches of soil placed over residential properties as part of the interim remedial measure were quantitatively considered in calculating EPCs under the future scenario.
• "Covered by a geotextile fabric and a minimum of 4-inches of gravel per the work plan. . . ." Four inches of gravel is insufficient to permanently exclude potential exposure to underlying soil. Also, the geotextile membrane may become compromised over time resulting in potential exposure to underlying soil.
• "Excluded: property bumed down." This is not an acceptable reason for excluding a sample. Even though the property bumed down, receptors may rebuild or use the property for different purposes under both current and fiiture conditions.
Therefore, Table 2-1 should be revised to indicate that these samples were inappropriately
excluded from the risk assessment, and the uncertainties associated with excluding samples
for the reasons listed above should be discussed in the uncertainty analysis (Section 4.6).
52. Table 4-22. Table 4-22 presents uncertainties associated with the human health risk
assessment. EPA does not agree with statements in the risk assessment that contaminant
concentrations in groundwater are decreasing. Contaminant concentrations have decreased
from historic highs in some of the outer monitoring wells, but continued decreasing trends are
not evident at all monitoring wells. Of more importance are the contaminant concentrations
at the source areas, as reflected by treatment system influent concentrations. Contaminant
concentrations dropped in some of these wells in the first several years after the system began
operating; however, over the last 10 years, relatively high concentrations have remained in
most of these wells with no continued downward trend. This is especially evident for
recovery well W405, which is being used as the worst-case or default reference point. Since
the recovery system began operating in 1987, PCP values measured in influent from this well
have ranged from 840 parts per billion (ppb) to 9900 ppb, with 8000 ppb detected in 1987,
31
and 9900 ppb and 7700 ppb detected during 2005 and 2006, respectively, as shown in Table
23 of the 2006 Annual Report. These monitoring data suggest significant mass of PCP
contamination remains in the ground beneath this area. Also, near Fox Creek, an area of
NAPL was found in the area of the new wells.
Therefore, Table 4-22 in particular, and the risk assessment in general, should be revised to
discuss the fact that groundwater concentrations in recovery wells and at the treatment system
influent have leveled off after initial decreases and are not continuing to decline.
Specifically, Table 4-22 should revise the "potential magnitude of effect" to indicate that
groundwater concentrations have not continued to decrease, but rather have plateaued.
53. Appendix D. Appendix D presents supporting information and calculations for the HHRA.
Various problems identified with portions of Appendix D are as follows:
• Appendix D2 - A portion of page 4 is cut off; this should be corrected.
• Appendix D3 - The print area in the table in this sub-appendix needs to be fixed—the right side of the table has been cut off; this should be corrected.
• Appendix D4 - The following editorial issues were identified in this sub-appendix and should be corrected:
i. Several cells indicate a #DrV/0! error message (see pages 286 and 300 of 508).
ii. Where cancer risks or noncancer hazards are not available or not applicable for certain COPCs, it seems "—" should be entered instead of a risk or hazard of "O.OOE+00." Some COPCs have "O.OOE+00" entered for risk or hazard and some have "—"; no explanation is provided for the difference.
iii. Several pages are blank except for the header (see pages 14, 16, and 20 of 508).
iv. In several places throughout this sub-appendix, print areas need to be adjusted—columns are cut off etc.
V. The last column on the right is cut off on several pages (for example, pages 197, 210, 278, 291, 351, and 387 of 508), and appears by itself on subsequent pages (for example, pages 211, 224, 292, 305, and 388 of 508). Print areas tliroughout the sub-appendix should be reviewed and fixed where necessary.
32
vi. Page breaks need to be fixed so rows/headers are displayed correctly (for example, see pages 225 and 230 of 508).
• Parameter_Risk.xls file (Oral Tox Criteria worksheet): The dermal subchronic RfDo for manganese is hard-wired as "NA." Because there is an oral subchronic RfDo for manganese, it seems there should be a value for the dermal subchronic RfDo as well (calculated as Rfl)o * ABSGI).
• App_D4-14 to D4-16_Stnd_Child_Risk.xls file (A+B - Future - Area B Worksheet), beginning with cell J226 and going to the cells to the right (Area B): Considering this is a Future scenario worksheet, it is unclear why values from the Sum B -Current worksheet are being used instead of values from the Sum B - Future worksheet. Similar locations of the A+B Future - CDA worksheet pull in values from the Sum B Future worksheet. It is unclear why these values are handled differently at this particular location. This should be corrected.
• App_D4-14 to D4-16_Stnd_Child Risk.xls file: In the produce calculations used to determine the final hazards for the Allen-C exposure area, the Original Concentrations Pre-interim Remedial Measures (Pre-IRM) concentrations from the Soil A worksheet in the EPCs.xls file were used as inputs. This seems to contradict the statements made in the HHRA that produce is not currently grown in unamended soil.
• App_D4-21 to D4-24_Utility_AltSF.xls file: hi the hih Out Part A worksheet, a column labeled "Subchronic Inhalation RfD" lists values for manganese and naphthalene only. It appears that these values are linked to the Parameter_Risk.xls file. Inhalation Tox Criteria worksheet, and "Chronic RfD" column. There is a "Subchronic RfC" column in the Parameter_Risk.xls file. Inhalation Tox Criteria worksheet, but it has a RfC for dieldrin only. It seems that these subchronic RfDs/RfCs should be consistent—not in containing the same values but in listing values for the same chemicals.
Magnesium - surface water: 82,000 )ag/L (Suter and Tsao 1996)
Potassium - surface water: 53,000 [ig/L (Suter and Tsao 1996)
32. Tables 5-30 through 5-32. The total organic carbon (TOC) values for the control sediments
should be included in the table.
33. Table 5-43. The title of this table should be revised from 4-43 to 5-43.
34. Appendix E6. Section 7.1.2. Page E6-17. A reference for the fifth main bullet regarding the
proportion of all organic matter is missing and should be added.
41
REFERENCES
Barr Engineering Company (Barr). 2005. Validated Analytical Data - House Dust, Laboratory Batch Numbers: K2408652, St. Regis Paper Company Site - Cass Lake, Minnesota. Febmary 8.
Georgia Department of Natural Resources (GDNR). 2005. Rules and Regulations for Water Quality Control. Chapter 391-3-6. On-line Address: http://www.epa.gov/waterscience/standards/wqslibrary/ga/ga_4_wqs.pdf
Long, E.R., and others. 1995. "Incidence of Adverse Biological Effects with Ranges of Chemical Concentratons in Marine and Estuarine Sediments." Environmental Management. Volume 19, Pages 81 through 97.
Suter, G.W. II and Tsao, C.L. 1996. "Toxicological Benclimarks for Screening Potential Contaminants of Concem for Effects on Aquatic Biota: 1996 Revision. ES/ER/TM-96/R2.
U.S. Environmental Protection Agency (EPA). 1989. Risk Assessment Guidance for Superfund, Volume I: Human Health Evaluation Manual (Part A) (RAGS). Interim Final. Office of Emergency and Remedial Response. Washington, D.C. EPA/540/1-89/002. December.
EPA. 2003. "World Trade Center Indoor Environment Assessment: Selecting Contaminants of Potential Concem and Setting Health-Based Benchmarks." Prepared by the Contaminants of Potential Concem (COPC) Committee of the World Trade Center Indoor Air Task Force Working Group. Available at: http: //www. epa. go v/wtc/copc_benchmark.pdf