DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. 

### OSWER 9200.3-56

PUBLIC REVIEW DRAFT

DRAFT RECOMMENDED INTERIM PRELIMINARY REMEDIATION GOALS
FOR DIOXIN IN SOIL AT CERCLA AND RCRA SITES

Prepared by:

U.S. Environmental Protection Agency Office of Superfund Remediatio n and Technology Innovation Washington, D.C.

December 30, 2009DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. LIST OF ACRONYMS AND ABBREVIATIONS

ARAR Applicable or Relevant and Appropriate Requirement ATSDR Agency for Toxic Substances and Disease Registry CERCLA Comprehensive Environmental Re sponse, Compensation, and Liability Act CSF Cancer Slope Factor ECEH European Centre for Environmental Health EPA U.S. Environmental Protection Agency
HAD Health Assessment Document HEAST Health Effects Assessment Summary Table
HI Hazard Index HQ Hazard Quotient IPCS International Programme on Chemical Safety IRIS Integrated Risk Information System
LOAEL Lowest-Observed-Adverse-Effect-Level
MCL Maximum Contaminant Level
MRL Minimal Risk Level NAS National Academy of Sciences
NCEA National Center for Environmental Assessment NCP National Contingency Plan
NOAEL No-Observed-Adverse-Effect-Level NPL National Priority List NTP National Toxicology Program ODW Office of Drinking Water OEM Office of Emergency Management ORD Office of Research and Development OSRTI Office of Superfund Remedi ation and Technology Innovation OSWER Office of Solid Waste and Emergency Response
OW Office of Water PCB Polychlorinated biphenyl PCDD Polychlorinated dibenzodioxin PCDF Polychlorinated dibenzofuran pg Picogram (10 -12 grams)
PM2.5 Particulate material less than 2.5 um
PM10 Particulate material less than 10 um POCD Program Operations and Coordination Division ppb Parts per billion
PPRTV Provisional Peer Re viewed Toxicity Value ppt Parts per trillion PRG Preliminary Remediation GoalDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. LIST OF ACRONYMS AND ABBREVIATIONS - continued

PTMI Provisional Tole rable Monthly Intake PWG Pathology Working Group RAGS Risk Assessment Guidance for Superfund RBA Relative Bioavailability RCRA Resource Conservation and Recovery Act
RfD Reference Dose
ROD Records of Decision
RSC Relative Source Contribution STSC Superfund Technical He alth Risk Support Center TCDD 2,3,7,8-Tetrachlorodibenzo-p-dioxin TDI Tolerable Daily Intake TEF Toxicity Equivalency Factors TEQ TCDD Toxic Equivalent WHO World Health OrganizationDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 1 - PUBLIC REVIEW DRAFT

DRAFT RECOMMENDED INTERIM PRELIMINARY REMEDIATION GOALS
FOR DIOXIN IN SOIL AT CERCLA AND RCRA SITES

OVERVIEW

In May 2009, the U.S. Environmental Protecti on Agency’s (EPA) Administrator Lisa P.
Jackson decided that EPA needs to acceler ate work underway to reassess the human health risks from exposur es to dioxin. EPA’s Science Plan for Activities Related to
Dioxins in the Environment (EPA 2009a) details a plan, wi th interim milestones, for completion of the Agency’s dioxin reassessment and other efforts related to dioxins in the environment. In a letter dated May 26, 2009, to the community of the Tittabawassee River/Saginaw River and Bay Contamination Si te in Michigan, the Administrator stated:

“As we move forward to develop remediati on strategies at this site, the science on dioxin’s health and ecological effects will obv iously play an important role in our decisions. Although EPA scientists, supporte d by external peer review bodies, have
invested considerable time and effort in evaluating the scientific literature on dioxin,
we need to be sure that EPA’s assessme nt of dioxin’s risk s to people and the environment is brought to bear at this and other dioxin-contaminated sites in a timely manner. Accordingly, I am, in parallel w ith this letter, announ cing a commitment to
accelerate our scientific work on dioxin. Our goal is to issue a final dioxin assessment by the end of 2010. In addition, our Office of Research and Development and Office of Solid Waste and Emergenc y Response will review current dioxin cleanup guidance set by the Agency and th e States with the aim of recommending interim preliminary remediation goals informed by the latest science and the work of state agencies. We will announce these in terim PRGs by the end of the year.”

EPA’s Office of Research and Developmen t (ORD) expects to complete the dioxin reassessment by the end of 2010, subject to furt her consideration of the science and the scope and complexity of the revisions th at will need to be made. ORD will be responding to all National Academy of Sc iences (NAS) comments received on EPA’s
draft 2003 dioxin reassessment.DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 2 - EPA’s Office of Solid Waste and Emergenc y Response (OSWER) has developed draft recommended interim Preliminary Remediation Goals (PRGs) for dioxin in soil, informed by the best available science and work of state agencies at this time. On October 13, 2009, EPA posted a proposed plan for developing the interim PRGs, (available at: www.epa.gov/superfund/policy/remedy/sfreme dy/remedies/dioxininterimplan.html) and requested comments on the proposed plan. EPA has taken these comments into account, establishing a docket (available at: http://www.regulations.gov and go to Docket No. EPA-HQ-SFUND-2009-1002) where comments received to date can be found. EPA has considered these comments in formul ating the draft recommended interim PRGs (available at: http://www.regulations.gov and go to Docket No. EPA-HQ-SFUND-2009- 0907).

EPA expects to finalize these draft recomm ended interim PRGs for soil in June 2010 after receipt and evaluation of public comments on all aspects of this draft interim guidance. Until these draft recommended interim PRGs are finalized, EPA will continue
to use the 1998 recommended interim PRGs (EPA 1998). The fina lized recommended
PRGs are intended for interim use until EPA issues its final dioxin reassessment (hereafter “recommended interim PRGs” refers to PRGs that once finalized are to be used
in the interim until EPA issues its final dioxin reassessment). At that time, EPA intends to issue updated recommended PRGs based on the final dioxin reassessment. Also at that time, EPA intends to re-evaluate cleanup d ecisions at Comprehensive Environmental Response, Compensation, and Liability Ac t (CERCLA) and Resource Conservation and Recovery Act (RCRA) sites that were base d on the 2010 recommended PRGs to ensure that cleanups remain protective for human health.

PURPOSE

The purpose of this guidance is two-fold:

1. To recommend the use of PRGs to prot ect against cancer a nd non-cancer effects associated with human exposure to dioxin in soil at CERCLA and RCRA sites, and,

2. To discuss the interim use of these recommended PRGs for soil at CERCLA and
RCRA sites

These draft recommended interim PRGs ar e intended for use in evaluating dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) a nd other dioxin-like compounds in soil. Dioxin-like compounds, including other pol ychlorinated dibenz odioxins (PCDDs), dibenzofurans (PCDFs) and biphenyls (PCBs) may collectively be evaluated using theDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 3 - recommended PRGs for dioxin after adjustment to account for relative toxicity using toxicity equivalency factors (TEFs) to cal culate dioxin toxicity equivalent (TEQ)
concentrations. EPA recommends the use of the TEFs developed by the World Health Organization (WHO) (van den Berg et al. 1998, 2006) based on review of the toxicological literature. For example, if a soil contained 10 ppt of dioxin (i.e, TCDD) and also contained 20 ppt of some other dioxin-like chemical that was 1/10 as toxic as dioxin, the toxicity equivalent concentration for the other dioxin-like compound would be 2 ppt, and the total TEQ concentration for the soil would be 10 + 2 = 12 ppt dioxin TEQ. The total dioxin TEQ concentration would then be compared to the recommended PRG. EPA acknowledges that there is uncertainty asso ciated with risk estimates based on TEQs. Therefore, risk assessors should identify the fraction of the TEQ attr ibutable to dioxin
and to each chemical class of dioxin-like compounds (i.e., PCDDs, PCDFs, and PCBs).

For CERCLA and RCRA sites, Regions ge nerally should consider using the recommended interim PRGs in this guidance as a starting point for residential and commercial/industrial soil cleanup levels. EP A encourages State and Tribal programs
that do not use PRGs to consider the r ecommended interim PRGs as starting point
concentrations to de velop cleanup levels.

This guidance supersedes OSWER’s previ ous PRG guidance for dioxin in soil (EPA 1998). These draft recommended interim soil PRGs are national levels protective for cancer and non-cancer effects from human expos ure by ingestion and dermal contact with surface soils. Inhalation exposure is not included for the draft recommended interim PRGs, because at present, there is no availa ble inhalation unit risk value for dioxin that
has been derived in accordance with curre nt guidance for inhalation risk assessment (EPA 2009d). However, inhalation exposure to dioxin (particulates and vapor) is expected to be low (< 2.4%) compared to oral exposure in most cases (see Attachment 1). Therefore, risks due to inhalation of particulates and vapors are expected to be minimal. Regions should continue to develop PRGs on a site-specific basis for other media (e.g., sediments, which involve biotransfer and bioaccumulation through indirect pathways) and for ecological assessments.

This guidance is consistent with OSWER’ s guidance (EPA 2003a) on using a hierarchy of existing chemical toxicity value sources; it does not represent a new or independent review of dioxin toxicity, which ORD is curre ntly conducting as part of the final dioxin reassessment. As a result, there is uncertain ty associated with these draft recommended interim PRGs because they do not take into account peer review comments on the new science that was reviewed by the NAS, and ne w science that was released since the NAS
review. A final dioxin reassessm ent is still under development.DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 4 - This draft guidance presents current OS WER technical and po licy recommendations regarding PRGs for soil contaminated with di oxin. While OSWER developed this draft guidance for facility response actions unde r CERCLA and RCRA corrective action, other regulators, including the States , may find it useful in their programs, although they may
choose to use alternative assessments consistent with their own programs and policies. In addition, EPA may use and accept other techni cally sound approaches after appropriate review, either at its own initia tive or at the suggestion of ot her interested parties. This draft guidance does not impose any requirements or obligations on EPA, the States, other Federal agencies, or the regulated community. It is important to understand that this
document does not substitute for statutes th at EPA administers or their implementing regulations, nor is it a regul ation itself. Thus, this document does not impose legally binding requirements on EPA, the States, or the regulated community, and may not apply to a particular situation based upon the speci fic circumstances. Rather, the document suggests approaches that may be used at particular sites as appropriate, given site-specific
circumstances.

BACKGROUND

Description of PRGs

Consistent with CERCLA and the National Contingency Plan (NCP), protection of human health and the environment is a requi rement for selected remedies (see 40 CFR §300.430(f)(1)(i)(A)). In the CERCLA remedy se lection process, PRGs typically are used when developing cleanup levels. At CE RCLA sites, PRGs t ypically are “specific statements of desired endpoint concentrations of risk levels (55 FR 8713, March 8, 1990) that are conservative, default endpoint con centrations used in screening and initial development of remedial alternatives before consideration of information from sitespecific risk assessments”. In accordance with the NCP (see 40 CFR §300.430(e)(2)(i)(A)), PRGs are generally at the low end of the risk range and typically are used in screening and initial devel opment of remedial alternatives before
consideration of more detailed informati on from the site-specific risk assessment.

The NCP (40 CFR §300.430( e)(2)(i)(A )) states:

“Remediation goals shall establish acceptable exposure levels that are protective
of human health and the environment and shall be developed by considering the following:DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 5 - (A) Applicable or relevant and approp riate requirements (ARARs) under federal
environmental or state environmental or f acility siting laws, if available, and the following factors: ( 1 ) For systemic toxicants, acceptable exposure levels shall represent concentration levels to which the human population, including sensitive subgroups, may be exposed without advers e effect during a lifetime or part of a lifetime, incorporating an adequate margin of safety; ( 2 ) For known or suspected carcinogens, acceptable exposure levels are generally concentration levels that represent an excess upper bound
lifetime cancer risk to an individual of between 10 -4 and 10 -6 using information on the relationship between dose and response. The 10 -6 risk level shall be used as the point of departure for determining remediation goals for alternatives when ARARs are not available or are not sufficiently protective because of the presence of multiple contaminants at a site or multiple pathways of exposure; ( 3 ) Factors related to technical limitations such as detection/quantification limits for contaminants; ( 4 ) Factors related to uncertainty; and ( 5 ) Other pertinent information.”

1998 OSWER Guidance on PRGs for Dioxin in Soil

This draft interim guidance, when finaliz ed, will supersede the 1998 OSWER directive
entitled “Approach for Addressing Dioxin in Soil at CERCLA and RCRA Sites” (EPA 1998). The 1998 OSWER directive recommended th at a soil concentrat ion of 1 part per billion (ppb), which is equivalent to 1,000 parts per trillion (ppt) of dioxin (as TEQ) be generally used as a starti ng point for developing cleanup levels for CERCLA removal
sites and as a PRG for CERCLA remedial sites for dioxin TEQ in surface soil involving a residential exposure scenario. For commer cial/industrial exposure scenarios, a soil
concentration within the range of 5 ppb (5,000 ppt) to 20 ppb (20,000 ppt) dioxin TEQ was recommended as a starting point for deve loping cleanup levels for CERCLA sites. A range in soil concentrations was recommende d for commercial/ industrial soils due to the greater variability in exposures associated wi th the commercial/industrial scenarios. The PRGs were also generally recommended as a starting point for actions taken at RCRA
corrective action sites. These levels were recommended unless extenuating site-specific
circumstances warranted a different level.

Based on the oral cancer slope factor (CSF) developed by EPA (1985), EPA (1998)
estimated that the lifetime exce ss cancer risks to residents from oral exposure to dioxin in soil at a PRG of 1,000 ppt dioxin TEQ was a bout 2.5E-04, and that lifetime excess cancerDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 6 - risks to workers at a PRG of 5,000 ppt dioxin TEQ corresponds to a risk of about 1.3E04. Dermal exposure was not considered for either residential or commercial/industrial land use. EPA (1998) noted that these risks we re at the higher end of the range of excess
cancer risks.

Need to Update the 1998 OSWER PRGs

In developing this guidance, the Agency has evaluated several attributes of the current
PRGs for dioxin in soil that are not consistent with the best available science on dioxin. These inconsistencies include the following:

• The derivation procedure did not consider potential non-cancer effects of dioxin

• The value for residents considered oral exposure only, and did not include dermal

exposure

• The value for workers is based on an i ndoor worker (oral exposure only), while the most exposed worker is usually an out door worker with both oral and dermal

exposure

Based on a consideration of a number of factor s, the Administrator has determined that it is important to develop update d interim PRGs to be used unt il the release of the final dioxin reassessment. The following sections describe the approach used by EPA to provide and select new recomm ended interim PRGs for dioxin.

RECOMMENDATIONS

Recommended Toxicity Values

The most common health effect in peopl e exposed to large amounts of dioxin is chloracne. Chloracne cases have typically been the result of accidents or significant contamination events. Chloracne is a severe skin disease with acne-like lesions that occur mainly on the face and upper body. Othe r effects of exposure to large amounts of dioxin include skin rashes, sk in discoloration, excessive body hair, and possibly mild liver damage.

One of the main concerns over health effects from dioxins is the risk of cancer in adults. Several studies suggest that workers exposed to high levels of dioxins at their workplace over many years have an increased risk of can cer. Animal studies have also shown an increased risk of cancer from long-term exposure to dioxins.

Finally, based on data from animal studies, th ere is some concern that exposure to low levels of dioxins over long periods (or high level exposures at sensitive times) mightDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 7 - result in reproductive or developmental effects (FDA, 2008). Consequently, both a cancer slope factor and a non-can cer toxicity value are used to derive PRGs for cancer and non-cancer effects.

Hierarchy for Selecting Interim Toxicity Values

OSWER has developed a recommended hier archy (EPA 2003a) for the selection of toxicity values, including thos e used in developing PRGs. As discussed in EPA (2003a), the first tier of toxicological information is found in EPA’s Integrated Risk Information System (IRIS), and is developed by EPA’ s ORD National Center for Environmental Assessment (NCEA). Generally, any values in IR IS are considered to be Tier 1. If no data are available in IRIS, the next prefer ence (Tier 2) is Provisional Peer Reviewed Toxicity Values (PPRTVs) developed by EP A NCEA’s Superfund Technical Health Risk Support Center (STSC). If toxicity values ar e not available from either Tier 1 or 2, other high quality sources of toxicity information can be used. These are considered Tier 3 values in this hierarchy.

As discussed in EPA (2003a), toxicity values generally are not appropriate for use as Tier 3 values until they have been through peer review, the peer review comments have been addressed, and the analysis is made publicly av ailable. Also, toxicity values should be based on similar methods and procedures as those used for Tier 1 and Tier 2, and the methods and processes used to develop the va lues should be transparent. It should be noted that these procedures are specifi c to CERCLA/RCRA cleanup programs and are not necessarily the approach taken by other EPA programs.

At present, EPA has not derived any Tier 1 or Tier 2 toxicity values for dioxin, either for cancer or non-cancer effects. Consequen tly, for the purposes of providing these recommended interim PRGs for dioxin, EPA re viewed available toxicity values to identify the most appropriate Tier 3 values (EPA 2009b, 2009c). The recommended interim Tier 3 toxicity values that are discussed in this guidance may be appropriate for the Regions to use to assess human health risks until toxicity values for dioxin are
available in EPA’s IRIS database or until fu rther scientific analysis indicates that alternate values should be used. When a new IRIS toxicity assessment is finalized, EPA intends to review cleanup level decisions to ensure that sites addressed using these interim toxicity values remain protective, give n the revised toxicity values. If important
new scientific information becomes available before a new IRIS toxicity assessment is finalized, EPA may issue additional guida nce addressing the recommended interim toxicity values discusse d in this guidance.

Recommended Cancer Slope FactorDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 8 - Because EPA does not have a Tier 1 or Tier 2 cancer toxicity value for dioxin, EPA reviewed available cancer slope factors fo r dioxin (EPA 2009b) to determine whether they would meet EPA’s Tier 3 cr iteria. Five primary candidate values were identified, as
follows:

• EPA’s Office of Health and Environmen tal Assessment (EPA 1985) developed an oral cancer slope fact or of 1.56E-04 (pg-kg-day) -1 . This was based on the combined incidence of lung, palate, and nasal carcinomas, and liver hyperplastic
nodules or carcinomas in female rats in the study by Kociba et al. (1978).

• EPA (1997a) (EPA’s Health Effects A ssessment Summary Table, or HEAST)
included an oral CSF of 1.5E-04 (pg-kg-day) -1 . The citation for the CSF in HEAST lists EPA (1985) as one of the sources for the HEAST value.

• California (CalEPA) (1986, 2002) developed an oral can cer slope factor of 1.3E04 (pg/kg-day) -1 . This is based on the occurren ce of hepatocellular adenomas and carcinomas in male mice in a study by the National Toxicology Program (NTP 1982).

• Michigan (MDEQ 1998) utilizes an oral cancer slope fact or of 7.5E-05 (pg/kgday) -1 , which is based on a re-analysis of the histological slides of livers from female rats from the Kociba et al. (19 78) study using the liver tumor classification scheme proposed by NTP in 1986 (Maronpot et al. 1986, EPA 1990).

• Minnesota (MNDOH 2003) uses an oral cancer slope factor of 1.4E-03 (pg/kgday) -1 , which is based on the draft re-evalu ation of the exposure-response data for liver cancer in female rats reported in the draft EPA (2003b) dioxin reassessment.

More detailed descriptions of these five alternative slope factors are presented in
Attachment 2.

The slope factor identified by Minnesota is no t considered appropriate because it is based on the 2003 EPA draft dioxin reassessment (E PA 2003b), which has not been finalized. The slope factor identified by Michigan is based on an updated and peer-reviewed evaluation of the Kociba et al. (1978) data using the updated NTP tumor classification system. However, documentation of the slope factor of 75,000 (mg/kg-day) -1 , including its derivation, peer review and supporting info rmation, is very brief and the information that is publicly available is limited or not completely transparent. The slope factor listed in HEAST of 1.5E-04 (pg/kg-day) -1 is slightly different from the slope factor listed in the source document (EPA 1985) of 1.56E-04 (pg/kg-day) -1 . Because of this, the HEAST was not considered to be transparent as to the derivation of the CSF and how the value came to be changed slightly from that lis ted in the source document. Of the two remaining slope factors (EPA 1985, CalEPA 1986), both are publicly available,DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 9 - transparent as to their deri vation, and were adequately p eer-reviewed. However, the slope factor of 1.56E-04 (pg/kg-day) -1 derived by EPA (1985) is preferred because it is based on the incidence of all significant tumors combined, rather than the incidence of
liver tumors alone.

Recommended Non-Cancer Toxicity Factor

As noted above, EPA has not yet derived a Tier 1 or Tier 2 non-cancer toxicity value (Reference Dose, or RfD) for dioxin. Ther efore, EPA reviewed non-cancer toxicity values developed by States, foreign countri es, or other health agencies (EPA 2009b, 2009c). Based on a review of available docum ents, the following candidate values were
identified:

• A chronic oral Minimal Risk Level (MRL ) value of 1 pg/kg-day developed by the Agency for Toxic Substances and Disease Registry (ATSDR). This value is based on behavioral effects in the offspr ing of female monkeys exposed to dioxin in the diet for 16 months, including the period of gestation a nd lactation (ATSDR 1998).

• A chronic oral RfD value of 1 pg/kg-day developed by the EPA’s Office of Drinking Water (ODW) (EPA 1987) to s upport derivation of a lifetime health advisory for TCDD. This value is base d on the occurrence of reproductive effects
in animals.

• A range of Tolerable Daily Intake (TD I) values, ranging from about 1 pg/kg-day to 4 pg-kg-day, developed by the W HO (WHO 1991, 1998; JECFA 2002). These values are derived by identifying a no-eff ect tissue burden in exposed animals for a range of non-cancer effect s, and computing the average daily intake level that would yield the no-effect tissue burden in humans.

Each of these approaches is describe d in greater detail in Attachment 2.

Of these values, OSWER recommends the chronic oral MRL value of 1 pg/kg-day developed by ATSDR (1998) generally as th e most appropriate value for use in the development of non-cancer PRGs. This valu e is well documented and peer reviewed, and qualifies as an OSWER Tier 3 toxicity value. This toxicity value is consistent with the RfD of 1 pg/kg-day developed by EPA’s OD W (EPA 1987), and is also consistent with the low end of the range of TDI values developed by WHO (1991, 1998; JECFADRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 10 - 2002). Note that ATSDR (2008) has used the 1 pg/kg-day value to derive a soil screening concen tration of 50 ppt 1 dioxin TEQ.

Recommended Exposure Pathways and Parameters

EPA provides guidance on the calculation of PRGs in two main documents, including Risk Assessment Guidance for Superfund (RAG S) Volume I, Part B (Development of Risk-Based Preliminary Remediation Goals) (EPA 1991) and Supplemental Guidance for Developing Soil Screening Levels for Superfund Sites (EPA 2002a). For the purposes of this effort, EPA has utilized default e xposure equations and exposure parameters discussed in the more recent EPA guida nce (2002a) along with the RAGS dermal guidance (EPA 2004). For workers, RAGS B recommends evaluating only indoor workers, while EPA (2002a) recommends ev aluating both indoor and outdoor workers. Also, EPA (2002a) recommends evaluating non-cancer risk to a reside nt based on the soil intake rate of a child, which is considered more protective of children than the approach used in RAGS B (that uses a time-weight ed average intake rate across childhood and adulthood). Soil PRGs calculated using EPA 2002a equations are ge nerally appropriate provided that conditions at th e site are the same as th e conditions assumed in the calculations. Site managers wishing to us e PRGs developed with these protective equations should consider whether it may be appropriate to modify any of the assumptions in deriving site-specific PRGs.

The equations and exposure assumptions recommended by EPA (2002a, 2004) for oral and dermal exposure of residents and worker s (both indoor and outdoor workers) to soil are provided in Tables 1 to 4. In brief, some of the key exposure assumptions for these populations are as follows:

• Residents and outdoor workers are assu med to be exposed by both oral and dermal exposure

1 ATSDR’s soil screening levels are calculated in accordance with ATSDR’s Public Health Assessment Guidance Manual (ATSDR 2005). Th e dioxin soil screening level is based on ATSDR’s chronic oral MRL value of 1 pg/kg-day, assuming a soil intake rate of 0.2 g/day by a 10-kg child. Dermal exposure is not included. The assumption of a body weight of 10 kg is consistent with previous exposure factor recommendations from EPA, while EPA currently recommends a body weight of 15 kg for a child. Moreover, the 50 ppt screening level is not intended for use as a PRG, or to serve as a remedial goal. Rather, ATSDR uses the soil screening concentration as an initial comparison value for health assessments and to make public health recommendations, such as community health education or site access limitations..DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 11 - • Indoor workers are assumed to be exposed by oral exposure only, as no significant dermal exposure is expected.

• Inhalation exposure is not included for any population because at present, there is
no available inhalation unit risk value for dioxin that has been derived in accordance with current guidance for i nhalation risk assessment (EPA 2009d).

• Inhalation exposure to dioxin (particulates and vapor) is expected to be low (< 2.4%) compared to oral exposure in most cases (see Attachment 1).

• For evaluation of cancer PRGs , residential exposure is a ssumed to begin at birth and extend for 30 years. This includes exposure for 6 years as a child and 24 years as an adult. Worker exposures ar e assumed to occur for 25 years, but only
as an adult.

• For non-cancer PRGs, exposure as a resident is assumed to occur only as a child. This assumption is thought to be ge nerally conservative (EPA 2002), since exposure to soil is higher for a child than for an adult resident. For workers, exposure is assumed to occur only as an adult.

The equations shown in Tables 1 to 4 include two additional terms not explicitly included in the equations recommended by EPA (2002a):

• RBA . Relative bioavailability (RBA), for purposes of this guidance, is the ratio of the absorption of dioxin from soil co mpared to the absorption that occurred in the study used to derive the oral cancer slope factor or the oral reference dose for
dioxin. For the calculations included in this docume nt, the value of RBA is assumed to be 1.0 (i.e., dioxin absorption is the same as that occurring in the study.) This is an appropriate assumpti on for establishing a default PRG because use of a RBA factor of 1.0 will ensure prot ectiveness. However, this assumption may need to be revisited when pe rforming site-specific assessments.

• RSC . The Relative Source Contribution (R SC) is the amount of a daily safe
intake for non-cancer effects that is “allocated” to soil. RSCs should be applied only for effects that have a non-zero th reshold, and are used mainly by EPA in developing water standards (EPA 2000). In cases where other sources (e.g., the diet) contribute a substantia l fraction of the ingestion e xposure, then the RSC term may be set to some lower value. The na tional average dioxin contribution from
diet is estimated to be more than 90% (from beef, pork, poultry, other meats, dairy, eggs, milk, and fish). If we account ed for this 90% contribution from food,
then the RSC would be 0.1 and the PRG would be one-tenth of the non-cancer PRG value that we are currently recomm ending. However, an RSC adjustment for soil is not often used at Superfund sites, where soil is an exposure source for the following reasons. The available dietary data are for adults, but the PRGs areDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 12 - developed for children who are exposed to lower concentration levels in the current food supply. In addition, EPA’s responsibilities are to evaluate and manage only contaminant sources related to the site. For those individuals near Superfund sites, the contribution of soil derived dioxin exposures relative to food derived exposures is expected to be mu ch greater than the national average. Therefore, for all PRG calculations performed in this document, the value of RSC
is set to 1.0.

Draft Interim Recommended PRGs for Dioxin in Soil

Cancer PRGs

Based on the recommended oral cancer slope factor of 1.56E-04 (pg/kg-day) -1 discussed above, recommended interim soil PRGs for prot ection against cancer effects at the 1E-06 risk level may be computed in accordan ce with current EPA equations and default exposure assumptions shown in Table 1 and Table 2. The results are shown below:

Potential Soil PRGs for Dioxin Base d on Cancer (1E-06 Risk Level)

Land Use Receptor PRG (ppt TEQ)

Residential Resident 3.7
Indoor Worker 37 Commercial/
Industrial Outdoor Worker 17 All PRGs are shown to two significant figures

Non-Cancer PRGs

Based on the recommended oral non-cancer interim toxicity value of 1 pg/kg-day selected above, recommended interim non-cancer PRGs for residential and commercial/industrial land use that correspond to a Hazard Quotient (HQ) of 1 may be
calculated in accordance with current EPA equations and default exposure assumptions
shown in Table 3 and Table 4. These results are shown below:

Potential Soil PRGs for Dioxin Based on Non-Cancer Effects (HQ of 1)

Land Use Receptor PRG (ppt TEQ)

Residential Resident 72
Indoor Worker 2,000 Commercial/
Industrial Outdoor Worker 950 All PRGs are shown to two significant figuresDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 13 - Draft Recommended Interim PRGs

Based on consideration of oral and dermal exposures to dioxin and other dioxin-like compounds in soil, EPA recommends the interim PRGs for dioxin in soil calculated
based on non-cancer effects: 72 ppt dioxin TEQ in resident ial soil and 950 ppt dioxin TEQ in commercial/industrial soil

. EPA believes that these recommended interim PRGs generally provide adequate protection agai nst non-cancer effects. In addition, they generally are protective for cancer effects at ap proximately the 1E-05 risk level, which is within EPA’s protective risk range of 1E-04 to 1E-06 (see 40 CFR §300.430(e)(2)(i)(A)).
It should be noted that because these reco mmended interim PRGs correspond to a HQ of 1, they limit the upper bound cancer risk level to 1E-05 rather than the typical upper limit
of 1E-04. These recommended interim PRGs are set at a more protective cancer risk level than the 1998 PRGs, which reflect a cancer risk level of 2E -04. These draft recommended interim PRGs are expected to be higher than typical background levels for
residential and most commercial/industr ial soils, respectivel y (ATSDR 1998).

Land Use PRG (ppt TEQ)

Residential 72
Commercial/Industrial 950 All recommended PRGs are shown to two significant figures

EPA believes the draft recommended PRGs de scribed above if finalized would be appropriate for use on an interim basis until EP A releases its final dioxin reassessment.

However, EPA is also considering an altern ative concentration of 3.7 ppt dioxin TEQ in residential soil and 17 ppt dioxin TEQ in co mmercial/industrial soil as the point of departure for determining PRGs. These alternat ive draft PRGs are at the 1E-06 risk level
and therefore are also consistent with the NCP provision for PRGs (see 40 CFR §300.430(e)(2)(i)(A)(2)), which states 1E-06 is the point of departure for determining remediation goals. These alternative values are protective for non-cancer as well as
cancer effects. EPA notes that PRGs based on a 1E-06 cancer risk level would likely be within or possibly below background concentra tions of dioxins in U.S. soils. A recent EPA report found mean rural so il concentrations ranging from 0.2 to 11.4 ppt dioxin TEQ (EPA 2007). Generally, it is OSWER policy to not set site specifi c cleanup levels at concentrations below site specific natural background levels (EPA 2002b). Thus, if EPA
were to finalize these alternative values , soil background levels would need to be
identified at CERCLA sites in order to develop appropriate cleanup levels. While EPA isDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 14 - taking comments on all aspects of this draft gu idance, EPA is particularly interested in comments on the utility of these alternative values.

IMPLEMENTATION

This guidance does not affect or replace statutory or regulatory requirements (e.g., CERCLA Section 121 provisions on meeti ng or waiving ARARs) under CERCLA or RCRA. For example, the maximum contam inant level (MCL) for dioxin in drinking water is 30 pg/L, and this should continue to be considered as an ARAR for the cleanup under CERCLA of ground water that may be used as drinking water (unless a more stringent state ARAR requires a lower concentration).

These draft recommended interim PRGs are informed by the best available toxicity values as evaluated using OS WER’s toxicity hierarchy (EPA 2003a) and calculated using current EPA exposure assumptions, which have been updated since the 1998 PRG guidance (EPA 1998) was issued. Once fina lized, regions may consider using these
recommended interim PRGs at both CERCLA and RCRA sites where the Agency is determining dioxin soil cleanup levels. When EPA’s ORD finalizes its dioxin reassessment, OSWER will evaluate the imp act of the dioxin reassessment and will update these PRGs as appropriate.

These draft recommended interim soil PRGs ar e national levels prot ective for cancer and non-cancer effects from ingestion and dermal contact with surface soils in residential and commercial/industrial expos ure scenarios. Inhalation ex posure is not included for the draft recommended interim PRGs, because at present, there is no available inhalation unit risk value for dioxin that has been deri ved in accordance with current guidance for inhalation risk assessment (EPA 2009d). Ho wever, inhalation exposure to dioxin (particulates and vapor) is expected to be low (< 2.4%) compared to oral exposure in most cases (see Attachment 1). Therefore, ri sks due to inhalation of particulates and vapors are expected to be minimal. Once fi nalized, the interim guidance will supersede OSWER’s previous PRG guidance for dioxi n in soil (EPA 1998). These draft recommended interim soil PRGs are national levels protective for cancer and non-cancer effects from human contact (ingestion, dermal contact, and inhalati on exposure (this is minimal for dioxin particulates and vapors) ) with surface soils in residential and commercial/industrial exposure scenarios. Expo sure to dioxin by the inhalation route is not expected to be significant compared to oral exposure (see Attachment 1). Regions should continue to develop PRGs on a site-speci fic basis for other media, like sediments, that involve biotransfer and bioaccumulation up the aquatic food chain to fish consumed by humans and for ecological assessments where the receptors are terrestrial biota, such as plants and animals, not humans

.DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 15 - At CERCLA National Priority List (NPL) sites, includi ng, where appropriate, other Federal agency-lead and state-lead sites, Regions should consult with the Office of Superfund Remediation and Technology Innova tion (OSRTI) Site Assessment and Remedy Decisions Branch on all proposed dioxin cleanups that are conducted under Superfund. Consultation should be initiated atthe risk assessment stage, and continue through the process.

For removal actions, Regions should contac t Headquarters for concurrence on non-NPL removal actions where dioxin is a principa l contaminant of concern (EPA 1989). For non-time critical removal actions involving dioxin, consultation may involve both OEM
and OSRTI. The use of removal authority is dete rmined on a site-specific basis, and trigger levels for initiating a removal action ar e sometimes higher than the levels used as either PRGs (or starting point s) or final cleanup levels.

For sites where another Federal agency is th e lead agency, OSRTI will notify the Federal
Facilities Restoration Reus e Office of ongoing consultations regarding dioxin soil cleanup levels. The Office of Site Remedi ation Enforcement will provide support if
enforcement issues are identified. For consultation procedures, refer to OSWER Directive 9200.4-19 (EPA 1996) and OS WER Directive 9200.1-18FS (EPA 1997b).

Once finalized, Regions performing five-year- reviews of CERCLA remedial sites where
soils contaminated with dioxin or other diox in-like compounds have been left in place should consider this guidance on recommende d interim PRGs when evaluating whether the original remedies in the Records of Decision (ROD) remain protective for the
contaminated areas. Consistent with ex isting five-year-review guidance (EPA 2001),
OSWER recommends that the fi ve-year-reviews include an evaluation of existing site data, identification of the need for additio nal site data, and identification of areas potentially needing cleanup based on the review of this existing data. This information
can be used to evaluate whether additiona l data collection and/ or site cleanup is appropriate. Once the final dioxin reassessm ent has been released, OSWER may issue additional guidance on implementation of the PRGs.

In the case of EPA-lead RCRA corrective action sites, Regions should provide the Program Implementation and Information Division within the Office of Resource Conservation and Recovery (ORCR) with proposed dioxin soil cleanup levels (i.e., prior to notice and comment) in order to ensu re appropriate implementation of the recommended interim PRGs, once they are finalized. For State-lead RCRA corrective action sites, we would also encourage States to use the dioxin levels recommended by this guidance as starting poi nts in developing soil clea nup levels, unless they have developed their own standards or guidance. Because States are the primary implementersDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 16 - of the RCRA Corrective Action program, this guidance does not recommend specific procedures for implementation under RCRA. States are encouraged to share their approaches with the Regions in a manner cons istent with established procedures for EPA support and oversight of state RCRA Corrective Action programs.

Point of Contact

If you have any questions, please contact Marlene Berg by phone at 703-603-8701 or by
e-mail at berg.marlene@epa.gov

.DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 17 - References

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.

ATSDR. 2008. Update to the ATSDR Polic y Guideline for Dioxins and Dioxin-Like Compounds in Residential Soil. Agency for Toxic Substances and Disease Registry.
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EPA. 1985. Health Assessment Document fo r Polychlorinated Dibe nzo-p-Dioxins. U.S. Environmental Protection Agency, Office of Health and Environmental Assessment,
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EPA. 1989. Guidance on Non-NPL Removal Ac tions Involving Nationally Significant or Precedent Setting Issues. Directive No. 9360.0-19, 1989. Available online at: http://www.epa.gov/superfund/ policy/remedy/pdfs/93-60019-s.pdf

EPA. 1990. Toxic Steering Gr oup Meeting (July 10). Carci nogenicity Slope Factor for 2,3,7.8-TCDD: Overview and Recent Developments. U.S. Environmental ProtectionDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 18 - Agency. Available online at: http://www.michigan.gov/documents/deq/deq-whm-hwpdow-slope_factor_251918_7.pdf

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EPA. 1996. Headquarters Consultation for Di oxin Sites. U.S. Environmental Protection Agency, Office of Solid Waste and Emerge ncy Response. OSWER Directive 9200.4-19. December 13, 1996. Available online at: http://www.epa.gov/superfund/ policy/remedy/pdfs/92-00419-s.pdf

EPA. 1997a. Health Effects Assessment Summary Tables (HEAST). U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response. EPA-540-R-97-036. July 1997. Available online at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=2877

EPA. 1997b. Consolidated Guide to Consultation Procedures for Superfund Response
Decisions. U.S. Environmental Protecti on Agency, Office of Solid Waste and Emergency Response. OSWER Directive 9200.1-18FS. May 1997. Available online at: http://www.epa.gov/superfund/policy/remedy/cnsltsum.htm

EPA. 1998. Approach for Addressing Dioxi n in Soil at CERCLA and RCRA Sites. Memo from Timothy Fields, EPA Acting Admini strator, to Regional Directors. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response. OSWER Directive 9200.4-26. Apr il 13, 1998. Available online at: http://www.epa.gov/superfund/reso urces/remedy/pdf/92-00426-s.pdf

EPA. 2000. Methodology for Deriving Am bient Water Quality Criteria for the Protection of Human Health ( 2000). U.S. Environmental Protection Agency, Office of Science and Technology, Office of Water. EPA 822-B-00-004. October. Available
online at: http://www.epa.gov/waterscience /criteria/humanhealth/method/

EPA. 2001. Comprehensive Five-Year Review Guidance. U.S. Environmental Protection Agency, Office of Emergency a nd Remedial Response. EPA 540-R-01-007.
OSWER No. 9355.7-03B-P. June 2001. Available online at: ww.epa.gov/superfund/accomp/5year/index.htmDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 19 - EPA. 2002a. Supplemental Guidance for Developing Soil Screening Levels for Superfund Sites. U.S. Environmental Prot ection Agency, Office of Solid Waste and Emergency Response. OSWER 9355.4-24. December 2002. Available online at: http://www.epa.gov/superfund/health/conmedia/soil/index.htm

.

EPA. 2002b. Role of Background in the CERCLA Cleanup Program. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response. OSWER 9285.6-07P. April 26, 2002. Available online at: http://www.epa.gov/swerrims/riskassessment/pdf/role.pdf

EPA. 2003a. Human Health Toxicity Values in Superfund Risk Assessments. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, DC. OSWER Directive 9285.7- 53. December 5, 2003. Available online

at: http://www.epa.gov/oswer/riskassessment/pdf/hhmemo.pdf

EPA. 2003b. Exposure and Human Health Reasse ssment of 2,3,7,8-Tetrachlorodibenzop-Dioxin (TCDD) and Related Compounds , NAS review draft, Volumes 1-3 (EPA/600/P-00/001Cb, Volume 1), National Ce nter for Environmental Assessment, Washington, DC (Dec.). Available online at: http://www.epa.gov/nceawww1/ pdfs/dioxin/nas-review/

EPA. 2004. Risk Assessment Guidance for Superfund Volume I: Human Health Evaluation Manual (Part E, Supplemental Guidan ce for Dermal Risk Assessment) Final. U.S. Environmental Protection Agency, Offi ce of Emergency and Remedial Response. EPA/540/R/99/005. July. Available online at: http://www.epa.gov/oswer/riskassessment/ragse/index.htm

EPA. 2007. Pilot Survey of Levels of Polychlorinated Dibenzo-P-Dioxins (PCDDs), Polychlorinated Dibenzofurans (PCDFs), Polychlorinated Biphenyls (PCB) and Mercury in Rural Soils of the U.S. U.S. Environmental Protection Agency, Washington, DC.
EPA/600/R-05/043F. Available online at: http://cfpub.epa.gov/ncea/CFM /recordisplay.cfm?deid=150944

EPA. 2009a. EPA’s Science Plan for Activities Related to Dioxins in the Environment. U.S. Environmental Protection Agency. May 26, 2009. Available on-line at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=209690

EPA. 2009b. State Soil Clea nup Levels for Dioxin. U.S. Environmental Protection Agency, National Center for Environmental Assessment. December 2009. Available
on-line at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=217926DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 20 - EPA. 2009c. Review of International Soil Concentrations for Dioxin. U.S. Environmental Protection Agency, Office of Superfund Remediation and Technology
Innovation. OSWER 9200.3-54. Decembe r 28, 2009. Available on-line at: http://www.regulations.gov and go to Docket No. EPA-HQ-SFUND-2009-0907.

EPA. 2009d. Risk Assessment Guidance for Superfund. Volume I: Human health Evaluation manual. (Part F, Supplemental Guidance for Inhalation Risk Assessment. U.S. Environmental protection Agency, Office of Superfund Remediation and Technology Innovation. EPA-540-R-070-002. OSWER 9285.7-82. January 2009.
Available online at: http://www.epa.gov/oswer/risk assessment/ragsf/index.htm

Faqi AS, Dalsenter PR, Merker HJ, Chahoud I. 1998. Reproductive toxicity and tissue
concentrations of low doses of 2,3,7,8-tetrachlorodibenzo-p-dioxi n in male offspring rats exposed throughout pregnancy and lactation. Toxicol. Appl. Pharmacol., 150:383-392.

FDA. 2008. Dioxin Interagency Working Gr oup Questions and Answers about Dioxins. U.S. Food and Drug Administration. September 2008. Available on line at: http://www.fda.gov/Food/FoodSafety/FoodCont aminantsAdulteration/ChemicalContami nants/DioxinsPCBs/ucm077524.htm

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Kociba RJ, Keyes DG, Beyer JE, et al. 1978. Results of a Two-Year Chronic Toxicity and oncogenicity Study of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) in rats. Toxicol. Appl. Pharmacol. 46:279-303.

Lorber M, Patterson D, Huwe J, Kahn H.. 2009. Evaluation of background exposures of Americans to dioxin-like compounds in th e 1990s and the 2000s. Chemosphere 77:640– 651.

Maronpot RR, Montgomery CA, Boorman GA, McConnell EE. 1986. National Toxicology Program Nomenclature for Hepatopr oliferative Lesions of Rats. Toxicol.
Pathol. 14:263-273.DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 21 - MDEQ. 1998. Technical Support Documen t: Part 201 Generic Soil Direct Contact Criteria (excerpt). Michig an Department of Environmental Quality, Environmental Response Division. August 31, 1998 Available online at:http://www.michigan.gov/documents/deq/deq-whm-hwp-dowexcerpt_of_dcc_tsd_251913_7.pdf

MNDOH. 2003. Cancer Risk Assessment for Dioxins. Prepared by Minnesota Department of Health (MNDOH) at the requ est of the Risk Evaluation/Air Modeling Unit, Environmental Standards and Analysis Section of the Minnesota Pollution Control Agency (March 17); Available online at: www.canceractionny.org/cance rriskassessment.htm

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Murray FJ, Smith FA, Nitschke KD, Humi ston CG, Kociba RJ, Schwetz BA. 1979. Three-generation reproduction study of rats given 2,3,7,8-te trachlorodibenzo-p-dioxin (TCDD) in the diet. Toxicol. Appl. Pharmacol. 50:241–252.

Nisbet ICT, Paxton MB. 1982. Statistical As pects of Three-Generation Studies of the Reproductive Toxicity of TCDD an d 2,4,5-T. Am. Stat. 36:290-298.

NTP. 1982. Carcinogenesis Bioassay of 2,3,7,8-tetrachlorodibenzo-p-dioxin (CAS No. 1746-01-6) in Osborne-Mende l rats and B6C3F1 Mice (Gavage Study). National Toxicology Program. Technical Report Series, Issue 209:195.

Ohsako S, Miyabara Y, Nishimura N, Kurosawa S, Sakaue M, Ishimura R, Sato M, Takeda K, Aoki Y, Sone H, Tohyama C, Y onemoto J. 2001. Maternal exposure to a low dose of 2,3,7,8-tetrachlorodibenz o-p-dioxin (TCDD) suppres sed the development of reproductive organs of male rats: Dose-dep endent increase of mRNA levels of 5- reductase type 2 in contrast to decrease of androgen receptor in the pubertal ventral prostate. Toxicol. Sci. 60:132–143.

Sauer RM. 1990. Pathology Working Group: 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Sprague-Dawley Rats. PATHCO, Inc. Submitted to the Maine Scientific Advisory panel.

Schantz SL, Ferguson SA, Bowman RE. 1992. Effects of 2,3,7,8-te trachlorodi-benzo-pdioxin on behavior of monkeys in peer groups. Neurotoxicol. Teratol. 14:433–446.

Van den Berg M, Birnbaum L, Bosveld ATC, Brunström B, Cook P, Feeley M, Giesy JP, Hanberg A, Hasegawa R, Kennedy SW, Kubiak T, Larsen JC, van Leeuwen FXR, Liem AKD, Nolt C, Peterson RE, Poellinger L, Safe S, Schrenk D, Tillitt D, Tysklind M, Younes M, Wærn F, Zacharewski T. 1998. T oxic Equivalency Factors (TEFs) for PCBs,DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 22 - PCDDs, PCDFs for Humans and W ildlife. Environmental Health Perspectives Volume 106, Number 12, December 1998.

Van den Berg M, Birnbaum LS, Denison M, De Vito M, Farland W, Feeley M, Fiedler H, Hakansson H, Hanberg A, Haws L, Rose M, Safe S, Schrenk D, Tohyama C, Tritscher A, Tuomisto J, Tysklind M, Walker N, Peterson RE. 2006. The 2005 World Health Organization Reevaluation of Human and Ma mmalian Toxic Equivalency Factors for
Dioxins and Dioxin-Like Compounds. Toxicological Sciences 2006 93(2):223-241.
Available online at: http://toxsci.oxfordjournals.org/cgi/content/abstract/93/2/223

WHO. 1991. Summary Report – Consultation on Tolerable Da ily Intake from Food of
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12:101-128.

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Geneva. Available on-line at: http://www.who.int/pcs/doc s/dioxin-exec-sum/exe-sumfinal.htmlDRAFT

TABLE 1 RECOMMENDED EQUATION FOR CO MPUTING CANCER PRGS FOR
EXPOSURE OF RESIDENTS TO DIOXIN IN SOIL

RBAEVABSSFS ABSSF IFSFEF ATTR gpgPRG

d GI o adjsoilo ⋅⋅⋅⋅ +⋅⋅ ⋅ ⋅

= ] )/( [ days/yr365 )/(

/

Parameter (description) Units Default Value

TR (target cancer risk) dimensionless 1E-04 to 1E-06
AT (averaging time) years 70
EF (exposure frequency) days/yr 350

SF o ( oral slope factor) (pg-kg-day) -1 1.56E-04 (a)

IF soil/adj (age-adjusted soil ingestion factor) g-yr/(kg-d) 0.114

ABS GI (gastrointestinal absorption frac tion) pg absorbed/pg ingested 1.0
SFS (age adjusted dermal factor) g-yr/kg-event 0.360

ABS d (dermal absorption fraction) pg absorbed/pg on skin 0.03 (b)
EV (dermal exposure frequency) events/day 1
RBA (relative bioavailability) -- 1

Source: EPA 2002 Equation 3-1 Includes oral and dermal exposure. (a) Based on EPA (1985) (b) Based on EPA (2004)

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 23 -DRAFT

TABLE 2 RECOMMENDED EQUATION FOR CO MPUTING CANCER PRGS FOR
EXPOSURE OF WORKERS TO DIOXIN IN SOIL

RBASAEVABSAFABSSFoSFIREDEF ATBWTR gpgPRG

d GI o ⋅⋅⋅⋅⋅ +⋅⋅⋅ ⋅ ⋅ ⋅

= ] )/( )[( days/yr365 )/(

Default Value Parameter (description) Units Indoor Worker Outdoor
Worker
TR (target cancer risk) Dimensionless 1E-04 to 1E-06 1E-04 to 1E-06
BW (body weight) Kg 70 70
AT (averaging time) Years 70 70
EF (exposure frequency) days/yr 250 225
ED (exposure duration) Years 25 25

SF o ( oral slope factor) (pg-kg-day) -1 1.56E-04 (a) 1.56E-04 (a)
IR (soil ingestion rate) g/day 0.05 0.10

ABS GI (gastrointestinal absorption fraction) pg absorbed/pg ingested 1.0 1.0

ABS d (dermal absorption fraction) pg absorbed/pg on skin -- 0.03 (b)
EV (dermal exposure frequency) events/day -- 1

AF (dermal adherence factor) g/cm 2

-- 2E-04

SA (dermal surface area) cm 2

-- 3300
RBA (relative bioavailability) -- 1 1

Source: EPA 2002 Equation 4-1 Includes oral and dermal exposure for outside wo rkers. Dermal exposure not quantified for an
indoor worker. (a) Based on EPA (1985) (b) Based on EPA (2004)

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 24 -DRAFT

TABLE 3 RECOMMENDED EQUATION FOR COMP UTING NON-CANCER PRGS FOR
EXPOSURE OF RESIDENTS TO DIOXIN IN SOIL

RBA ABSRfDSAEVABSAFRfDIREDEF RSC ATBWTHQ gpgPRG

GI o d o soil ⋅⋅ ⋅⋅⋅+
⋅⋅ ⋅ ⋅ ⋅ ⋅

= )] (/) (/[ days/yr365 )/(

Parameter (description) Units Default
Value

THQ (target hazard quotient) dimensionless 1
BW (body weight - child) kg 15
AT (averaging time) years 6
EF (exposure frequency) days/yr 350
ED (exposure duration) years 6

RfD o ( oral reference dose) pg/kg-day 1.0 (a)

IR soil (soil ingestion rate) g/day 0.20

ABS GI (gastrointestinal absorption frac tion) pg absorbed/pg ingested 1.0

AF (dermal adherence factor) g/cm 2 2E-04

ABS d (dermal absorption fraction) pg absorbed/pg on skin 0.03 (b)
EV (dermal exposure frequency) events/day 1
SA (dermal surface area exposed - child) cm 2 2,800
RBA (relative bioavailability) -- 1

RSC (relative source contribution) -- 1

Source: EPA 2002 Equation 3-2 Includes oral and dermal exposure. (a) Based on ATSDR (1998) chronic oral MRL (b) Based on EPA (2004)

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 25 -DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. - 26 - TABLE 4 RECOMMENDED EQUATION FOR COMP UTING NON-CANCER PRGS FOR
EXPOSURE OF WORKERS TO DIOXIN IN SOIL

RBA ABSRfDSAEVABSAFRfDIREDEF RSC ATBWTHQ gpgPRG

GI o d o soil ⋅⋅ ⋅⋅⋅+
⋅⋅ ⋅ ⋅ ⋅ ⋅

= )] (/) (/[ days/yr365 )/(

Default Value Parameter (description) Units Indoor
Worker Outdoor
Worker
THQ (target hazard quotient) Dimensionless 1 1
BW (body weight) Kg 70 70
AT (averaging time) Years 70 70
EF (exposure frequency) days/yr 250 225
ED (exposure duration) Years 25 25

RfD o ( oral reference dose) pg/kg-day 1.0 (a) 1.0 (a)
IR (soil ingestion rate) g/day 0.05 0.10

ABS GI (gastrointestinal absorption fraction) pg absorbed/pg ingested -- 1.0

ABS d (dermal absorption fraction) pg absorbed/pg on skin -- 0.03 (b)
EV (dermal exposure frequency) events/day -- 1

AF (dermal adherence factor) g/cm 2

-- 2E-04

SA (dermal surface area) cm 2

-- 3,300
RBA (relative bioavailability) -- 1 1

RSC (relative source contribution) -- 1 1

Source: EPA 2002 Equation 4-2 Includes oral and dermal exposure for outdoor wo rkers. Dermal exposure not quantified for an
indoor worker. (a) Based on ATSDR (1998) chronic oral MRL (b) Based on EPA (2004)DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A1-1 ATTACHMENT 1

EVALUATION OF RELATI VE DIOXIN INTAKE
FROM INHALATION AND INGESTION EXPOSURE

Exposure to a contaminant in soil may occu r by a number of path ways, including direct ingestion of soil, dermal cont act with soil, inhalation of soil particulates in air, and inhalation of vapors of the chemical released from soil to air. This Attachment compares the relative magnitude of human exposure to dioxin in soil by the inhalation route (including both inhalation of dioxin on air borne particulates a nd inhalation of dioxin vapor) compared to intake by the oral r oute using EPA’s default residential and commercial/industrial land exposure parameters. The dermal pathway is not included in the comparison because dermal exposure is e xpressed in terms of absorbed dose, while the oral and inhalation pathways are expressed in terms of ad ministered dose. However, based on default exposure assumptions, the de rmal pathway is relatively minor compared to oral. This Attachment does not compare risks associated with oral and inhalation pathways because there is no available inhala tion unit risk value for dioxin that has been derived in accordance with current guidan ce for inhalation risk assessment (EPA 2009d).

Relative Contribution from Inhalation of Particulates

The ratio of the amount of dioxin inhaled on respirable soil part icles (e.g., PM10s or PM2.5s) compared to the amount of dioxin inge sted with soil can be calculated as
described below.

Dose Inhaled (mg/day) = C soil · C PM10 · BR Dose Ingested (mg/day) = C soil · IR

where:

C soil = concentration of dioxin in soil
C PM10 = concentration of soil particles less than 10 μm in size in air (mg/m 3 ) BR = breathing rate (m 3 /day) IR = soil ingestion rate (mg/day)

The concentration of PM10 part icles in air is given by:

C PM10 (mg/m 3 ) = (1E-06 mg/kg) / PEFDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A1-2 where PEF = particulate emission factor (m 3 /kg).

The ratio of the daily intakes of dioxin by these two routes is then:

Ratio(inhal/ingest) = BR / (IR · PEF)

EPA (1991) provides recommende d default values for breath ing rate and soil ingestion rate for residents and workers, and EPA ( 2002) provides a recommended default PEF for
residential and industrial land use. Based on these inputs, the resu lting ratio of daily intakes (inhalation compared to oral) are as follows:

Parameter Value Parameter Child Adult Worker BR (m 3 /day) 10 20 10 IR (kg/day) 2E-04 1E-04 1E-04 PEF (m 3 /kg) 1.36E+09 1.36E+09 1.36E+09

Ratio (inhalation of dioxin on particulates vs. oral intake from soil) 0.00004 0.00015 0.00007

As indicated, based on recommended default exposure parameters, the amount of dioxin inhaled as respirable particulates is likely to be small (<< 1%) compared to the amount ingested with soil.

Relative Contribution from Inhalation of Volatiles

Similarly, the ratio of the daily intake of a chemical due to inhala tion of the volatilized chemical in air to the chemical ingested on soil:

Ratio(inhal/ingest) = BR / (IR · VF)

where VF = volatilization factor (m 3 /kg).

The value of the VF term may be calculated using Equation 4-8 in EPA (2002). Recommended default inputs and chemical-sp ecific terms are shown in Table A1-1. Based on these parameters, the value of VF is estimated to be 8.4E+06 m 3 /kg. Based on this, the ratios of dioxin intake from vapor inhalation compared to soil ingestion are as
follows:DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A1-3 Parameter Value Parameter Child Adult Worker BR (m 3 /day) 10 20 10 IR (kg/day) 2E-04 1E-04 1E-04 VF (m 3 /kg) 8.4E+06 8.4E+06 8.4E+06 Ratio (inhalation of vapors vs. oral intake) 0.006 0.024 0.012

As seen, exposure by inhalation of dioxin released to air from soil is likely to be small (< 2.4%) compared to the amount of dioxin ingested in soil.DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A1-4 TABLE A1-1 RECOMMENDED DEFAULT INPUTS AND CHEMICAL-SPECIFIC VALUES USED IN VOLATILIZATION FACTOR CALCULATION

Parameter (description) Units Value Source

Q/Cvol (inverse of the ratio of geometric mean air concentration to volatilization flux at a center of a square source) g/m 2 -s per kg/m 3 68.18 [a]

T (exposure interval) s 9.5E+08 [a]

Ρ b (dry soil bulk density) g/cm 3 1.5 [a]

Θ a (air-filled soil porosity) L air /L soil n- Θ
w [a]
n (total soil porosity) L pore /L soil 1-( Ρ b / Ρ s ) [a]

Θ
w (water-filled soil porosity) L air /L soil 0.15 [a]

Ρ s (soil particle density) g/cm 3 2.65 [a]

f
oc (fraction organic carbon in soil) g/g 0.006 [a]

D i (diffusivity in air) cm 2 /s 4.7E-02 [b]

H' (Henry’s law constant) dimensionless 2.04E-03 [c,d]

D
w (diffusivity in water) cm 2 /s 8E-06 [b]

K d (soil-water partition coefficient) cm 3 /g K
oc Α f
oc [a]

K
oc (soil-organic carbon partition coefficient) cm 3 /g 3.98E+06 [e]

Chemical-specific values are shaded in grey.

[ a] EPA (2002) [b] GSI Chemical Database: http://www.gsi-net.com/en/publications/gsi-chemicaldatabase/single/240.html [c] SRC PHYSPROP Database: http://www.syrres.com/what-we-do/product.aspx?id=133 [d] Converted to dimensionless using EPA’s On- line Tools for Site Assessment Calculation http://www.epa.gov/athens/learn2model/part-two/onsite/henryslaw.html [e] SRC CHEMFATE Database: http://www.srcinc.com/what-we-do/databaseforms.aspx?id=381DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A2-1 ATTACHMENT 2

DESCRIPTION OF CANDIDATE CANCER AND
NON-CANCER TOXICITY VALUES FOR DIOXIN

A. DERIVATION OF CANCER SLOPE FACTORS

The first step in computing recommended cancer-based Preliminary Remediation Goals (PRGs) for dioxin is to select the cancer slope factor. A re view of the approaches used by U.S. states, territories (EPA 2009b) and other U.S. health ag encies has identified five potential values, as discussed below.

EPA (1985)

EPA’s Office of Health and Environmental A ssessment reviewed the toxicity data for dioxin and prepared a Health Assessment Document (HAD) in September 1985 (EPA 1985). The HAD evaluated the cancer dose-re sponse data from each of two published
studies in animals:

• A two-year oral feeding study in male and female rats (Kociba et al. 1978). The
HAD evaluation considered two alternative pathological analyses of the slides from the study, including th e findings of the original pathologist (Kociba) and also an independent reviewer (Squire ) employed by EPA’s Cancer Assessment Group.

• A two-year oral gavage st udy in male and female rats and mice performed by the National Toxicology Program (NTP) of th e National Cancer Institute (NTP 1982).

The HAD fit a number of alternat ive cancer dose response data sets from each of these studies to the linearized multistage model to deri ve a series of alternative estimates of an oral cancer slope factor. These results are summarized in Table A2-1. The HAD found that the highest slope factor was obtained using the data from Kociba et al. (1978), using
the combined incidence of carcinomas in lung, carcinoma and hyperplastic nodules in liver, and carcinoma in nasal turbinates and hard palate in female rats. Based on the histopathological analysis of Kociba, the slope fact or was 1.51E-04 (pg/kg-day) -1 , while based on the histological analysis by Squi re, the slope factor was 1.61E-04 (pg/kg-day) -1

. The HAD identified the geometric mean of these two values (1.56E-04 (pg/kg-day) -1 ) asDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A2-2 the recommended slope factor. This approach was peer-reviewed by an expert panel assembled for a peer review workshop in Cincinnati in 1983, and by the Environmental Effects, Fate and Transport committee of EPA’s Science Advisory Board.

EPA (1997)

EPA’s Health Effects Assessment Summary Table (HEAST) (EPA 1997a) identifies an oral cancer slope fact or of 1.5E-04 (pg/kg-day) -1 . HEAST tables are described in EPA (1997) as containing “provisional risk asse ssment information” that “have not had enough review to be recognized as high qual ity, Agency-wide consensus information.” The primary source of the oral slope factor value for dioxin is the EPA (1985) HAD, but
the reason that the value lis ted is 1.5E-04 (pg/kg-day) -1 rather than 1.56E-04 (pg/kg-day) -

1 is not clear. The value was indicated as being provisional, and was qualified as being under further evaluation. Although the HAD (EPA 1985) is peer-reviewed, specific information on the peer review status of the value in HEAST has not been found.

CalEPA (1986, 2002)

California (CalEPA 1986, 2002) al so reviewed the cancer data from the study of Kociba et al. (1978) (including the hi stological analyses by both Ko ciba and Squire) and by NTP (1982). A number of different data sets were fit to the linearized multistage model to
derive inhalation unit risk values. These unit risk values, and the equivalent oral cancer slope factors, are summarized in Table A2-2. In this analysis, th e highest slope factor was found to occur using data from the NTP (1982) study on the incidence of carcinomas
and adenomas in male mouse liver. This slope factor was 1.3E-04 (pg/kg-day) -1 (CalEPA 1986). This slope factor wa s peer-reviewed in August 1986 by an independent ninemember Scientific Review Panel.

Michigan (MDEQ 1998)

Michigan uses a slope factor of 7.5E-05 (pg/kg-day) -1 , which is based on a re-analysis of the histological slides of liver s from female rats from the Ko ciba et al. (1978) study using the liver tumor classification scheme propos ed by NTP in 1986 (Maronpot et al. 1986). In this revised histological cl assification, lesions that were previously classified as “neoplastic nodules” and were c ounted as liver tumors are di vided into “hepatocellular hyperplasia” and “hepatocellu lar adenoma.” The term “hyperplasia” is reserved for proliferative lesions that are secondary responses to degene rative changes in the liver,
and these are not considered to be liver tumors. Foci of cellular alteration, including hepatocellular adenoma and hepatocellular ca rcinoma, are considered to represent aDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A2-3 spectrum of changes that comprise the natura l history of liver neoplasia, and these are counted as liver tumors (Maronpot et al. 1986).

The pathology slides from Kociba et al. (1978) were originally reclassified by Squire (an independent pathologist serving as a c onsultant to EPA’s Carcinogen Assessment Group), who reported that preliminary results from the re-reading indicated substantially lower liver tumor incidence (EPA 1990). Ba sed on a request from the Maine Science Advisory Panel, the slides were subseque ntly re-evaluated under the new system by seven independent pathologists referred to as the Pathology Working Group (PWG) (Sauer 1990, Goodman and Sauer 1992). Tabl e A2-3 summarizes th e results for liver lesions derived using the original and the re vised classification schemes. As shown, the incidence of liver tumors is substantially lower based on the new classification scheme than the original scheme. Based on total signi ficant tumors (liver, lung, nasal turbinates and hard palate), the cancer slope factor ba sed on the revised classification scheme is 7.5E-05 (pg/kg-day) -1 , as opposed to a value of 1.51E-04 using the original analysis (EPA 1990).

A three page document is publicly ava ilable on the Michigan Department of Environmental Quality website that summarizes the reevaluation of the Kociba data by the PWG; however, a description of the deri vation of the cancer sl ope factor is not included nor is information about external peer review of that deri vation. The findings of the PWG, however, were published in the peer reviewed literature. In short, documentation of the slope factor of 75,000 (mg/kg-day) -1 , including its derivation, peer review and supporting informati on, is very brief, and the information that is publicly available is limited or not completely transparent.

Minnesota (MNDOH 2003)

Minnesota uses a value of 1.4E-03 (pg/kg-day) -1 , which is based on the re-evaluation of the exposure-response data for liv er cancer in female rats reported in the EPA 2003 draft dioxin reassessment (EPA 2003b). In this appr oach, the tumor incidence data reported by Goodman and Sauer (1992) were used, whic h are based on the revised liver pathology scheme developed by NTP in 1986 (Maronpot et al. 1986). However, the dose metric was changed from administered dose (ug/kg-da y) to body burden (ug/g). This approach helps account for the large difference in ha lf-life of TCDD in hu mans and rats (EPA 2003b). The dose corresponding to a specified body burden was estimated using the following equation:

Intake (pg/kg-d) = Tissue Burden (pg/kg) · ln(2) / [t 1/2 · f]DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A2-4 where:

t 1/2 = half-life of dioxin in the body (days). A value of 2593 days was assumed for humans and 25 days in rats. f = fraction of an ingested dose that is absorbed (assumed to be 0.8)

Using the linearized multistage model and adjusting the dose metric as described, EPA (2003b) derived a cancer slope factor of 1.4E-03 (pg/kg-day) -1 . This value is 8.7 times higher than the cancer slope factor derive d by EPA (1985), and reflects the combined effect of using body burden rather than ingest ed dose (31 times higher) and the effect of using the revised histopathology in cidence data (3.6 times lower).

This approach and the resultan t slope factor have not undergone final Agency approval or final peer review.

B. DERIVATION OF NON-CANCER TOXICITY VALUES

The first step in computing recommended non-cancer-based PRG concentrations for
dioxin is to select a non-can cer toxicity value (RfD). 2 EPA currently does not have an Agency RfD for dioxin. Therefore, EPA re viewed non-cancer values used by states, foreign nations or other health agencies.

EPA Office of Drinking Water (1987)

In 1987, EPA’s Office of Drinking Water (ODW ) developed an oral RfD of 1 pg/kg-day for use in deriving a Lifetime Health Adviso ry value (EPA 1987). This RfD was based on a 3-generation reproductive st udy in rats (Murray et al. 197 9). In this study, animals were exposed to TCDD in the diet at concen trations that produced average doses of 0, 0.001, 0.01, or 0.1 ug/kg-day. Significant decreases in fertility and neonatal survival of offspring were observed in animals exposed to the 0.1 ug/kg-day dose level. At the dose of 0.01 ug/kg-day, signs of toxic ity included decreases in gest ational survival, decreased pup size at birth, and decreased neonatal survival and gr owth. For the 0.001 ug/kg-day dose group, no effect on fertility, litter size, or postnatal body weight was observed in any generation, and effects on neonatal survival were inconsistent. However, a re-evaluation of these data by Nisbet and Paxton (1982), us ing different statisti cal methods indicated

2 An RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitiv e subgroups) that is likely to be without an appreciable risk of deleterious effects duri ng a lifetime. It can be derived from a NOAEL, LOAEL, or benchmark dose, with uncertainty fact ors generally applied to reflect limitations of the data used..DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A2-5 that there was a reduction in the gestational index, decreased fetal weight, increased liver to body weight ratio, and increased inciden ce of dilated renal pelvis at the 0.001 ug/kg dose. From these results, EPA (1987) dete rmined that a dose of 0.001 ug/kg-day was the lowest-observed-adverse-effect-level (LOAEL), and calculated an RfD by dividing the LOAEL by an uncertainty fact or of 1,000, yielding a result of 1E-06 ug/kg-day (1 pg/kgday). The uncertainty factor of 1,000 was chosen in accordance with National Academy of Sciences (NAS) and EPA ODW guidelines for use with a LOAEL from an animal study. This uncertainty factor accounts for un certainty in extrapolation from animals to humans (10x), variation in sensitivity between humans (10x), and use of a LOAEL rather than a NOAEL (10x). ODW states that th is value has been peer-reviewed, but documentation of the peer review was not located.

ATSDR (1998)

ATSDR has derived a chronic or al Minimal Risk Level (MRL) 3 of 1 pg/kg-day (ATSDR 1998). This value is based on a study by Schant z et al. (1992) in which female monkeys were exposed to dioxin in the diet for 16 mont hs at 0, 5 or 25 ppt TC DD. After 7 months of exposure, the females were bred with unexposed males. Exposure of the females continued through mating, gestation and lact ation. Only one monkey in the high dose group delivered a viable offspring, so this gr oup was not studied furthe r. When offspring from the control group and the 5 ppt group were 8.6 months of age, they were placed in peer groups of 4 monkeys (2 exposed, 2 control) and allowed to play without interference. Behavioral pa tterns (social interactions, vo calizations, locomotion, selfdirected behavior, environment exploration) were monitored 4 days/week for 9 weeks. No overt signs of toxicity were observed in the mothers or the offspring, and birth weights were not adversely a ffected. However, significant alterations were observed in play behavior, displacement and self-direc ted behavior, with a tendency for offspring from exposed mothers to initiate more rough/-t umble play bouts, to retreat from play less often, and to engage in more self-directed behavior. Based on this, a dietary exposure level of 5 ppt was identified as a LOAEL. The estimated dose from this diet was 1.2E-04 ug/kg-day. This dose was adjust ed by dividing by an overall un certainty factor of 100 to account for use of a minimal LOAEL, inter- species extrapolation, and inter-individual variability. This yielded an MRL of 1E -06 ug/kg-day (1 pg/kg-day). All ATSDR Toxicity Profiles are peer revi ewed and publicly available.

3 An MRL is an estimate of the daily human exposure to a hazardous substance that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration of exposure. These substance-specific estimates, whic h are intended to serve as screening levels, are used by ATSDR health assessors and other res ponders to identify contaminants and potential health effects that may be of concern at hazardous waste sites.DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A2-6 WHO (1991, 1998); JECFA (2002)

The World Health Organization (WHO) has b een organizing expert consultations and workgroups for a number of year s to derive toxicity values for the evaluation of dioxin toxicity. The results of their first consulta tion was issued in 1990. At that time, WHO (1991, 1992) concluded that TCDD was carci nogenic in animals, acting as a nongenotoxic promoter-carcinogen. Therefore, the consultation deci ded to establish a Tolerable Daily Intake (TDI) 4 based on general toxicological effects. Based on liver, immunological and reproductive effects in anim als, the no-effect dose was estimated to be about 1,000 pg/kg-day. This value was adju sted to an equivalent human dose of 100 pg/kg-day using toxicokinetic da ta. After applying an uncerta inty factor of 10 to account for insufficient data on reproductive eff ects in humans, a TDI of 10 pg/kg-day was
recommended.

In 1998, the WHO European Centre for Environmental Health (WHO-ECEH) and International Programme on Chemical Safety (IPCS) performed a re-assessment of the available information on the toxicity of dioxin (WHO 1998), and reached the following key conclusions:

• The cancer effects of dioxin are mediated by a non-genotoxic m ode of action that is mediated via a receptor binding mechan ism. Consequently, cancer risk has a threshold, and exposures that do not cau se non-cancer effects will not increase
cancer risk.

• The most sensitive non-cancer effects caused by dioxin include developmental and reproductive effects in rats and monkeys.

• The most reliable metric of exposure for use in risk evaluation is tissue burden rather than ingested dose.

Based on these key conclusions, WHO (1998) es timated the TDI (pg/kg-day) for lifetime exposure in a series of 3 steps, as follows:

Step 1: Identify the tissue burden effect level for the most sensitive (and relevant) adverse responses. Based on st udies in rats and monkeys, the WHO estimated that the LOAEL tissue burdens ranged fr om 28-73 ng/kg (28,000-73,000 pg/kg).

4 A TDI is an estimate of the amount of a substance in air, food or drinking water that can be taken in daily over a lifetime without appreciable health risk. TDIs are calculated on the basis of laboratory toxicity data to which uncertainty factors are applied.DRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A2-7 Step 2: Given the tissue burden range, calcu late the TDI that would yield this tissue burden range. The WHO computed the TDI using a simple steady-state pharmacokinetic model of the following form:

TDI (pg/kg-d) = Tissue Burden (pg/kg) · [1-exp(-ln(2)/t 1/2 )] / f

where:

t 1/2 = half-life of dioxin in the body (days) f = fraction of an ingested dose that is absorbed

WHO utilized a half-life of 7.5 years (2,738 da ys), and an assumed fractional absorption of 0.5 (50%). Based on this, the TDI was estimated to range from 14-37 pg/kg-day.

Step 3: Adjust the TDI to account for uncertain ties. A factor of 10 was applied to address the following uncertainties: a) the us e of a range of LOAELs instead of a noeffect level, b) the possi ble differences in susceptibility between humans and experimental animals, c) the potential differences in susceptibilities within the human population, and d) differences in half-lives of elimination for the compounds of a complex TEQ mixture. After application of the uncertainty factor, the TDI (rounded) was estimated to range from 1-4 pg/kg-day. The WHO (1998) consultation stressed that the upper range of the TDI of 4 pg/kg-day s hould be considered a maximal tolerable intake on a provisional basis and that the ultimate goal is to reduce human intake levels to below 1 pg/kg-day.

More recently, the Joint FAO/WHO Expert Committee on Food Additives (JECFA 2002) re-evaluated dioxin toxicity based on two ne w reproductive studies (Ohsako et al. 2001 and Faqi et al. 1998) published since the previous assessment.

Faqi et al. (1998) exposed female rats s ubcutaneously with TCDD at 0, 25, 60 or 300 ng/kg, followed by weekly maintenance doses of 0, 5, 12 or 60 ng/kg, beginning 2 weeks before the beginning of mating and continua lly through mating, gestation and lactation. Male offspring were assessed for sexual develo pment and were bred to untreated females. Adverse effects on sperm were detected at all doses on postnatal day 170.

Ohsako et al. (2001) administered a singl e oral dose of 0, 12.5, 50, 200 or 800 ng/kg of TCDD to pregnant rats, and male offspring were assessed for reproductive development. Adverse effects that were noted on postna tal day 49 and/or day 120 included reduced anogenital distance (50, 200 or 800 ng/kg), reduced ventral pros tate weight (200 or 800 ng/kg), reduced androgen receptor messenger ribonucleic acid (mRNA) production inDRAFT

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. A2-8 ventral prostate (all doses) in creased 5-alpha-reductase type 2 mRNA in ventral prostate (all doses), and decrease androgen receptor mR NA in the ventral prostate (all doses).

JECFA (2002) used two altern ative models (linear model a nd power model) to estimate the relationship between fetal and maternal body burden and to cal culate a Provisional Tolerable Monthly Intake (PTMI) for each of these two new studies. The resulting
values are summarized in Table A2-4.

Based on these calculations, JECFA (2002) conc luded that the range of PTMI values was 40-100 pg/kg-month, and chose the mid-point of this range (70 pg/kg-month) as the final PTMI. Assuming 30 days/month, this is equivalent to a TDI of 2.3 pg/kg-day.

Because all of the evaluations described a bove were performed by panels of expert scientists, all of the TDI values derived are considered to be adequately peer-reviewed.DRAFTTABLE A2-1 CANCER SLOPE FACTORS DEVELOPED BY EPA (1985)StudyPathologistSpeciesGenderTissue(s)TumorType(s)CSF(pg/kg-day)-1Kociba et al. 1978KocibaRatMaleNasal turbinates/hard palateCarcinoma1.5E-05Kociba et al. 1978SquireRatMaleNasal turbinates/hardpalate/tongueCarcinoma1.7E-05Kociba et al. 1978KocibaRatFemaleLungNasal turbinate/hard palateLiverCarcinomaCarcinomaHyperplastic nodules or carcinoma1.51E-04Kociba et al. 1978SquireRatFemaleLungNasal turbinate/hard palateLiverCarcinomaCarcinomaHyperplastic nodules or carcinoma1.61E-04NTP 1982NTPRatFemaleLiverCarcinoma and neoplastic nodules3.3E-05NTP 1982NTPMouseMaleLiverCarcinoma7.5E-05NTP 1982NTPMouseFemaleSubcutaneous tissueBloodLiverFibrosarcomaLymphoma or leukemiaCarcinoma or adenoma4.6E-05Shaded cells indicate the slope factors recommended by EPA (1985) for use.THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BECONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY.A2-9DRAFTTABLE A2-2 CANCER SLOPE FACTORS DEVELOPED BY CALEPA (1986)StudyPathologistSpeciesGenderTissue(s)TumorType(s)iUR(ng/m3)-1x 103CSF(pg/kg-day)-1Kociba et al.1978KocibaRatMaleNasal turbinates/hard palateCarcinoma4.21.5E-05Kociba et al.1978SquireRatMaleNasal turbinates/hardpalate/tongueCarcinoma4.91.7E-05Kociba et al.1978KocibaRatFemaleLiverCarcinoma andneoplastic nodules279.5E-05Kociba et al.1978SquireRatFemaleLiverCarcinoma andneoplastic nodules258.8E-05NTP 1982NTPRatFemaleLiverCarcinoma andneoplastic nodules9.43.3E-05NTP 1982NTPMouseMaleLiverCarcinoma andadenomas381.3E-04NTP 1982NTPMouseFemaleSubcutaneous tissueFibrosarcoma2.48.4E-06Shaded cell indicates the slope factorrecommended by CalEPA (1986) for use.THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOTBE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY.A2-10DRAFTTABLE A2-3RECOMMENDED EQUATIONS FORCOMPUTING CANCER PRGS FOREXPOSURE OF RESIDENTS TO DIOIXN INSOIL LIVER TUMOROCCURRENCE IN FEMALE RATS (KOCIBA ET AL. 1978) BASED ONTWO ALTERNATIVE HISTOPATHOLOGICAL CLASSIFICATION METHODSOriginal Analysis (EPA 1985)Reanalysis (EPA 1990)Dose(ug/kg-day)HyperplasticnodulesHepatocellularcarcinomasTotal Animalswith LiverTumorsAdenomaHepatocellularCarcinomaTotal Animalswith LiverTumors08/861/869/862/860/862/860.0013/500/503/501/500/501/500.01018/502/5018/509/500/509/500.10023/4911/4934/4814/454/4518/45Source: EPA (1990, 2003b)THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BECONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY.A2-11DRAFTTHE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BECONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY.A2-12TABLE A2-4. RECOMMENDED EQUATIONFOR COMPUTING CANCER PRGS FOREXPOSURE OF WORKERS TO DIOXIN IN SOILTDI CALCULATIONS FROM JECFA (2002)Faqi et al. (1998)Ohsako et al. (2001)ParameterLinearModelPowerModelLinearModelPowerModelLOEL Maternal body burden (ng/kg)25257.67.6Equivalent body burden with repeated dosing (ng/kg)25391319Body burden from feed (ng/kg)3333Total body burden (ng/kg)28421622EHMIa(pg/kg per month)423630237330Safety factor9.69.63.23.2PTMI (pg/kg per month)446674103TDIb(pg/kg-day)1.52.22.53.4aEquivalent human monthly intakebCalculated based on 30 days per month