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 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 Remediation and Technology Innovation 

Washington, D.C. 

December 30, 2009 
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LIST OF ACRONYMS AND ABBREVIATIONS 

ARAR Applicable or Relevant and Appropriate Requirement 

ATSDR Agency for Toxic Substances and Disease Registry 

CERCLA Comprehensive Environmental Response, 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 Remediation 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 Reviewed Toxicity Value 

ppt Parts per trillion 

PRG Preliminary Remediation Goal 
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LIST OF ACRONYMS AND ABBREVIATIONS - continued 

PTMI Provisional Tolerable 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 Health 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 Organization 
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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 Protection Agency’s (EPA) Administrator Lisa P. 

Jackson decided that EPA needs to accelerate work underway to reassess the human 

health risks from exposures to dioxin. EPA’s Science Plan for Activities Related to 

Dioxins in the Environment (EPA 2009a) details a plan, with 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 Site in Michigan, the Administrator stated: 

“As we move forward to develop remediation strategies at this site, the science on 

dioxin’s health and ecological effects will obviously play an important role in our 

decisions. Although EPA scientists, supported 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 assessment of dioxin’s risks 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 with this letter, announcing 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 Emergency Response will review current dioxin 

cleanup guidance set by the Agency and the 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 interim PRGs by the end of the year.” 

EPA’s Office of Research and Development (ORD) expects to complete the dioxin 

reassessment by the end of 2010, subject to further consideration of the science and the 

scope and complexity of the revisions that will need to be made. ORD will be 

responding to all National Academy of Sciences (NAS) comments received on EPA’s 

draft 2003 dioxin reassessment. 
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EPA’s Office of Solid Waste and Emergency 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/sfremedy/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 formulating 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 recommended 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 finalized 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 decisions at Comprehensive Environmental 

Response, Compensation, and Liability Act (CERCLA) and Resource Conservation and 

Recovery Act (RCRA) sites that were based 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 protect against cancer and 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 are intended for use in evaluating dioxin 

(2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) and other dioxin-like compounds in soil. 

Dioxin-like compounds, including other polychlorinated dibenzodioxins (PCDDs), 

dibenzofurans (PCDFs) and biphenyls (PCBs) may collectively be evaluated using the 
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recommended PRGs for dioxin after adjustment to account for relative toxicity using 

toxicity equivalency factors (TEFs) to calculate 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 associated with risk estimates based on TEQs. 

Therefore, risk assessors should identify the fraction of the TEQ attributable to dioxin 

and to each chemical class of dioxin-like compounds (i.e., PCDDs, PCDFs, and PCBs). 

For CERCLA and RCRA sites, Regions generally should consider using the 

recommended interim PRGs in this guidance as a starting point for residential and 

commercial/industrial soil cleanup levels. EPA encourages State and Tribal programs 

that do not use PRGs to consider the recommended interim PRGs as starting point 

concentrations to develop cleanup levels. 

This guidance supersedes OSWER’s previous 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 exposure 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 available inhalation unit risk value for dioxin that 

has been derived in accordance with current 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 currently conducting as part of the final dioxin 

reassessment. As a result, there is uncertainty 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 new science that was released since the NAS 

review. A final dioxin reassessment is still under development. 
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This draft guidance presents current OSWER technical and policy recommendations 

regarding PRGs for soil contaminated with dioxin. While OSWER developed this draft 

guidance for facility response actions under 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 technically sound approaches after appropriate 

review, either at its own initiative or at the suggestion of other 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 that EPA administers or their implementing 

regulations, nor is it a regulation 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 specific 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 requirement for selected remedies (see 40 CFR 

§300.430(f)(1)(i)(A)). In the CERCLA remedy selection process, PRGs typically are 

used when developing cleanup levels. At CERCLA sites, PRGs typically are “specific 

statements of desired endpoint concentrations of risk levels (55 FR 8713, March 8, 1990) 

that are conservative, default endpoint concentrations 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 development of remedial alternatives before 

consideration of more detailed information 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: 
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(A) Applicable or relevant and appropriate requirements (ARARs) under federal 

environmental or state environmental or facility 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 adverse 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 finalized, 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 that a soil concentration 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 starting 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 commercial/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 developing cleanup levels for CERCLA sites. A 

range in soil concentrations was recommended for commercial/ industrial soils due to the 

greater variability in exposures associated with 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 excess cancer risks to residents from oral exposure to dioxin in 

soil at a PRG of 1,000 ppt dioxin TEQ was about 2.5E-04, and that lifetime excess cancer 
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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 were 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 indoor worker (oral exposure only), while 

the most exposed worker is usually an outdoor worker with both oral and dermal 

exposure 

Based on a consideration of a number of factors, the Administrator has determined that it 

is important to develop updated interim PRGs to be used until the release of the final 

dioxin reassessment. The following sections describe the approach used by EPA to 

provide and select new recommended interim PRGs for dioxin. 

RECOMMENDATIONS 

Recommended Toxicity Values

The most common health effect in people 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. Other effects of exposure to large amounts of 

dioxin include skin rashes, skin 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 cancer. Animal studies have also shown an 

increased risk of cancer from long-term exposure to dioxins. 

Finally, based on data from animal studies, there is some concern that exposure to low 

levels of dioxins over long periods (or high level exposures at sensitive times) might 
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result in reproductive or developmental effects (FDA, 2008). Consequently, both a 

cancer slope factor and a non-cancer toxicity value are used to derive PRGs for cancer 

and non-cancer effects. 

Hierarchy for Selecting Interim Toxicity Values 

OSWER has developed a recommended hierarchy (EPA 2003a) for the selection of 

toxicity values, including those 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 IRIS are considered to be Tier 1. If no 

data are available in IRIS, the next preference (Tier 2) is Provisional Peer Reviewed 

Toxicity Values (PPRTVs) developed by EPA NCEA’s Superfund Technical Health Risk 

Support Center (STSC). If toxicity values are 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 available. 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 values should be transparent. It should be 

noted that these procedures are specific 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. Consequently, for the purposes of providing these 

recommended interim PRGs for dioxin, EPA reviewed 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 further 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, given the revised toxicity values. If important 

new scientific information becomes available before a new IRIS toxicity assessment is 

finalized, EPA may issue additional guidance addressing the recommended interim 

toxicity values discussed in this guidance. 

Recommended Cancer Slope Factor 
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Because EPA does not have a Tier 1 or Tier 2 cancer toxicity value for dioxin, EPA 

reviewed available cancer slope factors for dioxin (EPA 2009b) to determine whether 

they would meet EPA’s Tier 3 criteria. Five primary candidate values were identified, as 

follows: 

• EPA’s Office of Health and Environmental Assessment (EPA 1985) developed an 

oral cancer slope factor 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 Assessment 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 cancer slope factor of 1.3E04 (pg/kg-day)-1. This is based on the occurrence 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 factor 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. (1978) 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-evaluation 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 not considered appropriate because it is based 

on the 2003 EPA draft dioxin reassessment (EPA 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 information, 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 listed in the source document. Of the two 

remaining slope factors (EPA 1985, CalEPA 1986), both are publicly available, 
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transparent as to their derivation, and were adequately peer-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. Therefore, EPA reviewed non-cancer toxicity 

values developed by States, foreign countries, or other health agencies (EPA 2009b, 

2009c). Based on a review of available documents, 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 offspring of female monkeys exposed to dioxin 

in the diet for 16 months, including the period of gestation and 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 support derivation of a lifetime health 

advisory for TCDD. This value is based on the occurrence of reproductive effects 

in animals. 

• A range of Tolerable Daily Intake (TDI) values, ranging from about 1 pg/kg-day 

to 4 pg-kg-day, developed by the WHO (WHO 1991, 1998; JECFA 2002). These 

values are derived by identifying a no-effect tissue burden in exposed animals for 

a range of non-cancer effects, and computing the average daily intake level that 

would yield the no-effect tissue burden in humans. 

Each of these approaches is described 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 the most appropriate value for use in the 

development of non-cancer PRGs. This value 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 ODW (EPA 1987), and is also consistent 

with the low end of the range of TDI values developed by WHO (1991, 1998; JECFA 
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2002). Note that ATSDR (2008) has used the 1 pg/kg-day value to derive a soil 

screening concentration of 50 ppt1

 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 (RAGS) 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 exposure equations and exposure parameters 

discussed in the more recent EPA guidance (2002a) along with the RAGS dermal 

guidance (EPA 2004). For workers, RAGS B recommends evaluating only indoor 

workers, while EPA (2002a) recommends evaluating both indoor and outdoor workers. 

Also, EPA (2002a) recommends evaluating non-cancer risk to a resident 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-weighted average intake rate across childhood and 

adulthood). Soil PRGs calculated using EPA 2002a equations are generally appropriate 

provided that conditions at the site are the same as the conditions assumed in the 

calculations. Site managers wishing to use 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 workers (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 assumed 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). The 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.. 
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• 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 inhalation 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 assumed 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 are 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 generally 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 compared 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 document, 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 assumption for establishing a default PRG because 

use of a RBA factor of 1.0 will ensure protectiveness. However, this assumption 

may need to be revisited when performing site-specific assessments. 

• RSC. The Relative Source Contribution (RSC) 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 threshold, and are used mainly by EPA in 

developing water standards (EPA 2000). In cases where other sources (e.g., the 

diet) contribute a substantial fraction of the ingestion exposure, then the RSC term 

may be set to some lower value. The national 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 accounted 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 recommending. 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 are 
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. 

- 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 much 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 protection against cancer effects at the 1E-06 

risk level may be computed in accordance 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 Based on Cancer (1E-06 Risk Level) 

Land Use Receptor PRG 

(ppt TEQ) 

Residential Resident 3.7 

Commercial/ Indoor Worker 37 

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 

Commercial/ Indoor Worker 2,000 

Industrial Outdoor Worker 950 

 All PRGs are shown to two significant figures 
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. 

- 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 residential soil and 950 ppt dioxin 

TEQ in commercial/industrial soil. EPA believes that these recommended interim PRGs 

generally provide adequate protection against non-cancer effects. In addition, they 

generally are protective for cancer effects at approximately 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 recommended 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/industrial soils, respectively (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 described above if finalized would be 

appropriate for use on an interim basis until EPA releases its final dioxin reassessment. 

However, EPA is also considering an alternative concentration of 3.7 ppt dioxin TEQ in 

residential soil and 17 ppt dioxin TEQ in commercial/industrial soil as the point of 

departure for determining PRGs. These alternative 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 concentrations of dioxins in U.S. soils. A recent 

EPA report found mean rural soil concentrations ranging from 0.2 to 11.4 ppt dioxin TEQ 

(EPA 2007). Generally, it is OSWER policy to not set site specific 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 is 
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. 

- 14 - 

taking comments on all aspects of this draft guidance, 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 meeting or waiving ARARs) under CERCLA or 

RCRA. For example, the maximum contaminant 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 OSWER’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 finalized, 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 impact of the dioxin reassessment and will 

update these PRGs as appropriate. 

These draft recommended interim soil PRGs are national levels protective for cancer and 

non-cancer effects from ingestion and dermal contact with surface soils in residential 

and commercial/industrial exposure scenarios. Inhalation exposure 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 derived in accordance with current 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. Once finalized, the interim guidance will supersede 

OSWER’s previous 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 contact (ingestion, dermal contact, and inhalation exposure (this is 

minimal for dioxin particulates and vapors)) with surface soils in residential and 

commercial/industrial exposure scenarios. Exposure 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-specific 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, including, where appropriate, other 

Federal agency-lead and state-lead sites, Regions should consult with the Office of 

Superfund Remediation and Technology Innovation (OSRTI) Site Assessment and 

Remedy Decisions Branch on all proposed dioxin cleanups that are conducted under 

Superfund. Consultation should be initiated at the risk assessment stage, and continue 

through the process. 

For removal actions, Regions should contact Headquarters for concurrence on non-NPL 

removal actions where dioxin is a principal 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 determined on a site-specific basis, and 

trigger levels for initiating a removal action are sometimes higher than the levels used as 

either PRGs (or starting points) or final cleanup levels. 

For sites where another Federal agency is the lead agency, OSRTI will notify the Federal 

Facilities Restoration Reuse Office of ongoing consultations regarding dioxin soil 

cleanup levels. The Office of Site Remediation Enforcement will provide support if 

enforcement issues are identified. For consultation procedures, refer to OSWER 

Directive 9200.4-19 (EPA 1996) and OSWER Directive 9200.1-18FS (EPA 1997b). 

Once finalized, Regions performing five-year-reviews of CERCLA remedial sites where 

soils contaminated with dioxin or other dioxin-like compounds have been left in place 

should consider this guidance on recommended interim PRGs when evaluating whether 

the original remedies in the Records of Decision (ROD) remain protective for the 

contaminated areas. Consistent with existing five-year-review guidance (EPA 2001), 

OSWER recommends that the five-year-reviews include an evaluation of existing site 

data, identification of the need for additional 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 additional data collection and/or site cleanup is 

appropriate. Once the final dioxin reassessment 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 ensure 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 points in developing soil cleanup levels, unless they have 

developed their own standards or guidance. Because States are the primary implementers 
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. 

- 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 consistent 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 - 

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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. 

- 18 - 

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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. 

- 19 - 

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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. 

- 20 - 

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DRAFT 

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN 

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REPRESENT ANY AGENCY DETERMINATION OR POLICY. 

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DRAFT 

THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN 

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DRAFT 

TABLE 1 

RECOMMENDED EQUATION FOR COMPUTING CANCER PRGS FOR 

EXPOSURE OF RESIDENTS TO DIOXIN IN SOIL 

IFSFEF ABSSF RBAEVABSSFS

ATTR gpgPRG

adjsoilo o GI d +⋅⋅ ⋅⋅⋅⋅

⋅ ⋅ = [ )/( ]

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 

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

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

ABSGI (gastrointestinal absorption fraction) pg absorbed/pg ingested 1.0 

SFS (age adjusted dermal factor) g-yr/kg-event 0.360 

ABSd (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 COMPUTING CANCER PRGS FOR 

EXPOSURE OF WORKERS TO DIOXIN IN SOIL 

RBASAEVABSAFABSSFoSFIREDEF

ATBWTR gpgPRG

o GI d +⋅⋅⋅ ⋅⋅⋅⋅⋅

⋅ ⋅ ⋅ = )[( )/( ]

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 

SFo (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 

ABSGI (gastrointestinal absorption 

fraction) pg absorbed/pg ingested 1.0 1.0 

ABSd (dermal absorption fraction) pg absorbed/pg on skin -- 0.03 (b) 

EV (dermal exposure frequency) events/day -- 1 

AF (dermal adherence factor) g/cm2 -- 2E-04 

SA (dermal surface area) cm2 -- 3300 

RBA (relative bioavailability) -- 1 1 

Source: EPA 2002 Equation 4-1 

Includes oral and dermal exposure for outside workers. 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 COMPUTING NON-CANCER PRGS FOR 

EXPOSURE OF RESIDENTS TO DIOXIN IN SOIL 

ABSRfDSAEVABSAFRfDIREDEF RBA

ATBWTHQ RSC gpgPRG

soil o d o GI ⋅⋅ ⋅⋅⋅+ ⋅⋅

⋅ ⋅ ⋅ ⋅ = (/[ (/) )]

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 

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

IRsoil (soil ingestion rate) g/day 0.20 

ABSGI (gastrointestinal absorption fraction) pg absorbed/pg ingested 1.0 

AF (dermal adherence factor) g/cm2 2E-04 

ABSd (dermal absorption fraction) pg absorbed/pg on skin 0.03 (b) 

EV (dermal exposure frequency) events/day 1 

SA (dermal surface area exposed - child) cm2 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 COMPUTING NON-CANCER PRGS FOR 

EXPOSURE OF WORKERS TO DIOXIN IN SOIL 

ABSRfDSAEVABSAFRfDIREDEF RBA

ATBWTHQ RSC gpgPRG

soil o d o GI ⋅⋅ ⋅⋅⋅+ ⋅⋅

⋅ ⋅ ⋅ ⋅ = (/[ (/) )]

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 

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

IR (soil ingestion rate) g/day 0.05 0.10 

ABSGI (gastrointestinal absorption 

fraction) pg absorbed/pg ingested -- 1.0 

ABSd (dermal absorption fraction) pg absorbed/pg on skin -- 0.03 (b) 

EV (dermal exposure frequency) events/day -- 1 

AF (dermal adherence factor) g/cm2 -- 2E-04 

SA (dermal surface area) cm2 -- 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 workers. Dermal exposure not quantified for an 

indoor worker. 

(a) Based on ATSDR (1998) chronic oral MRL 

(b) Based on EPA (2004) 
DRAFT 

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A1-1 

ATTACHMENT 1 

EVALUATION OF RELATIVE DIOXIN INTAKE 

FROM INHALATION AND INGESTION EXPOSURE 

Exposure to a contaminant in soil may occur by a number of pathways, including direct 

ingestion of soil, dermal contact 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 airborne particulates and inhalation of dioxin 

vapor) compared to intake by the oral route using EPA’s default residential and 

commercial/industrial land exposure parameters. The dermal pathway is not included in 

the comparison because dermal exposure is expressed in terms of absorbed dose, while 

the oral and inhalation pathways are expressed in terms of administered dose. However, 

based on default exposure assumptions, the dermal pathway is relatively minor compared 

to oral. This Attachment does not compare risks associated with oral and inhalation 

pathways because there is no available inhalation unit risk value for dioxin that has been 

derived in accordance with current guidance for inhalation risk assessment (EPA 2009d). 

Relative Contribution from Inhalation of Particulates

The ratio of the amount of dioxin inhaled on respirable soil particles (e.g., PM10s or 

PM2.5s) compared to the amount of dioxin ingested with soil can be calculated as 

described below. 

Dose Inhaled (mg/day) = Csoil · CPM10 · BR 

Dose Ingested (mg/day) = Csoil · IR 

where: 

 Csoil = concentration of dioxin in soil 

CPM10 = concentration of soil particles less than 10 μm in size in air (mg/m3) 

 BR = breathing rate (m3

/day) 

IR = soil ingestion rate (mg/day) 

The concentration of PM10 particles in air is given by: 

 CPM10 (mg/m3

) = (1E-06 mg/kg) / PEF 
DRAFT 

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A1-2 

where PEF = particulate emission factor (m3

/kg). 

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

 Ratio(inhal/ingest) = BR / (IR · PEF) 

EPA (1991) provides recommended default values for breathing 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 resulting ratio of daily 

intakes (inhalation compared to oral) are as follows: 

Parameter Value Parameter Child Adult Worker 

BR (m3/day) 10 20 10 

IR (kg/day) 2E-04 1E-04 1E-04 

PEF (m3/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 inhalation of the volatilized 

chemical in air to the chemical ingested on soil: 

 Ratio(inhal/ingest) = BR / (IR · VF) 

where VF = volatilization factor (m3

/kg). 

The value of the VF term may be calculated using Equation 4-8 in EPA (2002). 

Recommended default inputs and chemical-specific terms are shown in Table A1-1. 

Based on these parameters, the value of VF is estimated to be 8.4E+06 m3

/kg. Based on 

this, the ratios of dioxin intake from vapor inhalation compared to soil ingestion are as 

follows: 
DRAFT 

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A1-3 

Parameter Value Parameter Child Adult Worker 

BR (m3/day) 10 20 10 

IR (kg/day) 2E-04 1E-04 1E-04 

VF (m3/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 

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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/m2

-s per kg/m3 68.18 [a] 

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

Ρb (dry soil bulk density) g/cm3 1.5 [a] 

Θa (air-filled soil porosity) Lair/Lsoil n- Θw [a] 

n (total soil porosity) Lpore/Lsoil 1-( Ρb/ Ρs) [a] 

Θw (water-filled soil porosity) Lair/Lsoil 0.15 [a] 

Ρs (soil particle density) g/cm3 2.65 [a] 

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

Di (diffusivity in air) cm2/s 4.7E-02 [b] 

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

Dw (diffusivity in water) cm2/s 8E-06 [b] 

Kd (soil-water partition coefficient) cm3/g Koc Α foc [a] 

Koc (soil-organic carbon partition coefficient) cm3/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=381 
DRAFT 

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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 review of the approaches used 

by U.S. states, territories (EPA 2009b) and other U.S. health agencies has identified five 

potential values, as discussed below. 

EPA (1985) 

EPA’s Office of Health and Environmental Assessment reviewed the toxicity data for 

dioxin and prepared a Health Assessment Document (HAD) in September 1985 (EPA 

1985). The HAD evaluated the cancer dose-response 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 the findings of the original pathologist (Kociba) and 

also an independent reviewer (Squire) employed by EPA’s Cancer Assessment 

Group. 

• A two-year oral gavage study in male and female rats and mice performed by the 

National Toxicology Program (NTP) of the National Cancer Institute (NTP 1982). 

The HAD fit a number of alternative cancer dose response data sets from each of these 

studies to the linearized multistage model to derive 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 factor was 1.51E-04 (pg/kg-day)-1, while 

based on the histological analysis by Squire, 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) as 
DRAFT 

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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 factor of 1.5E-04 (pg/kg-day)-1. HEAST tables are described in EPA 

(1997) as containing “provisional risk assessment information” that “have not had 

enough review to be recognized as high quality, 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 listed 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) also reviewed the cancer data from the study of Kociba 

et al. (1978) (including the histological analyses by both Kociba 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, the 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 was 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 livers from female rats from the Kociba et al. (1978) study using 

the liver tumor classification scheme proposed by NTP in 1986 (Maronpot et al. 1986). 

In this revised histological classification, lesions that were previously classified as 

“neoplastic nodules” and were counted as liver tumors are divided into “hepatocellular 

hyperplasia” and “hepatocellular adenoma.” The term “hyperplasia” is reserved for 

proliferative lesions that are secondary responses to degenerative changes in the liver, 

and these are not considered to be liver tumors. Foci of cellular alteration, including 

hepatocellular adenoma and hepatocellular carcinoma, are considered to represent a 
DRAFT 

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FORMALLY DISSEMINATED BY EPA AND SHOULD NOT BE CONSTRUED TO 

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A2-3 

spectrum of changes that comprise the natural 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 consultant to EPA’s Carcinogen Assessment 

Group), who reported that preliminary results from the re-reading indicated substantially 

lower liver tumor incidence (EPA 1990). Based on a request from the Maine Science 

Advisory Panel, the slides were subsequently re-evaluated under the new system by 

seven independent pathologists referred to as the Pathology Working Group (PWG) 

(Sauer 1990, Goodman and Sauer 1992). Table A2-3 summarizes the results for liver 

lesions derived using the original and the revised 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 significant tumors (liver, lung, nasal turbinates 

and hard palate), the cancer slope factor based 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 available on the Michigan Department of 

Environmental Quality website that summarizes the reevaluation of the Kociba data by 

the PWG; however, a description of the derivation of the cancer slope factor is not 

included nor is information about external peer review of that derivation. 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 information, 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 liver cancer in female rats reported in the EPA 2003 draft 

dioxin reassessment (EPA 2003b). In this approach, the tumor incidence data reported by 

Goodman and Sauer (1992) were used, which 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-day) to body burden (ug/g). This approach 

helps account for the large difference in half-life of TCDD in humans 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) / [t1/2 · f] 
DRAFT 

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A2-4 

 

where: 

t1/2 = 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 derived by EPA (1985), and reflects the combined 

effect of using body burden rather than ingested dose (31 times higher) and the effect of 

using the revised histopathology incidence data (3.6 times lower). 

This approach and the resultant 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-cancer toxicity value (RfD). 2

 EPA currently does not have an 

Agency RfD for dioxin. Therefore, EPA reviewed 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 Advisory value (EPA 1987). This RfD was based 

on a 3-generation reproductive study in rats (Murray et al. 1979). In this study, animals 

were exposed to TCDD in the diet at concentrations 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 toxicity included decreases in gestational survival, decreased 

pup size at birth, and decreased neonatal survival and growth. 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), using different statistical 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 sensitive subgroups) that is likely to be without an 

appreciable risk of deleterious effects during a lifetime. It can be derived from a NOAEL, 

LOAEL, or benchmark dose, with uncertainty factors generally applied to reflect limitations of 

the data used.. 
DRAFT 

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A2-5 

 

that there was a reduction in the gestational index, decreased fetal weight, increased liver 

to body weight ratio, and increased incidence of dilated renal pelvis at the 0.001 ug/kg 

dose. From these results, EPA (1987) determined 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 factor 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 uncertainty 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 this value has been peer-reviewed, but 

documentation of the peer review was not located. 

ATSDR (1998) 

ATSDR has derived a chronic oral Minimal Risk Level (MRL)3

 of 1 pg/kg-day (ATSDR 

1998). This value is based on a study by Schantz et al. (1992) in which female monkeys 

were exposed to dioxin in the diet for 16 months at 0, 5 or 25 ppt TCDD. After 7 months 

of exposure, the females were bred with unexposed males. Exposure of the females 

continued through mating, gestation and lactation. Only one monkey in the high dose 

group delivered a viable offspring, so this group was not studied further. 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 patterns (social interactions, vocalizations, 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 affected. However, significant alterations were observed in 

play behavior, displacement and self-directed behavior, with a tendency for offspring 

from exposed mothers to initiate more rough/-tumble 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 adjusted by dividing by an overall uncertainty 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 reviewed 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, which are intended to serve as screening levels, are 

used by ATSDR health assessors and other responders 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 been organizing expert consultations and 

workgroups for a number of years to derive toxicity values for the evaluation of dioxin 

toxicity. The results of their first consultation was issued in 1990. At that time, WHO 

(1991, 1992) concluded that TCDD was carcinogenic in animals, acting as a nongenotoxic promoter-carcinogen. Therefore, the consultation decided to establish a 

Tolerable Daily Intake (TDI)4 based on general toxicological effects. Based on liver, 

immunological and reproductive effects in animals, the no-effect dose was estimated to 

be about 1,000 pg/kg-day. This value was adjusted to an equivalent human dose of 100 

pg/kg-day using toxicokinetic data. After applying an uncertainty factor of 10 to account 

for insufficient data on reproductive effects 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 mode of action that 

is mediated via a receptor binding mechanism. Consequently, cancer risk has a 

threshold, and exposures that do not cause 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) estimated 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 studies in rats and monkeys, the WHO estimated that the 

LOAEL tissue burdens ranged from 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 

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A2-7 

Step 2: Given the tissue burden range, calculate 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)/t1/2)] / f 

where: 

t1/2 = 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 days), 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 uncertainties. A factor of 10 was applied to 

address the following uncertainties: a) the use of a range of LOAELs instead of a noeffect level, b) the possible 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 should 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 new reproductive studies (Ohsako et al. 2001 

and Faqi et al. 1998) published since the previous assessment. 

Faqi et al. (1998) exposed female rats subcutaneously 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 continually through mating, gestation and lactation. 

Male offspring were assessed for sexual development 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 single 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 postnatal day 49 and/or day 120 included reduced 

anogenital distance (50, 200 or 800 ng/kg), reduced ventral prostate weight (200 or 800 

ng/kg), reduced androgen receptor messenger ribonucleic acid (mRNA) production in 
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. 

A2-8 

ventral prostate (all doses) increased 5-alpha-reductase type 2 mRNA in ventral prostate 

(all doses), and decrease androgen receptor mRNA in the ventral prostate (all doses). 

JECFA (2002) used two alternative models (linear model and power model) to estimate 

the relationship between fetal and maternal body burden and to calculate 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) concluded 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 above were performed by panels of expert 

scientists, all of the TDI values derived are considered to be adequately peer-reviewed. 
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TABLE A2-1 CANCER SLOPE FACTORS DEVELOPED BY EPA (1985) 

Study Pathologist Species Gender Tissue(s) Tumor Type(s) Kociba et al. 1978 Kociba Rat Male Nasal turbinates/hard palate Carcinoma Kociba et al. 1978 Squire Rat Male Nasal turbinates/hard palate/tongue Carcinoma Kociba et al. 1978 Kociba Rat Female 

Lung Nasal turbinate/hard palate Liver 

Carcinoma Carcinoma Hyperplastic nodules or carcinoma 

Kociba et al. 1978 Squire Rat Female 

Lung Nasal turbinate/hard palate Liver 

Carcinoma Carcinoma Hyperplastic nodules or carcinoma 

NTP 1982 NTP Rat Female Liver Carcinoma and neoplastic nodules NTP 1982 NTP Mouse Male Liver Carcinoma NTP 1982 NTP Mouse Female 

Subcutaneous tissue Blood Liver 

Fibrosarcoma Lymphoma or leukemia Carcinoma or adenoma 

Shaded 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 SHOCONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. 
DRAFT 

TABLE A2-2 CANCER SLOPE FACTORS DEVELOPED BY CALEPA (1986) 

Study Pathologist Species Gender Tissue(s) Tumor Type(s) iUR (ng/m3)-1 Kociba et al. 1978 Kociba Rat Male Nasal turbinates/hard palate Carcinoma 4.2 Kociba et al. 1978 Squire Rat Male Nasal turbinates/hard palate/tongue Carcinoma 4.9 Kociba et al. 1978 Kociba Rat Female Liver Carcinoma and neoplastic nodules 27 Kociba et al. 1978 Squire Rat Female Liver Carcinoma and neoplastic nodules 25 NTP 1982 NTP Rat Female Liver Carcinoma and neoplastic nodules 9.4 NTP 1982 NTP Mouse Male Liver Carcinoma and adenomas 38 NTP 1982 NTP Mouse Female Subcutaneous tissue Fibrosarcoma 2.4 

 Shaded cell indicates the slope factor recommended by CalEPA (1986) for use. THE FINDINGS AND CONCLUSIONS IN THIS DOCUMENT HAVE NOT BEEN FORMALLY DISSEMINATED BY EPA AND BE CONSTRUED TO REPRESENT ANY AGENCY DETERMINATION OR POLICY. 
DRAFT 

TABLE A2-3 

RECOMMENDED EQUATIONS FOR COMPUTING CANCER PRGS FOR 

EXPOSURE OF RESIDENTS TO DIOIXN IN 

SOIL LIVER TUMOR OCCURRENCE IN FEMALE RATS (KOCIBA ET AL. 1978) BASE

TWO ALTERNATIVE HISTOPATHOLOGICAL CLASSIFICATION METHODS 

Original Analysis (EPA 1985) Reanalysis (EPA 1990) 

Dose 

(ug/kg-day) Hyperplastic nodules Hepatocellular carcinomas Total Animals with Liver Tumors Adenoma Hepatocellular Carcinoma Tota

w

T

0 8/86 1/86 9/86 2/86 0/86 

0.001 3/50 0/50 3/50 1/50 0/50 0.010 18/50 2/50 18/50 9/50 0/50 0.100 23/49 11/49 34/48 14/45 4/45 

Source: EPA (1990, 2003b) 

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

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

TABLE A2-4. RECOMMENDED EQUATION FOR COMPUTING CANCER PRGS FO

EXPOSURE OF WORKERS TO DIOXIN IN SOIL 

TDI CALCULATIONS FROM JECFA (2002) 

Parameter Faqi et al. (1998) Ohsako et al

Linear Model 

Power 

Model 

Linear Model 

LOEL Maternal body burden (ng/kg) 25 25 7.6 Equivalent body burden with repeated dosing (ng/kg) 25 39 13 Body burden from feed (ng/kg) 3 3 3 Total body burden (ng/kg) 28 42 16 EHMIa (pg/kg per month) 423 630 237 Safety factor 9.6 9.6 3.2 PTMI (pg/kg per month) 44 66 74 TDIb (pg/kg-day) 1.5 2.2 2.5 

a Equivalent human monthly intake b Calculated based on 30 days per month