Risk-based PRGs are derived from equations combining exposure assumptions with chemical-specific toxicity values.

PRGs are based on default exposure parameters and factors that represent Reasonable Maximum Exposure (RME) conditions for long-term/chronic exposures and are based on the methods outlined in EPA's Risk Assessment Guidance for Superfund, Part B Manual (1991) and Soil Screening Guidance documents (1996 and 2002).

Site-specific information may warrant modifying the default parameters in the equations and calculating site-specific PRGs. In completing such calculations, the user should answer some fundamental questions about the site. For example, information is needed on the contaminants detected at the site, the land use, impacted media and the likely pathways for human exposure.

Whether these generic PRGs or site-specific screening levels are used, it is important to clearly demonstrate the equations and exposure parameters used in deriving PRGs at a site. A discussion of the assumptions used in the PRG calculations should be included in the decision document for a CERCLA site.

In a 2003 memo, EPA Superfund revised its hierarchy of human health toxicity values, providing three tiers of toxicity values. Three tier 3 sources were identified in that guidance, but it was acknowledged that additional tier 3 sources may exist. The 2003 guidance did not attempt to rank or put the identified tier 3 sources into a hierarchy of their own; however, when developing this calculator for the RAIS, a hierarchy was needed for all sources. The toxicity values used in this calculator are consistent with the 2003 guidance. Toxicity values from the following sources, in the order in which they are presented below, are used as the defaults in this calculator.

EPA's Integrated Risk Information System (IRIS)

Federal Register. Thursday December 7, 2000. Part II, Environmental Protection Agency. 40 CFR Parts 9, 141, and 142 - National Primary Drinking Water Regulations; Radionuclides; Final Rule. p 76713.

World Health Organization toxicity equivalence factors (TEFs).  Van den Berg et al. (2006) presents the WHO 2005 TEFs for carcinogenic dioxins and furans and polychlorinated biphenyls. Ahlborg et al. (1994) presents the WHO 1994 TEFs for carcinogenic polychlorinated biphenyls 170 and 180 inToxic equivalency factors for dioxin-like PCBs: Report on a WHO-ECEH and IPCS consultation, December 1993. Chemosphere, Vol. 28, No. 6, 1049-1067. Polycyclic aromatic hydrocarbon TEFs are presented in Provisional Guidance for Quantitative Risk Assessment of Polycyclic Aromatic Hydrocarbons.

The Provisional Peer Reviewed Toxicity Values (PPRTVs) derived by EPA's Superfund Health Risk Technical Support Center (STSC) for the EPA Superfund program.

The California Environmental Protection Agency/Office of Environmental Health Hazard Assessment's toxicity values-http://www.oehha.ca.gov/risk/ChemicalDB/index.asp

The Agency for Toxic Substances and Disease Registry (ATSDR) minimal risk levels (MRLs)-http://www.atsdr.cdc.gov/mrls/index.html

Other sources such as NCEA that were provided to the RAIS for use on the Oak Ridge Reservation.

The EPA Superfund program's Health Effects Assessment Summary. (Note that the HEAST website is not open to users outside of EPA, but access can be obtained for use on Superfund sites by contacting Rich Kapuscinski at Kapuscinski.Rich@epa.gov).

Values withdrawn from IRIS or HEAST.

When using toxicity values other than tier 1, users are encouraged to carefully review the basis for the value, and to document its use in decision documentation on a site.

2.3.1 Noncancer Toxicity Values

Noncancer toxicity values are reference doses and reference concentrations. The current, or recently completed, EPA toxicity assessments used in these screening tables (IRIS and PPRTV) define a reference dose, or RfD, as 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, or using categorical regression, with uncertainty factors generally applied to reflect limitations of the data used. RfDs are generally the toxicity value used most often in evaluating noncancer health effects at Superfund sites. Various types of RfDs are available depending on the exposure route (oral or inhalation), the critical effect (developmental or other), and the length of exposure being evaluated (chronic or subchronic). Some of the PRGs in this calculator also use Agency for Toxic Substances and Disease Registry (ATSDR) chronic oral minimal risk levels (MRLs) as oral chronic RfDs and intermediate oral MRLs as subchronic RfDs. The HEAST RfDs used in these PRGs were based upon then current EPA toxicity methodologies, but did not use the more recent benchmark dose or categorical regression methodologies.

2.3.1.1 Chronic Oral Reference Doses

A chronic oral RfD is defined as an estimate (with uncertainty spanning perhaps an order of magnitude or greater) of a daily oral exposure level for the human population, including sensitive subpopulations, that is likely to be without an appreciable risk of deleterious effects during a lifetime. Chronic oral RfDs are specifically developed to be protective for long-term exposure to a compound. As a guideline for Superfund program risk assessments, chronic oral RfDs generally should be used to evaluate the potential noncarcinogenic effects associated with exposure periods greater than 7 years (approximately 10 percent of a human lifetime). Chronic oral reference doses and ATSDR chronic oral MRLs are expressed in units of mg/kg-day.

2.3.1.2 Subchronic Oral Reference Doses

EPA has begun developing subchronic oral RfDs, which are useful for characterizing potential noncarcinogenic effects associated with shorter-term exposures by the oral route. As a guideline for Superfund program risk assessments, subchronic oral RfDs should generally be used to evaluate the potential noncarcinogenic effects of exposure periods between two weeks and seven years. Such short-term exposures can result when a particular activity is performed for a limited number of years or when a chemical with a short half-life degrades to negligible concentrations within several months. Subchronic oral reference doses and ATSDR intermediate oral MRLs are expressed in units of mg/kg-day.

2.3.2 Reference Concentrations

The current, or recently completed, EPA toxicity assessments used in these screening tables (IRIS and PPRTV assessments) define a reference concentration (RfC) as an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation 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 concentration, or using categorical regression with uncertainty factors generally applied to reflect limitations of the data used. Various types of RfCs are available depending on the exposure route (oral or inhalation), the critical effect (developmental or other), and the length of exposure being evaluated (chronic or subchronic). These screening tables also use ATSDR chronic inhalation MRLs as chronic RfCs, intermediate inhalation MRLs as subchronic RfCs and California Environmental Protection Agency (chronic) Reference Exposure Levels (RELs) as chronic RfCs. These screening tables may also use some RfCs from EPAs HEAST tables.

2.3.2.1 Chronic Inhalation Reference Concentrations

The chronic inhalation reference concentration is generally used for continuous or near continuous inhalation exposures that occur for 7 years or more. EPA chronic inhalation reference concentrations are expressed in units of mg/m³. Cal EPA RELs are presented in µg/m³ and have been converted to mg/m³ for use in these screening tables. Some ATSDR inhalation MRLs are derived in parts per million (ppm) and some in mg/m³. For use in this table, all were converted into mg/m³.

2.3.2.2 Subchronic Inhalation Reference Concentrations

The subchronic inhalation reference concentration is generally used for inhalation exposures that are between 2 weeks and 7 years. Subchronic inhalation reference concentrations are expressed in units of mg/m3. As noted above, some ATSDR (intermediate) inhalation MRLs were derived in ppm and converted for use in this table into mg/m3.

2.3.3 Cancer Toxicity Values

Slope factors and unit risk values are used to assess cancer risk. A slope factor and the accompanying weight-of-evidence determination are the toxicity data most commonly used to evaluate potential human carcinogenic risks. Generally, the slope factor is a plausible upper-bound estimate of the probability of a response per unit intake of a chemical over a lifetime. The slope factor is used in risk assessments to estimate an upper-bound lifetime probability of an individual developing cancer as a result of exposure to a particular level of a potential carcinogen. Slope factors should always be accompanied by the weight-of-evidence classification to indicate the strength of the evidence that the agent is a human carcinogen. The ATSDR does not derive cancer toxicity values (e.g. slope factors or inhalation unit risks). Some slope factors used in these screening tables were derived by the California Environmental Protection Agency, whose methodologies are quite similar to those used by EPA's IRIS and PPRTV assessments.

2.3.3.1 Oral Slope Factors

The oral slope factor evaluates the probability of an individual developing cancer from oral exposure to contaminant levels over a lifetime. Oral slope factors are expressed in units of (mg/kg-day)^-1

2.3.3.2 Inhalation Unit Risk

The IUR is defined as the upper-bound excess lifetime cancer risk estimated to result from continuous exposure to an agent at a concentration of 1 µg/m³ in air. Inhalation unit risk toxicity values are expressed in units of (µg/m³)^-1.

2.3.4 Toxicity Equivalence Factors

Some chemicals are members of the same family and exhibit similar toxicological properties; however, they differ in the degree of toxicity. Therefore, a toxicity equivalence factor (TEF) must first be applied to adjust the measured concentrations to a toxicity equivalent concentration.

The following table contains the various dioxin-like toxicity equivalency factors for Dioxins, Furans and PCBs (Van den Berg et al. (2006)), which are the World Health Organization 2005 values.

* Di-ortho values come from Ahlborg, U.G., et al. (1994), which are the WHO 1994 values from Toxic equivalency factors for dioxin-like PCBs: Report on WHO-ECEH and IPCS consultation, December 1993 Chemosphere, Volume 28, Issue 6, March 1994, Pages 1049-1067.

Carcinogenic polycyclic aromatic hydrocarbons

Provisional Guidance for Quantitative Risk Assessment of Polycyclic Aromatic Hydrocarbons (EPA/600/R-93/089, July 1993), recommends that a toxicity equivalency factor (TEF) be used to convert concentrations of carcinogenic polycyclic aromatic hydrocarbons (cPAHs) to an equivalent concentration of benzo(a)pyrene when assessing the risks posed by these substances. These TEFs are based on the potency of each compound relative to that of benzo(a)pyrene. For the toxicity value database, these TEFs have been applied to the toxicity values. Although this is not in complete agreement with the direction in the aforementioned documents, this approach was used so that toxicity values could be generated for each cPAH. Additionally, it should be noted that computationally it makes little difference whether the TEFs are applied to the concentrations of cPAHs found in environmental samples or to the toxicity values as long as the TEFs are not applied to both. However, if the adjusted toxicity values are used, the user will need to sum the risks from all cPAHs as part of the risk assessment to derive a total risk from all cPAHs. A total risk from all cPAHs is what is derived when the TEFs are applied to the environmental concentrations of cPAHs and not to the toxicity values.

The following table presents the TEFs for cPAHs recommended in Provisional Guidance for Quantitative Risk Assessment of Polycyclic Aromatic Hydrocarbons.

Toxicity Equivalency Factors for Carcinogenic Polycyclic Aromatic Hydrocarbons

Several chemical specific parameters are needed for development of the PRGs. Different hierarchies are used for organic and inorganic compounds.

2.4.1 Sources

Many sources are used to populate the database of chemical-specific parameters. They are briefly described below.

1. The Estimation Programs Interface (EPI) SuiteTM was developed by the US Environmental Protection Agency's Office of Pollution Prevention and Toxics and Syracuse Research Corporation (SRC). These programs estimate various chemical-specific properties. The calculations for these SL tables use the experimental values for a property over the estimated values.

2. EPA Soil Screening Level (SSL) Exhibit C-1.

3. WATER8, which has been replaced with WATER9.

4. Syracuse Research Corporation (SRC). 2005. CHEMFATE Database. SRC. Syracuse, NY. Accessed July 2005.

5. Syracuse Research Corporation (SRC). 2005. PHYSPROP Database. SRC. Syracuse, NY. Accessed July 2005.

6. Yaws' Handbook of Thermodynamic and Physical Properties of Chemical Compounds. Knovel, 2003.
   (http://www.knovel.com).

7. EPA Soil Screening Level (SSL) Table C.4 (http://www.epa.gov/superfund/health/conmedia/soil/index.htm).

8. Baes, C.F. 1984. Oak Ridge National Laboratory. A Review and Analysis of Parameters for Assessing Transport of Environmentally Released Radionuclides through Agriculture. http://homer.ornl.gov/baes/documents/ornl5786.html. Values are also found in Superfund Chemical Data Matrix (SCDM)
   (http://www.epa.gov/superfund/sites/npl/hrsres/tools/scdm.htm).

9. NIOSH Pocket Guide to Chemical Hazards (NPG), NIOSH Publication No. 97-140, February 2004. (http://www.cdc.gov/niosh/npg/npg.html).

10. CRC Handbook of Chemistry and Physics . (Various Editions)

11. Perry's Chemical Engineers' Handbook (Various Editions).McGraw-Hill. Online version available at: http://www.knovel.com/web/portal/browse/display?_EXT_KNOVEL_DISPLAY_bookid=2203&VerticalID=0. Green, Don W.; Perry, Robert H. (2008).

12. Lange's Handbook of Chemistry (Various Editions). Online version available at: http://www.knovel.com/web/portal/browse/display?_EXT_KNOVEL_DISPLAY_bookid=1347&VerticalID=0. Speight, James G. (2005). McGraw-Hill.

13. U.S. EPA 2004. Risk Assessment Guidance for Superfund Volume I: Human Health Evaluation Manual (Part E, Supplemental Guidance for Dermal Risk Assessment) Final. OSWER 9285.7-02EP. July 2004. Document and websitehttp://www.epa.gov/oswer/riskassessment/ragse/index.htm">http://www.epa.gov/oswer/riskassessment/ragse/index.htm">http://www.epa.gov/oswer/riskassessment/ragse/index.htm.

2.4.2 Hierarchy by Parameter

Generally the hierarchies below will work for organic and inorganic compounds.

1. Organic Carbon Partition Coefficient (K_oc) (L/kg). Not applicable for inorganics. EPI estimated values; SSL, Yaw estimated values; EPI experimental values; Yaw Experimental values

2. Dermal Permeability Constant (K_p) (cm/hr). EPI estimated values; RAGS Part E.

3. Molecular Weight (MW) (g/mole). EPI; CRC89; PERRY; LANGE; YAWS

4. Water Solubility (S) (mg/L). EPI experimatal values; SSL; CRC; PERRY; LANGE; YAWS experimental values; Yaws estimated values; EPI estimated values; PHYSPROP

5. Unitless Henry's Law Constant (H'). EPI experimental values; SSL; YAWS experimental values; EPI estimated values; PHYSPROP

6. Henry's Law Constant (atm-m3/mole). EPI experimental values; SSL; YAWS experimental values; EPI estimated values; PHYSPROP

7. Diffusivity in Air (D_ia) (cm2/s). WATER9 equations; SSL

8. Diffusivity in Water (D_ia) (cm2/s). WATER9 equations; SSL

9. Fish Bioconcentration Factor (BCF) (L/kg). EPI experimental values; EPI estimated values

10. Soil-Water Partition Coefficient (K_d) (cm3/g). SSL; BAES

11. Density (g/cm3). CRC; PERRY; LANGE; IRIS

When using PRGs, the exposure pathways of concern and site conditions should match those taken into account by the calculator. (Note, however, that future uses may not match current uses. Future uses of a site should be logical as conditions which might occur at the site in the future.) Thus, it is necessary to develop a conceptual site model (CSM) to identify likely contaminant source areas, exposure pathways, and potential receptors. This information can be used to determine the applicability of PRGs at the site and the need for additional information. The final CSM diagram represents linkages among contaminant sources, release mechanisms, exposure pathways, and routes and receptors based on historical information. It summarizes the understanding of the contamination problem. A separate CSM for ecological receptors can be useful. Part 2 and Attachment A of the Soil Screening Guidance for Superfund: Users Guide (EPA 1996) contains the steps for developing a CSM.

As a final check, the CSM should address the following questions:

• Are there potential ecological concerns?
• Is there potential for land use other than those used in the PRG calculations (i.e., residential and commercial/industrial)?
• Are there other likely human exposure pathways that were not considered in development of the PRGs?
• Are there unusual site conditions (e.g. large areas of contamination, high fugitive dust levels, potential for indoor air contamination)?

The PRGs may need to be adjusted to reflect the answers to these questions.

Natural background concentrations should be considered prior to applying PRGs. Background levels will be addressed as they are for other contaminants at CERCLA sites. For further information, see EPA's guidance "Role of Background in the CERCLA Cleanup Program", April 2002, (OSWER 9285.6-07P).

As with any risk based screening tool, the potential exists for misapplication. In most cases, this results from not understanding the intended use of the PRGs. In order to prevent misuse of the PRGs, the following should be avoided:

• Applying PRGs to a site without adequately developing a conceptual site model that identifies relevant exposure pathways and exposure scenarios.
• Not considering the effects from the presence of multiple contaminants, where appropriate.
• Use of the PRGs or cleanup levels without adequate consideration of the other NCP remedy selection criteria on CERCLA sites.
• Use of outdated PRGs (as more recent toxicity values may exist).

4.1.1 Noncancer for Child

The residential soil land use equations, presented here for child exposures, contain the following exposure routes:

incidental ingestion of soil

inhalation of particulates emitted from soil

dermal contact with soil

Total

4.1.2 Noncancer for Adult

The residential soil land use equation, presented here for adult exposures, contains the following exposure routes:

incidental ingestion of soil

inhalation of particulates emitted from soil

dermal contact with soil

Total

4.1.3 Noncancer Age-adjusted

The residential soil land use equation, presented here for age-adjusted exposures, contains the following exposure routes:

incidental ingestion of soil

inhalation of particulates emitted from soil

dermal contact with soil

Total

4.1.4 Carcinogenic

The residential soil land use equation, presented here, contains the following exposure routes:

incidental ingestion of soil

inhalation of particulates emitted from soil

dermal contact with soil

Total

4.1.5 Mutagenic

The residential soil land use equation, presented here, contains the following exposure routes:

incidental ingestion of soil,

inhalation of particulates emitted from soil,

dermal contact with soil,

Total.

4.1.6 Vinyl Chloride - Carcinogenic

The residential soil land use equations, presented here, contain the following exposure routes:

incidental ingestion of soil,

inhalation of particulates emitted from soil,

dermal contact with soil,

Total.

4.1.7 Supporting Equations for Residential Soil

Child Supporting Equations.

Adult Supporting Equations.

Age-adjusted Supporting Equations.

4.2.1 Noncancer

The outdoor worker soil land use equation, presented here, contains the following exposure routes:

incidental ingestion of soil,

inhalation of particulates emitted from soil, and

dermal exposure.

Total.

4.2.2 Carcinogenic

The outdoor worker soil land use equation, presented here, contains the following exposure routes:

incidental ingestion of soil,

inhalation of particulates emitted from soil, and

dermal exposure.

Total.

4.3.1 Noncancer

The indoor worker soil land use equation, presented here, contains the following exposure routes:

incidental ingestion of soil,

inhalation of particulates emitted from soil, and

Total.

4.3.2 Carcinogenic

The indoor worker soil land use equations, presented here, contain the following exposure routes:

incidental ingestion of soil,

inhalation of particulates emitted from soil, and

Total.

4.4.1 Noncancer

The composite worker soil land use equation, presented here, combines the most protective exposure parameters from the outdoor worker and the indoor worker. The composite worker contains the following exposure routes:

incidental ingestion of soil,

inhalation of particulates emitted from soil, and

dermal exposure.

Total.

4.4.2 Carcinogenic

The composite worker soil land use equation, presented here, contains the following exposure routes:

incidental ingestion of soil,

inhalation of particulates emitted from soil, and

dermal exposure.

Total.

4.5.1 Noncancer

The excavation worker/construction outdoor worker soil land use equations, presented here, contain the following exposure routes:

incidental ingestion of soil,

inhalation of particulates emitted from soil, and

dermal exposure.

Total.

4.5.2 Carcinogenic

The excavation/construction outdoor worker soil land use equations, presented here, contain the following exposure routes:

incidental ingestion of soil,

inhalation of particulates emitted from soil, and

dermal exposure.

Total.

4.6.1 Noncancer for Child

The recreational soil/sediment land use equations, presented here for child exposures, contain the following exposure routes:

incidental ingestion of soil/sediment,

inhalation of particulates emitted from soil/sediment, and

dermal contact with soil/sediment.

Total.

4.6.2 Noncancer for Adult

The recreational soil/sediment land use equations, presented here for adult exposures, contain the following exposure routes:

incidental ingestion of soil/sediment,

inhalation of particulates emitted from soil/sediment, and

dermal contact with soil/sediment.

Total.

4.6.3 Noncancer Age-adjusted

The recreational soil/sediment land use equations, presented here for age-adjusted exposures, contain the following exposure routes:

incidental ingestion of soil/sediment,

inhalation of particulates emitted from soil/sediment, and

dermal contact with soil/sediment.

Total.

4.6.4 Carcinogenic

The recreational soil/sediment land use equations, presented here, contain the following exposure routes:

incidental ingestion of soil/sediment,

inhalation of particulates emitted from soil/sediment, and

dermal contact with soil/sediment.

Total.

4.6.5 Mutagenic

The recreational soil/sediment land use equations, presented here, contain the following exposure routes:

incidental ingestion of soil/sediment,

inhalation of particulates emitted from soil/sediment, and

dermal contact with soil/sediment.

Total.

4.6.6 Vinyl Chloride - Carcinogenic

The recreational soil/sediment land use equations, presented here, contain the following exposure routes:

incidental ingestion of soil/sediment,

inhalation of particulates emitted from soil/sediment, and

dermal contact with soil/sediment.

Total.

4.6.7 Supporting Equations for Recreational Soil/Sediment

Child Supporting Equations.

Adult Supporting Equations.

Age-adjusted Supporting Equations.

4.7.1 Noncarcinogenic for Child

The tapwater land use equation, presented here for child exposures, contains the following exposure routes:

ingestion of water,

dermal contact with water, and

inhalation of volatiles.

Total.

4.7.2 Noncarcinogenic for Adult

The tapwater land use equation, presented here for adult exposures, contains the following exposure routes:

ingestion of water,

dermal contact with water, and

inhalation of volatiles.

Total.

4.7.3 Noncarcinogenic for Age-adjusted

The tapwater land use equation, presented here for age-adjusted exposures, contains the following exposure routes:

ingestion of water,

dermal contact with water, and

inhalation of volatiles.

Total.

4.7.4 Carcinogenic

The tapwater land use equation, presented here, contains the following exposure routes:

ingestion of water,

dermal contact with water, and

inhalation of volatiles.

Total.

4.7.5 Mutagenic

The tapwater land use equation, presented here, contains the following exposure routes:

ingestion of water,

dermal contact with water,

inhalation of volatiles.

Total.

4.7.6 Vinyl Chloride - Carcinogenic

The tapwater land use equation, presented here, contains the following exposure routes:

ingestion of water,

dermal contact with water, and

inhalation of volatiles.

Total.

4.7.7 Supporting Equations for Resident Tapwater

Child Supporting Equations.

Adult Supporting Equations.

Age-adjusted Supporting Equations.

4.8.1 Noncarcinogenic

The tapwater land use equation, presented here, contains the following exposure routes:

ingestion of water,

dermal contact with water, and

inhalation of volatiles.

Total.

4.8.2 Carcinogenic

The tapwater land use equation, presented here, contains the following exposure routes:

ingestion of water,

dermal contact with water, and

inhalation of volatiles.

Total.

4.9.1 Noncarcinogenic for Child

The surface water land use equations, presented here for child exposures, contain the following exposure routes:

ingestion of water, and

dermal contact with water.

Total.

4.9.2 Noncarcinogenic for Adult

The surface water land use equations, presented here for adult exposures, contain the following exposure routes:

ingestion of water, and

dermal contact with water.

Total.

4.9.3 Noncarcinogenic for Age-adjusted

The surface water land use equations, presented here for age-adjusted exposures, contain the following exposure routes:

ingestion of water, and

dermal contact with water.

Total.

4.9.4 Carcinogenic

The surface water land use equations, presented here, contain the following exposure routes:

ingestion of water, and

dermal contact with water.

Total.

4.9.5 Mutagenic

The surface water land use equations, presented here, contain the following exposure routes:

ingestion of water, and

dermal contact with water.

Total.

4.9.6 Vinyl Chloride - Carcinogenic

The surface water land use equations, presented here, contain the following exposure routes:

ingestion of water, and

dermal contact with water.

Total.

4.9.7 Supporting Equations for Recreator Surface Water

Child Suporting Equations.

Adult Suporting Equations.

Age-adjusted Suporting Equations.

4.10.1 Resident

4.10.1.1 Noncarcinogenic

The ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.10.1.2 Carcinogenic

The ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.10.1.3 Mutagenic

The ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.10.1.4 Vinyl Chloride - Carcinogenic

The ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.10.2 Outdoor Worker

4.10.2.1 Noncarcinogenic

The ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.10.2.2 Carcinogenic

The ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.10.3 Indoor Worker

4.10.3.1 Noncarcinogenic

The ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.10.3.2 Carcinogenic

The ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.10.4 Composite Worker

4.10.4.1 Noncarcinogenic

The composite worker ambient air land use equation, presented here combines the most protective exposure parameters from the outdoor and indoor worker. The composite worker contains the following exposure routes:

inhalation of volatiles

4.10.4.2 Carcinogenic

The Ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.10.5 Excavation/construction Worker

4.10.5.1 Noncarcinogenic

The Ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.10.5.2 Carcinogenic

The Ambient air land use equation, presented here, contains the following exposure routes:

inhalation of volatiles

4.11.1 Concentration in Fish

4.11.1.1 Noncarcinogenic

The ingestion of fish equation, presented here, contains the following exposure route:

consumption of fish.

4.11.1.2 Carcinogenic

The ingestion of fish equation, presented here, contains the following exposure route:

consumption of fish.

4.11.2 Concentration in Surface Water

4.11.2.1 Noncarcinogenic

The ingestion of fish equation, presented here, contains the following exposure route:

consumption of fish.

4.11.2.2 Carcinogenic

The ingestion of fish equation, presented here, contains the following exposure route:

consumption of fish.

Note: the consumption rate for fish is not age adjusted for this land use.

4.12.1 Concentration in Fruit and Vegetables

4.12.1.1 Noncarcinogenic

The ingestion of fruits and vegetables equation, presented here, contains the following exposure route:

consumption of fruits and vegetables.

4.12.1.2 Carcinogenic

The ingestion of fruits and vegetables equation, presented here, contains the following exposure route:

consumption of fruits and vegetables.

4.12.2 Back-calculated Concentration in Water Only for Fruits and Vegetables

4.12.2.1 Noncarcinogenic

consumption of fruits and vegetables.

4.12.2.2 Carcinogenic

consumption of fruits and vegetables.

4.12.3 Back-calculated Concentration in Soil Only for Fruits and Vegetables

4.12.3.1 Noncarcinogenic

consumption of fruits and vegetables.

4.12.3.2 Carcinogenic

consumption of fruits and vegetables.

4.12.4 Back-calculated Concentration in Soil and Water for Fruits and Vegetables

Results of back-calculating exposure to soil and water are presented in an interactive graph. See Section 4.13.5 for details.

4.12.4.1 Noncarcinogenic

consumption of fruits and vegetables.

4.12.4.2 Carcinogenic

consumption of fruits and vegetables.

4.12.5 Concentration in Milk

4.12.5.1 Noncarcinogenic

The ingestion of milk equation, presented here, contains the following exposure route:

consumption of milk.

4.12.5.2 Carcinogenic

The ingestion of milk equation, presented here, contains the following exposure route:

consumption of milk.

4.12.6 Back-calculated Concentration in Water Only for Milk

4.12.6.1 Noncarcinogenic

consumption of milk.

4.12.6.2 Carcinogenic

consumption of milk.

4.12.7 Back-calculated Concentration in Soil Only for Milk

4.12.7.1 Noncarcinogenic

consumption of milk.

4.12.7.2 Carcinogenic

consumption of milk.

4.12.8 Back-calculated Concentration in Soil and Water for Milk

Results of back-calculating exposure to soil and water are presented in an interactive graph. See Section 4.13.5 for details.

4.12.8.1 Noncarcinogenic

consumption of milk.

4.12.8.2 Carcinogenic

consumption of milk.

4.12.9 Concentration in Beef

4.12.9.1 Noncarcinogenic

The ingestion of beef equation, presented here, contains the following exposure route:

consumption of beef.

4.12.9.2 Carcinogenic

The ingestion of beef equation, presented here, contains the following exposure route:

consumption of beef.

4.12.10 Back-calculated Concentration in Water Only for Beef

4.12.10.1 Noncarcinogenic

consumption of beef.

4.12.10.2 Carcinogenic

consumption of beef.

4.12.11 Back-calculated Concentration in Soil Only for Beef

4.12.11.1 Noncarcinogenic

consumption of beef.

4.12.11.2 Carcinogenic

consumption of beef.

4.12.12 Back-calculated Concentration in Soil and Water for Beef

Results of back-calculating exposure to soil and water are presented in an interactive graph. See Section 4.13.5 for details.

4.12.12.1 Noncarcinogenic

consumption of beef.

4.12.12.2 Carcinogenic

consumption of beef.

There are two inhalation variables in the above land use equations that require further explanation: the particulate emission factor (PEF) and the volatilization factor (VF). Discussion of target risk and target hazard quotient is also provided. Finally, there are supporting equations and practices presented for the dermal exposure to water route.

4.13.1 Particulate Emission Factor (PEF)

Inhalation of contaminants adsorbed to respirable particles (PM10) was assessed using a default PEF equal to 1.36 x 10⁹ m³/kg. This equation relates the contaminant concentration in soil with the concentration of respirable particles in the air due to fugitive dust emissions from contaminated soils. The generic PEF was derived using default values that correspond to a receptor point concentration of approximately 0.76 µg/m³. The relationship is derived by Cowherd (1985) for a rapid assessment procedure applicable to a typical hazardous waste site, where the surface contamination provides a relatively continuous and constant potential for emission over an extended period of time (e.g. years). This represents an annual average emission rate based on wind erosion that should be compared with chronic health criteria; it is not appropriate for evaluating the potential for more acute exposures. Definitions of the input variables are in Table 1.

With the exception of specific heavy metals, the PEF does not appear to significantly affect most soil screening levels. The equation forms the basis for deriving a generic PEF for the inhalation pathway. For more details regarding specific parameters used in the PEF model, refer to Soil Screening Guidance: Technical Background Document. The use of alternate values on a specific site should be justified and presented in an Administrative Record if considered in CERCLA remedy selection.

Note: the generic PEF evaluates wind-borne emissions and does not consider dust emissions from traffic or other forms of mechanical disturbance that could lead to greater emissions than assumed here.

4.13.2 Volatilization Factor (VF)

The soil-to-air VF is used to define the relationship between the concentration of the contaminant in soil and the flux of the volatilized contaminant to air. VF is calculated from the equation below using chemical-specific properties and either site-measured or default values for soil moisture, dry bulk density, and fraction of organic carbon in soil. The Soil Screening Guidance: User's Guide describes how to develop site measured values for these parameters.

VF is only calculated for volatile organic compounds (VOCs). VOCs, for the purpose of this guidance, are chemicals with a Henry's Law constant of 1 x 10^-5 atm-m³/mole or greater and with a molecular weight of less than 200 g/mole.

Diffusivity in Water (cm²/s)

Diffusivity in water can be calculated from the chemical's molecular weight and density, using the following correlation equation based on WATER9 (U.S. EPA, 2001):

If density is not available, diffusivity in water can be calculated using the correlation equation based on U.S. EPA (1987). The value for diffusivity in water must be greater than zero. No maximum limit is enforced.

Diffusivity in Air (cm²/s).

Diffusivity in air can be calculated from the chemical's molecular weight and density, using the following correlation equation based on WATER9 (U.S. EPA, 2001):

If density is not available, diffusivity in air can be calculated using the correlation equation based on U.S. EPA (1987). For dioxins, diffusivity in air can be calculated from the molecular weight using the correlation equation based on EPA's Dioxin Reassessment (U.S. EPA, 2000).

4.13.3 Target Risk and Hazard Quotient

Additional significant inputs which can be modified when using the calculator are the target levels of cancer and non-cancer risk. The target risk levels for calculating generic PRGs are an extension of the Superfund program's "Role of the Baseline Risk Assessment in Superfund Remedy Selection Decisions" (OSWER Directive 9355.0-30) guidance which states:

"Where the cumulative carcinogenic site risk to an individual based on reasonable maximum exposure for both current and future land use is less than 10^-4 and the non-carcinogenic hazard quotient is less than 1, action generally is not warranted unless there are adverse environmental impacts. However, if Maximum Contaminant Levels (MCLs) or non-zero Maximum Contaminant Level Goals (MCLGs) are exceeded, action generally is warranted."

Action is generally not warranted when the cumulative site risk level is less than 10^-4 for carcinogens or a hazard quotient of 1 for non-carcinogens. Since PRGs are meant to be protective levels, the default risk level for PRGs for individual chemicals correspond to a 10^-6 risk level for carcinogens and a Hazard Quotient (HQ) of 1 for non-carcinogens.

The site decision document for the site should explain the rationale for using cancer and non-cancer risk levels other than the default values in calculated PRGs.

4.13.4 Dermal Contact with Water Supporting Equations

Calculating PRGs for the dermal exposure to water route, following RAGS Part E Supplemental Guidance for Dermal Risk Assessment), requires calculation of B, t^* and τ. Note that the RAIS has replaced RAGS Part E's use of t_event with ET (exposure time) to maintain consistency with our other exposure routes.

• B is the dimensionless ratio of the permeability coefficient of a compound through the stratum corneum relative to its permeability coefficient across the viable epidermis.
  
  
• t* is the time to reach steady state.
  
  
• τ is the lag time per event.
  
  

RAGS Part E stresses the determination of whether a chemical is within the effective predictive domain (EPD) for the determination of dermal permeability constant (K_p) applicability. The RAIS PRG output provides determination of whether or not a chemical is within the EPD. The RAIS PRG output also displays our determination of the fraction of the chemical that is ultimately absorbed (FA). FA depends strongly on the chemical's lipophilic characteristic and molecular weight as expressed in the B parameter and the lag time. RAGS Part E has determined that dermal exposures contributing less than 10% of oral exposures are insignificant. However, the RAIS presents dermal PRGs regardless of contribution percent.

4.13.5 Using the Back-calculated to Soil and Water Interactive Graph

The PRGs for Cadmium are based on the oral RfD for water which is slightly more conservative (by a factor of 2) than the RfD for food. Because the PRGs are considered screening values, we elected to use the more conservative RfD for cadmium. However, reasonable arguments could be made for applying an RfD for food (instead of the oral RfD for water) for some media such as soils.

Residential PRGs for Lead (Region 9 EPA and California EPA) are derived based on pharmacokinetic models. Both EPA's Integrated Exposure Uptake Biokinetic (IEUBK) Model and California's LeadSpread model are designed to predict the probable blood lead concentrations for children between six months and seven years of age who have been exposed to lead through various sources (air, water, soil, dust, diet and in utero contributions from the mother). Run in the reverse, these models also allow the user to calculate lead PRGs that are considered "acceptable" by EPA or the State of California.

EPA uses a second Adult Lead Model to estimate PRGs for an industrial setting. This PRG is intended to protect a fetus that may be carried by a pregnant female worker. It is assumed that a cleanup goal that is protective of a fetus will also afford protection for male or female adult workers. The model equations were developed to calculate cleanup goals such that there would be no more than a 5% probability that fetuses exposed to lead would exceed a blood lead level (PbB) of 10 F g/dL. An updated screening level for soil lead at commercial/industrial (i.e., nonresidential) sites of 800 ppm is based on a recent analysis of the combined phases of NHANES III that chooses a cleanup goal protective of all subpopulations.

For more information on EPA's lead models and other lead-related topics, please go to:

http://www.epa.gov/oerrpage/superfund/health/contaminants/lead/index.htm.

For more information on California's LeadSpread Model and Cal-Modified PRGs for lead, please go to:

http://www.dtsc.ca.gov/AssessingRisk/leadspread.cfm.

The IRIS RfD (0.14 mg/kg-day) for manganese is from all sources, including diet. The author of the IRIS assessment for manganese recommended that the dietary contribution from the normal U.S. diet (an upper limit of 5 mg/day) be subtracted when evaluating non-food (e.g. drinking water or soil) exposures to manganese, leading to a RfD of 0.071 mg/kg-day for non-food items. The explanatory text in IRIS further recommends using a modifying factor of 3 when calculating risks associated with non-food sources due to a number of uncertainties that are discussed in the IRIS file for manganese, leading to a RfD of 0.024 mg/kg-day. This modified RfD has been used in the derivation of some manganese screening levels, such as earlier Region 9 PRGs for soil and water. For more information regarding the Manganese RfD, users are advised to contact the author of the IRIS assessment on Manganese.

The oral RfD for Thallium, used in this website, is derived from the IRIS oral RfD for Thallium Sulfate by factoring out the molecular weight (MW) of the sulfate ion. Thallium Sulfate (Tl₂S0₄) has a molecular weight of 504.82. The two atoms of Thallium contribute 81% of the MW. Thallium Sulfate's oral RfD of 8E-05 multiplied by 81% gives a Thallium oral RfD of 6.48E-05.

The oral RfD toxicity value for Vanadium, used in this website, is derived from the IRIS oral RfD for Vanadium Pentoxide by factoring out the molecular weight (MW) of the oxide ion. Vanadium Pentoxide (V₂0₅) has a molecular weight of 181.88. The two atoms of Vanadium contribute 56% of the MW. Vanadium Pentoxide's oral RfD of 9E-03 multiplied by 56% gives a Vanadium oral RfD of 5.04E-03.

"Uranium Soluble Salts" uses the IRIS oral RfD of 3E-03. For the insoluble salts of Uranium, the oral RfD of 6E-04 may be used from the Federal Register, Thursday December 7, 2000. Part II, Environmental Protection Agency. 40 CFR Parts 9, 141, and 142 - National Primary Drinking Water Regulations; Radionuclides; Final Rule. p 76713.

For Chromium (VI) (Cr6), IRIS shows an air unit risk of 1.2E-2 per (µg/m 3). However, the supporting documentation in the IRIS file states that this toxicity value is based on an assumed 1:6 ratio of Cr6:Cr3. Because of this assumption and in an effort to be transparent, RSLs based on this cancer toxicity value are presented as "Chromium, Total (1:6 ratio Cr VI:III)" numbers.

In the RSL Table, the Cr6 specific value (assuming 100% Cr6) is derived by multiplying the IRIS Cr6 value by 7. This is considered to be a conservative and protective and is consistent with the State of California's interpretation of the Mancuso study that forms the basis of Cr6's toxicity values.

It is recommended that valent-specific data for Chromium be collected when Chromium is likely to be an important contaminant at a site, and when Cr6 may exist. In the absence of valent-specific data, screening levels for total Chromium are provided. If you are working on a chromium site, you may want to contact the appropriate regulatory officials in your region to determine what their position is on this issue.

The IRIS oral RfD of 2E-03 for 2,4-Dinitrotoluene is used as a surrogate for 2-Amino-4,6-Dinitrotoluene and 4-Amino-2,6-Dinitrotoluene.

Aroclor 1016 is considered low risk and assigned appropriate toxicity values. All other Aroclors are assigned the high risk toxicity values.

The soil saturation concentration, "sat", corresponds to the contaminant concentration in soil at which the absorptive limits of the soil particles, the solubility limits of the soil pore water, and saturation of soil pore air have been reached. Above this concentration, the soil contaminant may be present in free phase, i.e., nonaqueous phase liquids (NAPLs) for contaminants that are liquid at ambient soil temperatures and pure solid phases for compounds that are solid at ambient soil temperatures.

Equation 4-10 is used to calculate "sat" for each volatile contaminant. As an update to RAGS HHEM, Part B (USEPA 1991a), this equation takes into account the amount of contaminant that is in the vapor phase in soil in addition to the amount dissolved in the soil's pore water and sorbed to soil particles.

Chemical-specific "sat" concentrations must be compared with each VF-based PRG, because a basic principle of the PRG volatilization model is not applicable when free-phase contaminants are present. How these cases are handled depends on whether the contaminant is liquid or solid at ambient temperatures. Liquid contaminant that have a VF-based PRG that exceeds the "sat" concentration are set equal to "sat" whereas for solids (e.g., PAHs), soil screening decisions are based on the appropriate PRGs for other pathways of concern at the site (e.g., ingestion).

Risk-based PRGs for some chemicals in soil may exceed unity (>1,000,000 mg/kg), which cannot occur in the environment.

The ceiling limit of 10⁺⁶ mg/kgis equivalent to a chemical representing 10% by weight of the soil sample. At this contaminant concentration (and higher), the assumptions for soil contact may be violated (for example, soil adherence and windborne dispersion assumptions) due to the presence of the foreign substance itself.

Some of the cancer causing analytes in this tool operate by a mutagenic mode of action for carcinogenesis. There is reason to surmise that some chemicals with a mutagenic mode of action, which would be expected to cause irreversible changes to DNA, would exhibit a greater effect in early-life versus later-life exposure. Cancer risk to children in the context of the U.S. Environmental Protection Agency's cancer guidelines (U.S. EPA, 2005) includes both early-life exposures that may result in the occurrence of cancer during childhood and early-life exposures that may contribute to cancers later in life. In keeping with this guidance, separate cancer risk equations are presented for mutagens. The mutagen vinyl chloride has a unique set of equations. Consult Supplemental Guidance for Assessing Susceptibility from Early-Life Exposure to Carcinogens, EPA/630/R-03/003F, March 2005 for further information.http://www.epa.gov/oswer/riskassessment/sghandbook/chemicals.htm provides more detailed information about what chemicals are considered mutagens.