° The Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities ( HHRAP) ( U. S. EPA, 1998b) provided the primary source of chemical specific parameter values and default environmental parameters. We conducted the multipathway modeling using the IEM 2M model which was developed based on the same equations that gave rise to the HHRAP. We started with the HHRAP default inputs, and replaced specific inputs as necessary, either due to updated science, or due to policy choices that we made in order to be consistent with the mandate to assess risks to the individual most exposed. ° The Mercury Study Report to Congress ( U. S. EPA, 1997b) provided waterbody and watershed defaults.

Human Health Multipathway Assessment Exposure Assessment The exposure assessment methodology for the multipathway analysis includes the estimation of the HAP emission rates, release characteristics and fate and transport in the air. The HAP's environmental fate and transport from the air to the terrestrial and aquatic environments and the characterization of people's exposure pathways completes the process. We used central tendency exposure factors for the subsistence farmer scenario for the following exposure pathways: ° inhalation ° soil ingestion ° produce ingestion ° animal product ingestion including beef, dairy products, and pork ° fish ingestion at a recreational fisher level ° drinking water ingestion 3 We used mean exposure factors from the Exposure Factors Handbook ( U. S. EPA, 1997a) for households who farm ( Chapter 13) with the estimated media concentrations to estimate exposure. For fish ingestion , we used the data on recreational fishers found in Chapter 10. We calculated time weighted averages for children ( 0 6 years) and adults ( 7 70 years), to create farmer adult and farmer child receptors. ( This is the same definition of childhood as the HHRAP, which uses an defines childhood as the exposure received during the first 6 years.)

We included consideration of preparation losses, using table 13 5. We did not include loses from cooking. In table 13 5, the value for cooking losses refers to loss of moisture and drippings, not necessarily the loss of contaminant. Cooking loss may or may not result in the loss of contaminant. Since we do not have data on the effect of moisture and dripping loss on contaminant loss, we did not include this parameter in our exposure factor calculation. Finally, from Table 13 71 in the exposure factors handbook we identified the fraction of food intake that is home produced as reported by households who farm. According to the table, 16% of fruits, 31% of vegetables, 31% of meats, and 25% of dairy intake are home produced. No information was available in Chapter 10 of the exposure factors handbook to describe the percent intake of fish for recreation fishers. Intake rates and otehr exposure parameters used in the assessment are presented in Attachment A. Pathway specific assumptions are presented below:

Soil Ingestion Pathway  We estimated an average soil concentration for a default farm area following the HHRAP. The air concentrations and deposition rates used were the maximums. The mixing depth of the HAP into the soil was 1 cm for the soil ingestion pathway.

Produce Ingestion Pathway  We estimated exposure from produce ingestion based on the HAP concentration in produce we calculated. For produce ingestion rates, the Handbook groups fruiting vegetables with leafy vegetables, and potatoes with root vegetables. Because of the grouping the types of produce we considered were: legumes, grains, leafy vegetables, root vegetables, and fruits. HHRAP does not account for washing of produce. We have however investigated the extent to which data showing pollutant loss from washing exists. We found studies reporting that, for certain types of produce, pesticide losses due to washing ranges from 25 80%. Further, soil bacterial losses range from 90 99%. We assumed a 90% pollutant reduction from washing above ground vegetables in our multipathway analysis.

Animal Product Ingestion Pathway  We estimated exposures to HAP concentrations in beef, pork, and dairy products. We accounted for food preparation losses.

Drinking Water Ingestion Pathway  We used the dissolved HAP concentrations in water we estimated for the water ingestion pathway. Drinking water treatment facilities treat municipal water, and although the level of treatment may vary, at a minimum it would include removing suspended solids.

Fish Ingestion Pathway  We assumed that the farmer consumed fish caught from the local waterbody at the rate of a recreational fisher. 4 Risk Estimation We obtained toxicological dose response values from the OAQPS tables and evaluated inhalation noncarcinogenic effects for lead, cadmium and mercury and ingestion noncarcinogenic effects for cadmium and mercury. The dose response values are presented with other inputs in Attachment A. For lead, while, CAL EPA has an oral ingestion slope factor for lead, the EPA's IRIS states, " Quantifying lead's cancer risk involves many uncertainties, some of which may be unique to lead. Age, health, nutritional state, body burden, and exposure duration influence the absorption, release, and excretion of lead. In addition, current knowledge of lead pharmacokinetics indicates that an estimate derived by standard procedures would not truly describe the potential risk." EPA uses a slightly different approach in order to assess the hazard from ingestion exposures to lead. We used the IEM 2M to obtain media concentrations, then we use an additional model called the Integrated Exposure, Uptake and Biokinetic Model ( IEUBK) ( EPA 540/ R 93/ 081) to estimate blood lead levels forthe highest risk facility location  Minnesota. An updated memoorandum is included in Attachment C that describes how IEUBK was applied. This memo also contains the media concentrations, intake rates, and results of the IEUBK modeling. The results are also presented in Attachment B.

Ecological Screening Analysis We used the media concentrations developed for the human health assessment to estimate screening level ecological impacts. We used the media concentrations from the highest risk facility location  Minnesota. The methods used follow EPA's Guidelines for Ecological Risks Assessment ( USEPA 1998a, 1999). The screening level risk assessment was done using the method and toxicological dose response screening values identified in the draft secondary lead smelters analysis ( Cadmus. 2003). The screening level risk assessment identifies HAPs posing potential risks to ecological receptors and the relative magnitude of those potential risks. Inputs to the ecological analysis are provided in Attachment A.

Results Detailed results of the multipathway human health and ecological assessments are presented in Attachment B. We estimated noncancer hazards from all the ingestion pathways: water, meats, produce, soil, and fish. The highest noncancer total hazard index is 0.0058. This result occurred in Minnesota driven by cadmium exposure from the produce and fish ingestion pathways. Blood lead estimates from this source never exceeded the 0.0 milligram per deciliter ( mg/ dL) default output format of the IEUBK model. A blood lead level of 10 mg/ dL is considered a level where monitoring of the child is begun.

The ecological hazard quotients were all estimated to be less than one. The maximum estimate was 0.043 for cadmium exposure to through surface water to aquatic life. 5 References Cadmus 2003. Draft Final Report  ( Ecological) Residual Risk Assessment for Secondary Lead Smelters and Follow up Sab Review. Laramie, Wyoming. September 23, 2003.

EC/ R Incorporated 2001. Recommended Approach for Blood Lead Modeling for the Secondary Lead Residual Risk Assessment ( includes data on pollutant loss due to produce washing). July 27, 2001.

USEPA 1997a. Exposure Factors Handbook. Volume II Food Ingestion Factors. Office of Research and Development, Washington, DC. EPA/ 600/ P 95/ 002Fb. August 1997.

USEPA 1997b. Mercury Study Report to Congress Volume I: Executive Summary. Office of Air Quality Planning and Standards Research Triangle Park, NC. EPA 452/ R 97 003 December 1997.

USEPA 1998a. Guidelines for Ecological Risk Assessment. EPA 630/ R 95/ 002F.

USEPA 1998b. The Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities ( HHRAP). Office of Solid Waste and Emergency Response, Washington DC. EPA 530 D 98 001 A. July 1998.

USEPA 1999. Draft Screening Methodology For Ecological Risk Assessment. Manuscript.

USEPA 2002. Integrated Exposure, Uptake and Biokinetic Model ( IEUBK). Office of Solid Waste and Emergency Response. EPA 540/ R 93/ 081. Attachment A Assessment Inputs Table A. 1 Emission Rates and ISCST3 Inputs for the PCWP Multipathway Assessment Modeling Parameters Emission Rates Emissions ( tons/ year) Emissions ( g/ sec) Particle Fraction (%) ISC default model option Cadmium 1.28E 03 3.67E 05 100 rural land use Arsenic 6.86E 03 1.98E 04 100 wet and dry depletion Lead 6.30E 03 1.81E 04 100 no terrain Mercury elemental ( 80%) 3.74E 04 1.08E 05 0 Mercury divalent ( 20%) 9.35E 05 2.69E 06 50 Mercury total = 4.67E 04 1.35E 05 Stack Parameters Stack height ( m) Stack diameter ( m) Exit velocity ( m/ sec) Exit temp ( K) Model plant boiler/ dryer 21.5 1.5 18.5 360.9 Particle Size Distribution Mass median particle diameter ( um) Mass fraction (%) Liquid scavenging coefficient ( 1/ s mm h) Frozen scavenging coefficient ( 1/ smm h) Source AP 42 1.5 50 0.00006 0.00002 Wood fired boilers 7.5 40 0.00042 0.00014 density = 1 g/ cm3 15.0 10 0.00066 0.00022 Meteorological locations / years Surface Station WBAN # Upper Air WBAN #

Montgomery, AL / 1989 93 Montgomery, AL 13895 Centerville, AL 3881 Baton Rouge, LA / 1988 92 Baton Rouge, LA 13970 Lake Charles, LA 3937 Minneapolis, MN / 1988 91& 93 Minneapolis, MN 14922 St. Cloud, MN 14926 Raleigh, NC / 1988 91& 94 Raleigh, NC 13722 Greensboro, NC 13723 Salem, OR / 1990 94 Salem, OR 24232 Salem, OR 24232 Allentown, PA / 1990 94 Allentown, PA 14737 Albany, NY 14735 Table A. 2 IEM 2M Multipathway Analysis Air Concentration and Deposition Rate Inputs Input Type HAP Alabama Location Louisiana Location Minnesota Location Waterbody Values Watershed Values Receptor Values Waterbody Values Watershed Values Receptor Values Waterbody Values Watershed Values Receptor Values Air Concentration ( vapor)

( Fg/ m3) Lead 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 Cadmium 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 Divalent Mercury 1.35E 07 1.02E 07 2.58E 07 1.31E 07 1.04E 07 2.43E 07 1.08E 07 9.86E 08 2.67E 07 Elemental Mercury 1.08E 06 8.12E 07 2.06E 06 1.05E 06 8.32E 07 1.95E 06 8.66E 07 7.89E 07 2.14E 06 Dry Deposition ( Particulate)

( g/ m2 yr) Lead 1.17E 05 5.62E 06 2.79E 05 1.30E 05 6.52E 06 2.46E 05 1.66E 05 9.53E 06 4.65E 05 Cadmium 2.38E 06 1.14E 06 5.66E 06 2.64E 06 1.32E 06 4.99E 06 3.37E 06 1.93E 06 9.43E 06 Divalent Mercury 8.70E 08 4.17E 08 2.07E 07 9.67E 08 4.84E 08 1.83E 07 1.24E 07 7.08E 08 3.45E 07 Elemental Mercury 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 Wet Deposition ( vapor and particulate)

( g/ m2 yr) Lead 1.40E 05 2.34E 06 6.34E 05 1.37E 05 2.25E 06 6.86E 05 5.63E 06 1.11E 06 2.97E 05 Cadmium 2.84E 06 4.73E 07 1.28E 05 2.78E 06 4.56E 07 1.39E 05 1.14E 06 2.24E 07 6.03E 06 Divalent Mercury 1.86E 07 3.37E 08 8.01E 07 1.84E 07 3.25E 08 8.86E 07 7.22E 08 1.51E 08 3.70E 07 Elemental Mercury 6.58E 07 1.31E 07 2.64E 06 6.57E 07 1.26E 07 3.02E 06 2.43E 07 5.52E 08 1.19E 06 Total Air Concentration ( vapor and particulate)

( Fg/ m3) Lead NA NA 2.81E 05 NA NA 2.70E 05 NA NA 2.71E 05 Cadmium NA NA 5.70E 06 NA NA 5.46E 06 NA NA 5.49E 06 Divalent Mercury NA NA 4.67E 07 NA NA 4.43E 07 NA NA 4.68E 07 Elemental Mercury NA NA 2.06E 06 NA NA 1.95E 06 NA NA 2.14E 06 Input Type HAP North Carolina Location Pennsylvania Location Oregon Location Waterbody Values Watershed Values Receptor Values Waterbody Values Watershed Values Receptor Values Waterbody Values Watershed Values Receptor Values Air Concentration ( vapor)

( Fg/ m3) Lead 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 Cadmium 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 Divalent Mercury 1.17E 07 1.01E 07 2.81E 07 1.03E 07 9.60E 08 2.70E 07 1.08E 07 1.03E 07 5.27E 07 Elemental Mercury 9.36E 07 8.09E 07 2.25E 06 8.20E 07 7.68E 07 2.16E 06 8.68E 07 8.25E 07 4.22E 06 Dry Deposition ( Particulate)

( g/ m2 yr) Lead 5.79E 06 3.35E 06 1.59E 05 1.41E 05 7.87E 06 3.73E 05 5.20E 06 3.31E 06 3.85E 05 Cadmium 1.17E 06 6.80E 07 3.23E 06 2.86E 06 1.59E 06 7.56E 06 1.05E 06 6.70E 07 7.81E 06 Divalent Mercury 4.30E 08 2.49E 08 1.18E 07 1.05E 07 5.84E 08 2.77E 07 3.86E 08 2.46E 08 2.86E 07 Elemental Mercury 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 Wet Deposition ( vapor and particulate)

( g/ m2 yr) Lead 9.89E 06 1.87E 06 5.36E 05 1.10E 05 2.12E 06 8.41E 05 9.07E 06 1.97E 06 1.22E 04 Cadmium 2.00E 06 3.79E 07 1.09E 05 2.23E 06 4.29E 07 1.70E 05 1.84E 06 3.99E 07 2.48E 05 Divalent Mercury 1.27E 07 2.58E 08 6.73E 07 1.41E 07 2.92E 08 1.04E 06 1.14E 07 2.61E 08 1.50E 06 Elemental Mercury 4.33E 07 9.53E 08 2.21E 06 4.76E 07 1.08E 07 3.36E 06 3.72E 07 9.23E 08 4.77E 06 Total Air Concentration ( vapor and particulate)

( Fg/ m3) Lead NA NA 3.45E 05 NA NA 2.85E 05 NA NA 6.20E 05 Cadmium NA NA 6.99E 06 NA NA 5.78E 06 NA NA 1.26E 05 Divalent Mercury NA NA 5.37E 07 NA NA 4.81E 07 NA NA 9.87E 07 Elemental Mercury NA NA 2.25E 06 NA NA 2.16E 06 NA NA 4.22E 06 Table A. 3 IEM Multipathway Analysis Exposure Factors for Children Exposure Parameter Age Group ( years) Intake Rate from EFH ( gFW/

kgday a, b EFH Intake Rate Source Table Non home Produced Overall Mean Intake Rate ( from EFH Chapters 9 and 11)

( gFW/ kg day) Home Produced Overall Mean Intake Rate ( from EFH Chapter 13)

( gFW/ kg day) Households Who Farm Mean Intake from EFH Chapter 13 ( gFW/ kg day) Mean Preparation Loss from Tables 13 5 to 13 7 ( percent lost) Mean Moisture Content for Dry Weight Conversion:

from Tables 11 28 and 9

27 c, d, e, f, g ( percent moisture) Time Weighted Average Dry Weight Mean Home Produced Intake for Households Who Farm Adjusted for Preparation Loss h ( gDW/

kgday

Beef 0 1 1.24 11 3 1.09 2.45 2.63 24 72 0.92 1 2 1.92 3 5 1.83 Pork 0 1 0.45 11 4 0.41 1.23 1.3 36 70 0.43 1 2 0.77 3 5 0.74 Dairy 0 1 62.74 11 2 8.02 14 17.1 0 89 7.31 1 2 26.26 3 5 21.15 Fruits 0 1 11.53 9 7 1.79 1.49 2.32 20 87 0.79 1 2 7.10 3 5 2.60 13 61 NA Root Vegetables 0 1 2.03 9 11 1.36 1.16 1.39 8 86 0.27 1 2 2.52 13 65 NA 3 5 1.28 Legumes 0 1 1.36 9 10 0.39 1.01 1.3 16 86 0.32 1 2 2.46 13 64 NA 3 5 1.30 Leafy Vegetables 0 1 1.43 9 9 1.76 1.52 2.17 15 93 0.18 1 2 3.48 13 63 NA 3 5 1.74 a EFH = U. S. Environmental Protection Agency, 1997. Exposure Factors Handbook. EPA/ 600/ P 95/ 002Fa, Office of Research and Development and National Center for Environmental Assessment, Washington, D. C.

b Values from EFH Chapters 9 and 11 are presented on an " as consumed" basis and were adjusted to add preparation losses back into this starting value:

Intake Rate = EFH value/( 1 preparation loss)

c Dairy moisture content = weighted EFH average of butter, cream, milk, yogurt, and cheese d Fruits moisture content = EFH average of apples, pears, peaches, strawberries e Root vegetables moisture content = EFH average of potatoes, carrots, beets f Legumes mositure content = EFH average of corn, peas, pumpkin g Leafy vegetables moisture content = EFH average of all raw whole cabbage, lettuce, peppers, tomatoes h Final Intake Rate = time weighted average of original EFH intake rate*( home produced mean/ non home produced mean)*( farm mean/ overall mean)*( 100

preparation loss)*( 100 moisture content) Table A. 4 IEM Multipathway Analysis Exposure Factors for Adults Exposure Parameter Age Group ( years) Intake Rate from EFH ( gFW/

kgday a, b EFH Intake Rate Source Table Non home Produced Overall Mean Intake Rate ( from EFH Chapters 9 and 11)

( gFW/ kg day) Home Produced Overall Mean Intake Rate ( from EFH Chapter 13)

( gFW/ kg day) Households Who Farm Mean Intake from EFH Chapter 13 ( gFW/ kg day) Mean Prep.

Loss from Tables 13 5 to 13 7 ( percent lost) Mean Moisture Content for Dry Weight Conversion:

from Tables 11 28 and 9

27 c, d, e, f, g ( percent moisture) Time Weighted Avg. Dry Wt.

Mean Home Produced Intake for Households Who Farm Adjusted for Prep. Loss ( gDW/ kg day)

Beef 6 11 3.77 13 36 NA 2.45 2.63 24 72 0.48 12 19 1.72 20 39 2.06 40 69 1.84 Pork 6 11 0.55 11 4 0.41 1.23 1.3 36 70 0.24 12 19 1.28 13 54 NA 20 39 1.21 40 69 1.02 Dairy 6 11 13.33 11 2 8.02 14 17.1 0 89 1.18 12 19 6.29 20 39 7.41 13 28 NA 40 69 3.10 11 2 8.02 Fruits 6 11 2.52 13 61 NA 1.49 2.32 20 87 0.22 12 19 1.33 20 39 1.09 40 69 1.25 Root Vegetables 6 11 1.32 13 65 NA 1.16 1.39 8 86 0.16 12 19 0.94 20 39 0.87 40 69 1.13 Legumes 6 11 1.10 13 64 NA 1.01 1.3 16 86 0.14 12 19 0.78 20 39 0.76 40 69 0.93 Leafy Vegetables 6 11 1.39 13 63 NA 1.52 2.17 15 93 0.11 12 19 1.07 20 39 1.05 40 69 1.60 a EFH = U. S. Environmental Protection Agency, 1997. Exposure Factors Handbook. EPA/ 600/ P 95/ 002Fa, Office of Research and Development and National Center for Environmental Assessment, Washington, D. C.

b Values from EFH Chapters 9 and 11 are presented on an " as consumed" basis and were adjusted to add preparation losses back into this starting value: Intake Rate = EFH value/( 1 preparation loss)

c Dairy moisture content = weighted EFH average of butter, cream, milk, yogurt, and cheese d Fruits moisture content = EFH average of apples, pears, peaches, strawberries e Root vegetables moisture content = EFH average of potatoes, carrots, beets f Legumes mositure content = EFH average of corn, peas, pumpkin g Leafy vegetables moisture content = EFH average of all raw whole cabbage, lettuce, peppers, tomatoes h Final Intake Rate = time weighted average of original EFH intake rate*( home produced mean/ non home produced mean)*( farm mean/ overall mean)*( 100

preparation loss)*( 100 moisture content) Table A. 5 Additional IEM Multipathway Analysis Exposure Factors for Children and Adults Exposure Parameter Parameter Value Sourcea, b Body Weight, child aged 0  5 ( kg) 1.54E+ 01 EFH Table 7 3, average of ages 0 5 Exposure duration as a child 6.00E+ 00 HHRAP Lifetime ( yrs) 7.00E+ 01 HHRAP Child water consumption rate, L/ day 7.40E 01 EFH Table 3 30, time weighted average mean intake for ages 0 5 Child soil ingestion rate ( mgFW/ day) 1.00E+ 02 EFH Table 4 23, mean child Child grain ingestion rate ( gDW/ kg/ day) 9.20E 01 EFH Table 12 18, time weighted average mean intake for ages 0 5 of corn values in g DW/ day adjusted to gDW/ kg/ day Child fish ingestion rate ( gFW/ kg/ day) 3.70E 01 EFH Table 10 61, mean child for ages 1 to 5 Body Weight, adult aged 20  49 ( kg) 7.18E+ 01 HHRAP Exposure duration as an adult 6.40E+ 01 HHRAP Lifetime ( yrs) 7.00E+ 01 HHRAP Adult water consumption rate, L/ day 1.40E+ 00 EFH Table 3 30, mean adult Adult soil ingestion rate ( g/ day) 5.00E+ 01 EFH Table 4 23, mean adult Adult grain ingestion rate ( gDW/ kg/ day) 2.70E 01 EFH Table 12 18, time weighted average mean intake for ages 6 70 of corn values in g DW/ day adjusted to gDW/ kg/ day Adult fish ingestion rate ( gFW/ kg/ day) 1.70E 01 EFH Table 10 61, time weighted average mean intake for ages 6 to 70 Contact Fractions Fraction of day exposed to contaminated air 1 HHRAP Fraction of consumed products contaminated 1 HHRAP a EFH = U. S. Environmental Protection Agency, 1997. Exposure Factors Handbook. EPA/ 600/ P 95/ 002Fa, Office of Research and Development and National Center for Environmental Assessment, Washington, D. C.

b HHRAP = U. S. Environmental Protection Agency, 1998. Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities ( HHRAP). EPA 530 D 98 001A, Office of Solid Waste and Emergency Response, Washington, D. C. Table A. 6 Other Inputs Used in IEM 2M Modeling for the Multipathway Analysis Constants RC: ideal gas const ( m3 atm/ mole K) 8.21E 05 pa: air density ( g/ cm3) 1.19E 03 ua: viscosity of air ( g/ cm sec) 1.84E 04 Psed: solids density ( kg/ L or g/ cm3) 2.65E+ 00 Cdrag: drag coefficient 1.10E 03 kappa: Von Karman's coefficient 4.00E 01 lam2: boundary thickness ( dimensionless) 4.00E+ 00 Depth for base volatilization ( m) 5.00E 03 Agricultural Parametersa Grains Legumes Root vegetables Fruits Leafy vegetables Forage Silage RP ( interception fraction) b 0 0.008 0 0.05 0.15 0.47 0.44 TP ( Length of plant's exposure, yrs) 0.123 0.123 0.123 0.123 0.157 0.123 0.123 YP ( Yield of plant, kg dw/ m2) 0.3 0.104 0.334 0.107 0.177 0.31 0.84 VG ( surface area volume to whole plant volume correction) for lipophilic ( high K ow) chemicals 1 0.01 1 0.01 1 1 0.5 VG ( surface area volume to whole plant volume correction) for water soluble ( low K ow) chemicals 1 1 1 1 1 1 1 Beef Dairy Pork Grain consumption ( kg/ day) 0.47 2.6 3 Forage consumption ( kg/ day) 8.8 11 0 Silage consumption ( kg/ day) 2.5 3.3 1.3 Soil consumption ( kg/ day) 0.39 0.41 0.34 a U. S. Environmental Protection Agency, 1998. Methodology for Assessing Health Risks Associated With Multiple Pathways of Exposure to Combustor Emissions. EPA 600 R98 137. Office of Research and Development and National Center for Environmental Assessment, Cincinnati,

OH.

b Interception fractions are zero for grains and root vegetables since they are considered " protected" vegetables. Direct deposition from air to the vegetables does not occur. Table A. 7 IEM 2M Multipathway Analysis Dose Response Values Dose Response Factor lead elemental mercury divalent mercury cadmium Cancer Slope Factor ingestion ( kg day/ mg) NA NA NA NA URE: Unit Risk Estimate ( m3/ ug) NA NA NA 1.8E 03 ( IRIS)

RfC ( ug/ m3) 1.5E+ 00 3.0E 01 0.09 mercuric chloride ( CAL EPA) 2.0E 02 ( CAL EPA)

RfD: Reference Dose ( mg/ kg/ day) ingestion NA NA 3.0E 04  mercuric chloride all food except fish ( IRIS) 1.0E 03  food ( IRIS)

1.0E 04  methyl mercury fish only ( IRIS) 5.0E 04  water ( IRIS)

Source NAAQS IRIS IRIS/ CAL EPA IRIS/ CAL EPA CAL: California Environmental Protection Agency, 2002. Technical Support Document for Describing Available Cancer Potency Factors.

Office of Environmental Health Hazard Assessment, Sacramento, California. Online at http:// www. oehha. org/ air/ hot_ spots/ pdf/ TSDNov2002. pdf IRIS: U. S. Environmental Protection Agency. Integrated Risk Information System Substance File. Online at http:// www. ipa. gov/ iris. html NAAQS: National Ambient Air Quality Standard for Lead. Online at http:// www. epa. gov/ ttnnaaqs/ standards/ pb/ data/ npsaaqsl_ fr. pdf Table A. 8 IEM 2M Multipathway Analysis Compound Specific Parameters Compound Specific Parametera Lead Elemental Mercury Divalent Mercury Cadmium D w: water diffusion coeff. ( cm2/ s) 6.28E 06 3.01E 05 5.25E 06 9.45E 06 MW: molecular weight ( g/ mole) 2.07E+ 02 2.01E+ 02 2.72E+ 02 1.12E+ 02 D ( or D a): Atmospheric diffusion coefficient ( cm2/ sec) 5.43E 02 1.09E 02 4.53E 02 8.16E 02 H: Henry's Law Constant ( atm m3/ mole) 0.00E+ 00 7.10E 03 7.10E 10 0.00E+ 00 Kd s: soil water part coeff ( mL/ g or L/ kg) 9.00E+ 02 1.00E+ 03 5.80E+ 04 7.50E+ 01 Kd w: susp sed water part coeff ( L/ kg) 9.00E+ 02 1.00E+ 03 1.00E+ 05 7.50E+ 01 Kd bs: benthic sed water partition coefficient ( L/ kg) 9.00E+ 02 3.00E+ 03 5.00E+ 04 7.50E+ 01 ksg: soil loss degradation constant ( 1/ yr) 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 K ow: octanol/ water partitioning coefficient ( unitless) NA NA NA NA Br i: plant soil bioconcentration factor ( ug/ g DW plant per ug/ g soil) grains ( Br ag) 9.00E 03 0.00E+ 00 1.45E 02 6.20E 02 legumes ( Br ag) 1.36E 02 0.00E+ 00 1.45E 02 1.25E 01 root vegetables ( Br root veg) 9.00E 03 0.00E+ 00 3.60E 02 6.40E 02 fruits ( Br ag) 1.36E 02 0.00E+ 00 1.45E 02 1.25E 01 leafy vegetables ( Br ag) 1.36E 02 0.00E+ 00 1.45E 02 1.25E 01 forage ( Br forage) 4.50E 02 0.00E+ 00 0.00E+ 00 3.64E 01 silage ( Br ag) 1.36E 02 0.00E+ 00 1.45E 02 1.25E 01 Bv i: air to plant biotransfer factor ( ug/ g DW plant per ug/ g air) grains 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 legumes ( Br ag) 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 fruits ( Br ag) 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 leafy vegetables ( Br ag) 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 forage ( Bv forage) 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 silage ( Bv ag) 0.00E+ 00 0.00E+ 00 0.00E+ 00 0.00E+ 00 Ba j: biotransfer, jth animal ( day/ kg FW)

beef 3.00E 04 0.00E+ 00 5.22E 03 1.20E 04 dairy 2.50E 04 0.00E+ 00 2.26E 03 6.50E 06 pork 3.60E 04 0.00E+ 00 0.00E+ 00 1.91E 04 Fish Bioaccumulation Factors ( BAFs): BAF_ W( i): BAF for total water conc, L/ kg NA NA NA 2.50E+ 02 BAF_ D( i): BAF for diss water conc ( L/ kg) 8.00E+ 00 NA 6.80E+ 06 NA a Unless otherwise noted, source is U. S. Environmental Protection Agency, 1998. Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities, Appendix C. EPA 530 D 98 001A, Office of Solid Waste and Emergency Response, Washington, D. C. Table A. 9 IEM 2M Multipathway Analysis Default Site Dependent Parameters Site Dependent Parametersa PA LA MN OR AL NC TA ( average air temperature, C) b 10.7 20 7.2 11.2 18 15 TW ( average water temperature, C) c 10 25 10 15 25 15 P ( average annual precipitation, cm/ yr) b 110.5 143.8 71.9 99.5 136 106 RO ( average annual runoff, cm/ yr) c 25.4 22.5 7.6 25 18 18 EV ( average annual evapotranspiration, cm/ yr) c 63 100.7 70 75 65 80 W ( average wind speed, m/ s) b 5.1 4.1 4.7 3.1 2.9 3.4 Site Dependent Parametersa Default values used for each site I ( average annual irrigation, cm/ yr) 0 PS ( Support practice factor) 1 SDEL ( sediment delivery ratio to water body) 2.2 EF ( pollutant enrichment factor) 3 TC ( time of concentration, yr) 100 BD ( bulk soil density, g/ cm3) 1.5 ZD ( depth of incorporation, cm; no tillage) 1 ZTILL ( mixing depth for soil tillage, cm) 20 Theta ( soil moisture content, L/ L) 0.2 Theta_ V ( void space in soil, L/ L) 0.2 CN ( SCS soil curve number) 81.5 V ( fraction of vegetative cover) 0 R ( erosivity factor, / yr) 160 K ( erodibility factor, tons/ acre) 0.3 LS ( topographic factor, unitless) 2.5 C ( cover management factor, unitless) 0.3 SSW ( suspended solids concentration, mg/ L) 10 SSDEP ( m/ day) 0 v_ min: Mineralization for benthic solids ( m/ yr) 0.001 vs: Settling Velocity ( m/ yr) 730 vrs: Resuspension velocity ( m/ yr) 0.0037 E_ sw: Pore water diffusion coefficient ( m2/ yr) 0.158 v_ sbio: Settling rate for biotic solids ( m/ yr) 73 L_ sbio: Net internal production of biotic solids 100 k_ mort: Biotic mortality rate (/ day) 0.03 BS: Benthic sediment concentration ( kg/ L) 1 DB ( upper benthic depth, m) 0.02 BIO_ P ( aquatic plant biomass, mg/ L) 2 BIO_ F ( total fish biomass, mg/ L) 0.05 Bio_ F_ Tier3, mg/ L 0.02 WAL ( watershed info: land area of fallout, km2) d 37.3 Water Depth ( m) d 5 WAW: water body surface area ( km2) d 2.49 VW: water column volume ( m3) d 1.2E+ 07 VFX : long term dilution flow ( m3/ yr) d 4.8E+ 06 U: Average Current velocity ( m/ s) d NA a Unless otherwise noted, source is U. S. Environmental Protection Agency, 1998. Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities, Appendix C. EPA 530 D 98 001A, Office of Solid Waste and Emergency Response, Washington, D. C. b Comparative Climatic Data For the United States [ 1961 1990]. Southern Regional Climate Center. http:// www. srcc. lsu. edu/ 6190/ ccd. html d Interpolated from site specific values in the Mercury Study: Report to Congress. U. S. Environmental Protection Agency, 1997. Office of Air Quality Planning and Standards, and Office of Research and Development, Research Triangle Park, NC. d Default values from the Mercury Study: Report to Congress. U. S. Environmental Protection Agency, 1997. Office of Air Quality Planning and Standards, and Office of Research and Development, Research Triangle Park, NC.

Table A 10. Ecological Toxicity Screening Values ( Blank cells indicate that no screening values were found.) HAP Lead Cadmium Mercury ( Hg+ 2) Mercury ( elemental) Mercury methyl Screening values for air inhalation by 1.9E+ 03 1.4E+ 03 7.4E+ 02 7.4E+ 02 4.6E+ 02 Terrestrial Wildlife Receptor American Woodcock Cottontail Rabbit American Woodcock American Woodcock Cottontail Rabbit Plant screening values for herbivorous 3.0E+ 01 3.6E+ 00 4.8E+ 00 4.8E+ 00 1.2E 01 Terrestrial Wildlife Receptor Cottontail Rabbit Cottontail Rabbit Cottontail Rabbit Cottontail Rabbit Cottontail Rabbit Herbivore screening values for 4.2E+ 00 5.1E+ 00 1.7E+ 00 1.7E+ 00 2.0E 02 Terrestrial Wildlife Receptor Barn Owl Red Fox Barn Owl Barn Owl Barn Owl Soil screening values for vertebrates1 2.3E+ 02 2.8E+ 01 3.7E+ 01 3.7E+ 01 9.0E 01 Terrestrial Wildlife Receptor Short tail Shrew Short tail Shrew Short tail Shrew Short tail Shrew Short tail Shrew Surface water screening values for wildlife1 ( mg/ L) 4.9E+ 00 4.1E+ 00 5.6E+ 00 5.6E+ 00 1.4E 01 Terrestrial Wildlife Receptor Roughwinged Swallow Whitetail Deer Whitetail Deer Whitetail Deer Whitetail Deer Fish screening values for piscivorous 2.2E 03 2.9E 03 8.9E 04 8.9E 04 1.0E 05 Terrestrial Wildlife Receptor Belted Kingfisher Belted Kingfisher Belted Kingfisher Belted Kingfisher Belted Kingfisher Soil screening values for plants2 ( ug/ g) 5.0E+ 01 3.0E+ 00 3.0E 01 3.0E+ 00 Soil screening values for earthworms and microbial processes3 ( ug/ g) 5.0E+ 02 2.0E+ 01 1.0E 01 Surface water screening values for aquatic life4,5 ( mg/ L) 3.2E 03 1.1E 03 9.0E 04 1.3E 03 2.8E 06 1 Sample, B. E., D. M. Opresko, and G. W. Suter. 1996. Toxicological Benchmarks for Wildlife: 1996 Revision. ES/ ER/ TM 66/ R3. Prepared for the U. S. Department of Energy, Office of Environmental Management, DE AC05 84OR21400.

2 Will, M. E. and G. W. Suter, II. 1995a. Toxicological Benchmarks for Screening Potential Contaminants of Concern for Effects on Terrestrial Plants: 1995 Revision. ES/ ER/ TM 85/ R2. Prepared for the U. S. Department of Energy, Office of Environmental Managemen 3 Will, M. E. and G. W. Suter, II. 1995b. Toxicological Benchmarks for Potential Contaminants of Concern for Effects on Soil and Litter Invertebrates and Heterotrophic Process. ES/ ER/ TM 85/ R2. Prepared for the U. S. Department of Energy, Office of Environmen 4 For all HAP values except Mercury ( Hg+ 2): Suter, G. W., II, and C. L. Tsao. 1996. Toxicological Benchmarks for Screening Potential Contaminants of Concern for Effects on Aquatic Biota: 1996 Revision. ES/ ER/ TM 96/ R2. Prepared for the U. S. Department of En 5 For the Mercury ( Hg+ 2) value: USEPA ( Environmental Protection Agency). 1996. 1995 Updates: Water Quality Criteria Documents for the Protection of Aquatic Life in Ambient Water. EPA 820 96 001. Office of Water, Washington, DC. Attachment B Risk Results Table B. 1 Summary Multipathway Risk Estimates for the PCWP Assessment Multipathway Inhalation Risk Results Location Lifetime Excess Cancer Risk Total Inhalation Hazard Index Alabama 1E 08 0.00032 Louisiana 1E 08 0.00030 Minnesota 1E 08 0.00030 North Carolina 1E 08 0.00039 Oregon 2E 08 0.00069 Pennsylvania 1E 08 0.00032 Maximum 2E 08 0.00069 Maximum Ingestion Hazard Index Location Hazard Index Age Group HAP Driving Pathways Alabama 0.0007 child cadmium fish and produce ingestion Louisiana 0.0013 child cadmium fish ingestion Minnesota 0.0058 child cadmium fish ingestion North Carolina 0.0010 child cadmium fish ingestion Oregon 0.0014 child cadmium fish and produce ingestion Pennsylvania 0.0015 child cadmium fish ingestion Maximum 0.0058 Table B. 2 Summary Ecological Risk Estimates for the PCWP Asessment PCWP Production IEM 2M Ecological Risk Estimates Lead Cadmium Mercury ( Hg+ 2) Mercury ( elemental) Mercury methyl Sum of Mercury Hazard Quotient 0.012 0.043 0.0092 0.00052 0.000030 0.0092 Receptor aquatic life aquatic life earthworms &

microbes plants aquatic life earthworms &

microbes Media surface water surface water soil soil surface water soil Table B. 3 Detailed Multipathway Risk Estimates for the PCWP Assessment  Alabama Farmer and Summary of Multipathway Risk Recreational Fisher Cancer 70 year exposure Individual Lifetime Risk Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Cadmium 1E 08 Farmer and Summary of Multipathway Risk  Adult Recreational Fisher Noncancer 64 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 2E 05 Cadmium 3E 04 4E 04 1E 06 8E 05 1E 06 1E 04 1E 04 Mercury ( divalent/ methyl) 5E 06 4E 05 3E 06 9E 06 2E 05 6E 08 9E 08 Mercury ( elemental) 7E 06 Total Hazard Index 3E 04 4E 04 4E 06 9E 05 3E 05 1E 04 1E 04 Farmer and Summary of Multipathway Risk  Child Recreational Fisher Noncancer 6 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 2E 05 Cadmium 3E 04 6E 04 3E 06 2E 04 4E 06 7E 05 3E 04 Mercury ( divalent/ methyl) 5E 06 1E 04 6E 06 2E 05 1E 04 3E 08 2E 07 Mercury ( elemental) 7E 06 Total Hazard Index 3E 04 7E 04 8E 06 2E 04 1E 04 7E 05 3E 04 Table B. 4 Detailed Multipathway Risk Estimates for the PCWP Assessment  Louisiana Farmer and Summary of Multipathway Risk Recreational Fisher Cancer 70 year exposure Individual Lifetime Risk Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Cadmium 1E 08 Farmer and Summary of Multipathway Risk  Adult Recreational Fisher Noncancer 64 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 2E 05 Cadmium 3E 04 7E 04 2E 06 1E 04 2E 06 3E 04 3E 04 Mercury ( divalent/ methyl) 5E 06 4E 05 3E 06 1E 05 3E 05 4E 08 6E 08 Mercury ( elemental) 6E 06 Total Hazard Index 3E 04 8E 04 5E 06 1E 04 3E 05 3E 04 3E 04 Farmer and Summary of Multipathway Risk  Child Recreational Fisher Noncancer 6 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 2E 05 Cadmium 3E 04 1E 03 4E 06 3E 04 5E 06 2E 04 7E 04 Mercury ( divalent/ methyl) 5E 06 1E 04 6E 06 2E 05 1E 04 2E 08 1E 07 Mercury ( elemental) 6E 06 Total Hazard Index 3E 04 1E 03 1E 05 3E 04 1E 04 2E 04 7E 04 Table B. 5 Detailed Multipathway Risk Estimates for the PCWP Assessment  Minnesota Farmer and Summary of Multipathway Risk Recreational Fisher Cancer 70 year exposure Individual Lifetime Risk Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Cadmium 1E 08 Farmer and Summary of Multipathway Risk  Adult Recreational Fisher Noncancer 64 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 2E 05 Cadmium 3E 04 4E 03 1E 05 1E 04 5E 06 2E 03 2E 03 Mercury ( divalent/ methyl) 5E 06 3E 05 2E 06 7E 06 2E 05 6E 08 1E 07 Mercury ( elemental) 7E 06 Total Hazard Index 3E 04 4E 03 1E 05 1E 04 2E 05 2E 03 2E 03 Farmer and Summary of Multipathway Risk  Child Recreational Fisher Cancer 6 year exposure Individual Lifetime Risk Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Cadmium 1E 08 Farmer and Summary of Multipathway Risk  Child Recreational Fisher Noncancer 6 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 2E 05 Cadmium 3E 04 6E 03 2E 05 4E 04 1E 05 1E 03 4E 03 Mercury ( divalent/ methyl) 5E 06 1E 04 4E 06 2E 05 8E 05 3E 08 2E 07 Mercury ( elemental) 7E 06 Total Hazard Index 3E 04 6E 03 2E 05 4E 04 1E 04 1E 03 4E 03 Table B. 6 Detailed Multipathway Risk Estimates for the PCWP Assessment  North Carolina Farmer and Summary of Multipathway Risk Recreational Fisher Cancer 70 year exposure Individual Lifetime Risk Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Cadmium 1E 08 Farmer and Summary of Multipathway Risk  Adult Recreational Fisher Noncancer 64 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 2E 05 Cadmium 3E 04 6E 04 2E 06 9E 05 2E 06 2E 04 3E 04 Mercury ( divalent/ methyl) 6E 06 3E 05 2E 06 7E 06 2E 05 4E 08 6E 08 Mercury ( elemental) 7E 06 Total Hazard Index 4E 04 6E 04 5E 06 1E 04 3E 05 2E 04 3E 04 Farmer and Summary of Multipathway Risk  Child Recreational Fisher Noncancer 6 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 2E 05 Cadmium 3E 04 9E 04 5E 06 2E 04 4E 06 1E 04 5E 04 Mercury ( divalent/ methyl) 6E 06 1E 04 5E 06 2E 05 8E 05 2E 08 1E 07 Mercury ( elemental) 7E 06 Total Hazard Index 4E 04 1E 03 9E 06 3E 04 9E 05 1E 04 5E 04 Table B. 7 Detailed Multipathway Risk Estimates for the PCWP Assessment  Oregon Farmer and Summary of Multipathway Risk Recreational Fisher Cancer 70 year exposure Individual Lifetime Risk Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Cadmium 2E 08 Farmer and Summary of Multipathway Risk  Adult Recreational Fisher Noncancer 64 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 4E 05 Cadmium 6E 04 7E 04 4E 06 2E 04 3E 06 2E 04 3E 04 Mercury ( divalent/ methyl) 1E 05 6E 05 5E 06 2E 05 4E 05 4E 08 6E 08 Mercury ( elemental) 1E 05 Total Hazard Index 7E 04 7E 04 9E 06 2E 04 5E 05 2E 04 3E 04 Farmer and Summary of Multipathway Risk  Child Recreational Fisher Noncancer 6 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 4E 05 Cadmium 6E 04 1E 03 8E 06 5E 04 8E 06 1E 04 5E 04 Mercury ( divalent/ methyl) 1E 05 2E 04 1E 05 4E 05 2E 04 2E 08 1E 07 Mercury ( elemental) 1E 05 Total Hazard Index 7E 04 1E 03 2E 05 5E 04 2E 04 1E 04 5E 04 Table B. 8 Detailed Multipathway Risk Estimates for the PCWP Assessment  Pennsylvania Farmer and Summary of Multipathway Risk Recreational Fisher Cancer 70 year exposure Individual Lifetime Risk Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Cadmium 1E 08 Farmer and Summary of Multipathway Risk  Adult Recreational Fisher Noncancer 64 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 2E 05 Cadmium 3E 04 8E 04 2E 06 1E 04 2E 06 3E 04 4E 04 Mercury ( divalent/ methyl) 5E 06 5E 05 4E 06 1E 05 3E 05 6E 08 1E 07 Mercury ( elemental) 7E 06 Total Hazard Index 3E 04 9E 04 6E 06 1E 04 3E 05 3E 04 4E 04 Farmer and Summary of Multipathway Risk  Child Recreational Fisher Noncancer 6 year exposure Individual Hazard Quotient Substance inhalation total ingestion soil ingestion produce ingestion animal product ingestion water ingestion fish ingestion Lead 2E 05 Cadmium 3E 04 1E 03 5E 06 3E 04 6E 06 2E 04 8E 04 Mercury ( divalent/ methyl) 5E 06 2E 04 8E 06 3E 05 1E 04 3E 08 2E 07 Mercury ( elemental) 7E 06 Total Hazard Index 3E 04 2E 03 1E 05 4E 04 1E 04 2E 04 8E 04 Table B. 9 Detailed Output from the IEUBK Blood Lead Model Oregon PCWP Lead Uptake Blood Lead ( ug/ dL) Age ( yrs) Diet ( ug/ d) Water ( ug/ d) Soil/ Dust ( ug/ d) Total ( ug/ d) Total 0.5  1 0.008 0.006 0.03 0.017 0.0 1  2 0.011 0.012 0.03 0.026 0.0 2  3 0.011 0.012 0.03 0.026 0.0 3  4 0.009 0.017 0.03 0.029 0.0 4  5 0.009 0.017 0.03 0.029 0.0 5  6 0.009 0.017 0.03 0.029 0.0 6  7 0.013 0.015 0.03 0.031 0.0 Age ( yrs) Time outdoors ( hr) Inhalation Rate ( m3/ d) Lung Absorption (%) Air Conc. ( ug/ m3) Blood Lead ( ug/ dL) from Air 0.5  1 1 4.5 32 2.7 e 5 0.0 1  2 2 6.8 33 2.7 e 5 0.0 2  3 3 6.8 34 2.7 e 5 0.0 3  4 4 8.3 35 2.7 e 5 0.0 4  5 4 8.3 36 2.7 e 5 0.0 5  6 4 8.3 37 2.7 e 5 0.0 6  7 4 11.75 38 2.7 e 5 0.0 Table B. 10 Detailed Ecological Risk Estimates for the PCWP Assessment Screening Level Ecological Dose Response Values Lead Cadmium Mercury ( Hg+ 2) Mercury ( elemental) Mercury methyl Screening values for air inhalation by wildlife ( ug/ m3) 1.9E+ 03 1.4E+ 03 7.4E+ 02 7.4E+ 02 4.6E+ 02 Plant screening values for herbivorous wildlife ( ug/ g) 3.0E+ 01 3.6E+ 00 4.8E+ 00 4.8E+ 00 1.2E 01 Herbivore screening values for carnivorous wildlife ( ug/ g) 4.2E+ 00 5.1E+ 00 1.7E+ 00 1.7E+ 00 2.0E 02 Soil screening values for plants ( ug/ g) 5.0E+ 01 3.0E+ 00 3.0E 01 3.0E+ 00 Soil screening values for earthworms and microbial processes ( ug/ g) 5.0E+ 02 2.0E+ 01 1.0E 01 Soil screening values for vertebrates ( ug/ g) 2.3E+ 02 2.8E+ 01 3.7E+ 01 3.7E+ 01 9.0E 01 Surface water screening values for wildlife ( mg/ L) 4.9E+ 00 4.1E+ 00 5.6E+ 00 5.6E+ 00 1.4E 01 Surface water screening values for aquatic life ( mg/ L) 3.2E 03 1.1E 03 9.0E 04 1.3E 03 2.8E 06 Fish screening values for piscivorous wildlife ( mg/ g) 2.2E 03 2.9E 03 1.0E 05 PCWP Production IEM 2M Media Concentration Estimates 70 year facility operation; Minnesota Lead Cadmium Mercury ( Hg+ 2) Mercury ( elemental) Mercury methyl Air Concentration ( ug/ m3) 2.71E 05 5.49E 06 4.68E 07 2.14E 06 Forage Concentration ( ug/ g) 1.07E 02 6.66E 03 5.81E 05 7.34E 05 Herbivore concentration ( beef concentration as surrogate) ( ug/ g) 4.35E 05 8.13E 06 5.31E 06 No till farm soil concentration ( ug/ g) 9.12E 02 1.46E 02 9.20E 04 1.56E 03 No till farm soil concentration ( ug/ g) 9.12E 02 1.46E 02 9.20E 04 1.56E 03 No till farm soil concentration ( ug/ g) 9.12E 02 1.46E 02 9.20E 04 1.56E 03 Total surface water concentration ( mg/ L) 3.97E 05 4.70E 05 3.00E 09 4.37E 09 8.32E 11 Total surface water concentration ( mg/ L) 3.97E 05 4.70E 05 3.00E 09 4.37E 09 8.32E 11 Fish concentration ( mg/ g) 3.16E 07 1.17E 05 1.77E 10 1.77E 10 PCWP Production IEM 2M Ecological Risk Estimates Lead Cadmium Mercury ( Hg+ 2) Mercury ( elemental) Mercury methyl Sum of Mercury Hazard quotients for air inhalation by wildlife 1.5E 08 4.1E 09 6.3E 10 2.9E 09 3.5E 09 Plant hazard quotients for herbivorous wildlife 3.6E 04 1.9E 03 1.2E 05 1.5E 05 2.7E 05 Herbivore hazard quotients for carnivorous wildlife 1.0E 05 1.6E 06 3.2E 06 3.2E 06 Soil hazard quotients for plants 1.8E 03 4.9E 03 3.1E 03 5.2E 04 3.6E 03 Soil hazard quotients for earthworms and microbial processes 1.8E 04 7.3E 04 9.2E 03 9.2E 03 Soil hazard quotients for vertebrates 4.1E 04 5.2E 04 2.5E 05 4.3E 05 6.8E 05 Surface waterhazard quotients for wildlife 8.1E 06 1.1E 05 5.4E 10 7.8E 10 6.1E 10 1.9E 09 Surface water hazard quotients for aquatic life 1.2E 02 4.3E 02 3.3E 06 3.4E 06 3.0E 05 3.6E 05 Fish hazard quotients for piscivorous wildlife 1.4E 04 4.1E 03 1.8E 05 1.8E 05 Sum of Hazard Quotients 0.015 0.055 0.012 0.00058 0.000047 0.013 Maximum Hazard Quotient 0.012 0.043 0.009 0.00052 0.000030 0.0092 Attachment C IEUBK Modeling Documentation 1U. S. Environmental Protection Agency, 1994. Guidance Manual for the Integrated Exposure Uptake Biokinetic Model for Lead in Children. EPA/ 540/ R 93/ 081, Office of Emergency and Remedial Response, Washington, DC.

2U. S. Environmental Protection Agency, 1994. Technical Support Document: Parameters and Equations Used in the Integrated Exposure Uptake Biokinetic Model for Lead in Children. EPA/ 540/ R 94/ 040, Office of Emergency and Remedial Response, Washington, DC.

3U. S. Environmental Protection Agency, 1997. Exposure Factors Handbook. EPA/ 600/ P 95/ 002Fa, Office of Research and Development and National Center for Environmental Assessment, Washington, D. C. MEMORANDUM Date: January 28, 2004 Subject Results of IEUBK Modeling From: Darcie Smith, Lesley Stobert, and Nancy Jones EC/ R Incorporated To: Dennis Pagano, EPA/ OAQPS/ ESD The purpose of this memorandum is to present the inputs to and the results of blood lead level modeling using the Integrated Exposure Uptake Biokinetic Model for Lead in Children ( IEUBK, win32, Model 1.0, 2002). The blood lead concentrations in children resulting from emissions from one plywood production facility were estimated for a central tendency exposure scenario. The major inputs to the IEUBK model include lead air concentrations estimated using the Industrial Source Complex Model  Short Term Version 3 ( ISCST3) and media concentrations from the Indirect Exposure Methodology ( IEM 2M). The major outputs are the blood lead levels in

g/ dL for children ages 6 months to 7 years, by age group. Further information on IEUBK can be found in the guidance manual or technical support documents. 12 This memorandum is organized as follows: Section 1 presents the inputs used in IEUBK. Section 2 presents the IEUBK model results. Enclosure 1 presents the media concentrations from IEM 2M used in the IEUBK model. Enclosure 2 presents the values used to calculate dietary intake and the results of the calculations. Enclosure 3 presents the exposure factors used as inputs to the dietary intake calculations and as direct inputs to IEUBK.

1.0 IEUBK INPUTS The inhalation rate, water consumption rate, and the amount of soil/ dust ingested daily can be entered into IEUBK by age group. The central tendency exposure values from the Exposure Factor Handbook3 for were used and are presented in Tables 1 and 2. More detailed information about these factors is given in Enclosure 3. 2 Dietary intake of lead is another input to the IEUBK model, which depends both on the concentration of lead in food and the consumption rate of the food. The consumption rate also depends on the weight of the child. The lead concentration in each of several food types was obtained from IEM 2M modeling. These values, for each food type and for each age range, were multiplied by the consumption rate and body weight, and then summed for all foods by age range. Enclosure 2 presents the inputs and results of these calculations, Enclosure 3 presents more detailed information about the sources of the intake rates, and the final values are shown in Tables 1.

The outdoor air lead concentration, the lead concentration in drinking water, and the soil lead level are three additional values that can be input to IEUBK. The value for the outdoor air lead concentration was obtained from ISCST3 and was assumed to remain constant over all age ranges. The values for lead concentration in drinking water and outdoor soil lead levels were obtained from ISCST3 and IEM 2M modeling and were assumed to remain constant over all age ranges. In addition, the indoor dust level was assumed to equal the outdoor soil level for all age ranges and IEUBK default values for time spent outdoors were used. The input values for these parameters are listed in Table 2.

There are additional inputs to IEUBK that do not differ for age group of for exposure scenario. These inputs are listed in Table 2. The concentration values are outputs from IEM 2M. The absorption and other values are best estimate values that are used within IEUBK as defaults.

Table 1. Central Tendency Exposure Factors Used in IEUBK Modeling Age Central Tendency Exposure Scenario Inhalation Rate ( m3/ day) Water Consumption Rates ( L/ day) Soil/ Dust Ingestion Rates (

g/ g) Dietary Lead Intake (

g Pb/ day) Time Spent Outdoors ( hours/ day)

< 1 4.5 0.30 0.1 0.017 1 1 2 6.8 0.61 0.1 0.021 2 2 3 6.8 0.61 0.1 0.021 3 3 4 8.3 0.87 0.1 0.019 4 4 5 8.3 0.87 0.1 0.019 4 5 6 8.3 0.87 0.1 0.019 4 6 7 11.75 0.74 0.1 0.026 4 3 Table 2. Other IEUBK Inputs Used for All Ages and Exposure Scenarios Parameter Units Value Lead concentration in outdoor air

g/ m3 2.7 x 10 5 Lead concentration in drinking water

g/ L 3.95 x 10 8 Lead concentration in soil

g/ g 0.91 Lead concentration in dust

g/ g 0.91 Ratio of indoor to outdoor air lead concentration NA 1: 1 Mother's blood lead level at time of birth

g/ dL 2.5 Additional lead intake

g/ day 0.0 Lung absorption percentage lead absorbed 32 Total lead absorption from food and water ( at low intake) percentage lead absorbed 50 Total lead absorption from soil and dust ( at low intake) percentage lead absorbed 30 Total lead absorbed passively ( at high intake) for all ingestion pathways percentage lead absorbed 20 4 2.0 Results The results of the IEUBK modeling are presented in Table 3. All age groups were at of lead in the blood of less than 0.1

g/ dL.

Table 3. Results of IEUBK Modeling Age Blood Lead Level (

g/ dL)

Central Tendency Exposure Scenario < 1 0.0 1 2 0.0 2 3 0.0 3 4 0.0 4 5 0.0 5 6 0.0 6 7 0.0 5 ENCLOSURE 1 IEM 2M Media Concentration Outputs 6 HAP: Lead PARAMETER VALUE LEAD AIR CONCENTRATION ( ug/ m3) 2.7E 05 TOTAL PLANT CONCENTRATION ( ug/ g) Grains 1.2E 04 Legumes 4.2E 04 Root vegetables ( includes potatoes) 1.2E 04 Fruits 7.7E 04 Leafy vegetables ( exposed vegetables, including fruiting vegetables) 7.7E 04 ANIMAL PRODUCT CONCENTRATION ( ug/ g) Beef 4.4E 05 Dairy 4.7E 05 Pork 1.3E 05 TERRESTRIAL SOIL CONCENTRATIONS ( ug/ g) 9.1E 01 WATER CONCENTRATIONS ( mg/ L) 4.0E 05 FISH CONCENTRATIONS ( ug/ g) 3.2E 04 7 ENCLOSURE 2 Calculated Dietary Intake Values 8 Central Tendency Exposure Dietary Intake Rate Input to IEUBK Total Concentration ( ug Pb/ day) ( food concentration * BW * consumption rate) Food Age < 1 Age 1 to 2 Age 3 to 5 Age 6 to 11 Grains 4.8E 04 1.5E 03 2.0E 03 2.3E 03 Legumes 1.7E 03 2.0E 03 1.5E 03 2.2E 03 Root Vegs 2.3E 04 5.7E 04 4.1E 04 7.3E 04 Fruits 8.6E 03 9.0E 03 5.7E 03 9.7E 03 Leafy Vegs 5.5E 04 2.7E 03 1.9E 03 2.6E 03 Beef 2.0E 04 5.4E 04 7.3E 04 1.2E 03 Dairy 5.2E 03 3.7E 03 4.2E 03 4.7E 03 Pork 2.7E 05 7.7E 05 1.0E 04 1.4E 04 Fish 0.0E+ 00 1.4E 03 2.0E 03 2.7E 03 Total 1.7E 02 2.1E 02 1.9E 02 2.6E 02 Food Lead Concentration ( ug/ g) ( IEM 2M Output) Grains 1.2E 05 Legumes 4.2E 04 Root Vegs 1.2E 45 Fruits 7.7E 04 Leafy Vegs 7.7E 04 Beef 4.4E 05 Dairy 4.7E 05 Pork 1.3E 05 Fish 3.2E 04 Age Body Weight ( kg) < 1 7.2 1 to 2 12.3 3 to 5 17.5 6 to 11 30.8 Food Consumption Rate ( g DW / kg BW / day) ( from the Exposure Factors Handbook, shown in Enclosure 3) Food Age < 1 Age 1 to 2 Age 3 to 5 Age 6 to 11 Grains 0.56 1.00 1.00 0.63 Legumes 0.54 0.38 0.20 0.17 Root Vegs 0.27 0.39 0.20 0.20 Fruits 1.55 0.96 0.42 0.41 Leafy Vegs 0.10 0.28 0.14 0.11 Beef 0.65 1.00 0.96 0.87 Dairy 15.39 6.44 5.19 3.27 Pork 0.28 0.47 0.45 0.34 Fish 0.00 0.37 0.37 0.28 9 10 ENCLOSURE 3 Exposure Factors 11 Central Tendency Exposure Parameters Parameter Age Group Value Source Body Weights ( kg) Infant, < 1yr old 7.2 EFH Table 7 1. Mean value for 0 12 month olds, boys & girls Child, 1 2 yr old 12.3 EFH Table 7 3. Mean value for 1 2 year olds, boys & girls Child, 3 5 yr old 17.5 EFH Table 7 3. Mean value for 3 5 year olds, boys & girls Child, 6 11 yr old 30.8 EFH Table 7 3. Mean value for 6 11 year olds, boys & girls Inhalation Rates ( m3/ day) Infant, < 1yr old 4.5 EFH Table 5 23. Mean value for age < 1 Child, 1 2 yr old 6.8 EFH Table 5 23. Mean value for age 1 2 Child, 3 5 yr old 8.3 EFH Table 5 23. Mean value for age 3 5 Child, 6 11 yr old 11.75 EFH Table 5 23. Average of mean values for ages 6 8 and 9 11 males and females Water Ingestion Rates ( l/ day) Infant, < 1yr old 0.30 EFH Table 3 30. Mean value for age < 1 Child, 1 2 yr old 0.61 EFH Table 3 30. Mean value for age < 3 Child, 3 5 yr old 0.87 EFH Table 3 30. Mean value for age 3 5 Child, 6 11 yr old 0.74 EFH Table 3 30. Mean value for age 1 10 Soil Ingestion Rate ( g/ day) Child 0.10 EFH, p 4 25, recommended value for children ( mean, non pica)

Grain Ingestion Rate ( gDW/ kg/ day) Infant, < 1 yr old 0.56 EFH Table 12 18, corn values in g DW/ day, adjusted to gDW/ kg day Child, 1 5 yr old 1.00 Child, 6 13 yr old 0.63 Fish Ingestion Rates ( g/ kg/ day) Child, 1 2 yr old 0.37 EFH Table 10 61, Mean value for ages 0 5 Child, 3 5 yr old 0.37 EFH Table 10 61, Mean value for ages 0 5 Child, 6 11 yr old 0.28 EFH Table 10 61, Mean value for ages 6 10 EFH = U. S. Environmental Protection Agency, 1997. Exposure Factors Handbook. EPA/ 600/ P 95/ 002Fa, Office of Research and Development and National Center for Environmental Assessment, Washington, D. C. 12 Food Age Group ( years) Intake Rate from EFH ( gFW/ kg day) EFH Intake Rate Source Table Non home Produced Overall Mean Intake Rate from EFH Chapters 9 and 11)

( gFW/ kg day) Home Produced Overall Mean Intake Rate ( from EFH Chapter 13)

( gFW/ kg day) Households Who Farm Mean Intake from EFH Chapter 13 ( gFW/ kg day) Mean Preparation Loss from Tables 13 5 to 13 7 ( percent lost) Mean Moisture Content for Dry Weight Conversion: from Tables 11 28 and 9 27 2,3,4,5,6 ( percent moisture) Dry Weight Mean Home Produced Intake for Households Who Farm Adjusted for Preparation Loss 7 ( gDW/ kg day)

Beef 0 1 1.24 11 3 1.09 2.45 2.63 24 72 0.57 1 2 1.92 0.88 3 5 1.83 0.84 Pork 0 1 0.45 11 4 0.41 1.23 1.3 36 70 0.25 1 2 0.77 0.42 3 5 0.74 0.41 Dairy 0 1 62.74 11 2 8.02 14 17.1 0 89 1.97 1 2 26.26 0.82 3 5 21.15 0.66 Fruits 0 1 11.53 9 7 1.79 1.49 2.32 20 87 0.24 1 2 7.10 0.15 3 5 2.60 13 61 NA 0.07 Root Vegetables 0 1 2.03 9 11 1.36 1.16 1.39 8 86 0.18 1 2 2.52 13 65 NA 0.26 3 5 1.28 0.13 Legumes 0 1 1.36 9 10 0.39 1.01 1.3 16 86 0.16 1 2 2.46 13 64 NA 0.11 3 5 1.30 0.06 Leafy Vegetables 0 1 1.43 9 9 1.76 1.52 2.17 15 93 0.12 1 2 3.48 13 63 NA 0.34 3 5 1.74 0.17 1 Values from Chapters 9 and 11 are presented on an " as consumed" basis and were adjusted to add preparation losses back into this starting value:

Intake Rate = EFH value/( 1 preparation loss)

2 Dairy moisture content = weighted average of butter, cream, milk, yogurt, and cheese 3 Fruits moisture content = average of apples, pears, peaches, strawberries 4 Root vegetables moisture content = average of potatoes, carrots, beets 5 Legumes moisture content = average of corn, peas, pumpkin 6 Leafy vegetables moisture content = average of all raw whole cabbage, lettuce, peppers, tomatoes 7 Final Intake Rate = original EFH intake rate*( home produced mean/ non home produced mean)*( farm mean/ overall mean)*( 100 preparation loss)*( 100 moisture content) Appendix D Human Health Effects of HAPs Although numerous HAPs are emitted under this source category, several account for 95% of risk associated with this source category. A brief characterization of these HAPs is as follows:

Acrolein Acute ( short term) inhalation exposure to acrolein may result in upper respiratory tract irritation and congestion. The major effects from chronic ( long term) inhalation exposure to acrolein in humans consist of general respiratory congestion and eye, nose, and throat irritation. Acrolein is a strong dermal irritant, causing skin burns in humans. EPA considers acrolein a possible human carcinogen ( Group C), based on limited animal cancer data suggesting an increased incidence of tumors in rats exposed to acrolein in the drinking water.

Arsenic Inorganic arsenic exposure in humans by the inhalation route has been shown to be strongly associated with lung cancer, while ingestion of inorganic arsenic in drinking water by humans has been linked to a form of skin cancer and also to bladder, liver, kidney, and lung cancer. EPA has classified inorganic arsenic as a group A, known human carcinogen. The EPA inhalation cancer unit risk estimate for inorganic arsenic was used in this assessment. Chronic ( long term) inhalation exposure to inorganic arsenic in humans is associated with irritation of the skin and mucous membranes, and neurological injury. Animal studies of inhalation exposure have indicated developmental effects. Chronic oral exposure has resulted in gastrointestinal effects, anemia, peripheral neuropathy, skin lesions, hyperpigmentation, and liver or kidney damage in humans. The inhalation reference value used for the assessment of noncancer effects is a California REL value based on findings of developmental toxicity in mice ( CalEPA, 2000c). The EPA has not set an inhalation reference concentration for inorganic arsenic. This summary is based on IRIS ( USEPA 2003) and the ATSDR profile for arsenic ( ATSDR, 2000a).

Benzene The EPA has classified benzene as a Group A, known human carcinogen. Increased incidence of leukemia ( cancer of the tissues that form white blood cells) has been observed in humans occupationally exposed to benzene. The EPA has derived a range of inhalation cancer unit risk estimates for benzene; the value at the high end of the range was used in this assessment. Chronic inhalation of certain levels of benzene causes disorders in the blood in humans. Benzene specifically affects bone marrow ( the tissues that produce blood cells). Aplastic anemia,( 1) excessive bleeding, and damage to the immune system ( by changes in blood levels of antibodies and loss of white blood cells) may develop. In animals, chronic inhalation and oral exposure to benzene produces the same effects as seen in humans. Reproductive effects have been reported for women exposed by inhalation to high levels, and adverse effects on the developing fetus have been observed in animal tests. The inhalation reference value used for the assessment of noncancer effects is the IRIS RfC value of 3x10 2 mg/ m3, based on hematological effects in humans. Information used in this summary of benzene effects is based on IRIS ( USEPA 2003) and the ATSDR profile for benzene ( 1997a). Beryllium Human epidemiology studies are limited, but suggest a causal relationship between beryllium exposure and an increased risk of lung cancer. Inhalation exposure to beryllium has been demonstrated to cause lung cancer in rats and monkeys. EPA has classified beryllium as a Group B1, probable human carcinogen, and IARC has classified beryllium as carcinogenic to humans ( group 1).

Chronic ( long term) inhalation exposure of humans to beryllium has been reported to cause chronic beryllium disease ( berylliosis), in which granulomatous lesions ( noncancerous) develop in the lung. Acute ( short term) inhalation exposure to high levels of beryllium has been observed to cause inflammation of the lungs or acute pneumonitis ( reddening and swelling of the lungs) in humans; after exposure ends, these symptoms may be reversible. Inadequate information is available on the reproductive or developmental effects of beryllium in humans or animals following inhalation exposure. The RfC from IRIS, based on beryllium sensitization and progression to chronic beryllium disease was used in this assessment. This summary is based on IRIS support documents ( USEPA 1998) and the ATSDR Toxicological Profile for beryllium ( ATSDR, 2002a).

Cadmium An association between cadmium exposure and an increased risk of lung cancer has been reported from human studies, but these studies are inconclusive due to confounding factors. Animal studies have demonstrated an increase in lung cancer from long term inhalation exposure to cadmium. The U. S. Environmental Protection Agency ( EPA) has classified cadmium as a Group B1, probable human carcinogen. Chronic ( long term) inhalation or oral exposure to cadmium leads to a build up of cadmium in the kidneys that can cause kidney disease. Cadmium has been shown to be a developmental toxicant in animals, resulting in fetal malformations and other effects, but no conclusive evidence exists in humans. EPA has not established a RfC for cadmium. The " RfC" used for the assessment of noncancer effects is the California EPA REL based on kidney and respiratory effects in humans ( CalEPA 2000). The acute ( short term) effects of cadmium in humans through inhalation exposure consist mainly of effects on the lung, such as pulmonary irritation. This summary is based on IRIS ( USEPA 2003), and the ATSDR Toxicological Profile for cadmium ( ATSDR, 1999a).

Chromium Chromium occurs in the environment primarily in two valence states, trivalent chromium ( Cr III) and hexavalent chromium ( Cr VI). Exposure may occur from natural or industrial sources of chromium.

The respiratory tract is the major target organ for chromium ( VI) toxicity, for acute ( short term) and chronic ( long term) inhalation exposures. Human studies have clearly established that inhaled chromium ( VI) is a human carcinogen, resulting in an increased risk of lung cancer. Animal studies have shown chromium ( VI) to cause lung tumors via inhalation exposure. The U. S. Environmental Protection Agency ( EPA) has classified chromium ( VI) as a Group A, known human carcinogen. Other effects noted from chronic exposure include shortness of breath, coughing, and wheezing were reported from a case of acute exposure to chromium ( VI), while perforations and ulcerations of the septum, bronchitis, decreased pulmonary function, pneumonia, and other respiratory effects. Limited human studies suggest that chromium ( VI) inhalation exposure may be associated with complications during pregnancy and childbirth, while animal studies have not reported reproductive effects from inhalation exposure to chromium ( VI). The IRIS RfC for chromate particulates based on increased presence of lactate dehydrogenase in bronchioalveolar lavage fluid or exposed rats was used for this assessment.

Chromium III is much less toxic than chromium ( VI). The respiratory tract is also the major target organ for chromium ( III) toxicity, similar to chromium ( VI). Chromium ( III) is an essential element in humans, with a daily intake of 50 to 200 µ g/ d recommended for an adult. The body can detoxify some amount of chromium ( VI) to chromium ( III).

This summary is based on ATSDR Toxicological Profile for chromium ( ATSDR, 1998a) and support documents for IRIS ( USEPA, 1998b, c).

Formaldehyde Both acute ( short term) and chronic ( long term) exposures to formaldehyde irritate the eyes, nose, and throat, and may cause coughing, chest pains, and bronchitis. Reproductive effects, such as menstrual disorders and pregnancy problems, have been reported in female workers exposed to formaldehyde. Limited human studies have reported an association between formaldehyde exposure and leukemia, lung and nasopharyngeal cancer. Animal inhalation studies have reported an increased incidence of nasal squamous cell cancer. EPA considers formaldehyde a probable human carcinogen ( Group B2). Currently, EPA is re evaluating the carcinogenic potency of formaldehyde.

Lead EPA has classified lead as a group B2, probable human carcinogen. Human studies are inconclusive regarding lead exposure and cancer, while animal studies have reported an increase in kidney cancer from lead exposure by the oral route. Long term exposure to lead in humans results in effects on the blood, central nervous system ( CNS), blood pressure, kidneys, and Vitamin D metabolism. Children are particularly sensitive to the chronic effects of lead, with slowed cognitive development, reduced growth and other effects reported. The Centers for Disease Control use blood lead concentration of 10 ug/ dl in a child as the threshold for requiring monitoring and prevention activities ( ATSDR 1999b). Irreversible neurological effects can be the result of lead exposure in early childhood. Animal studies have reported effects similar to those found in humans, with effects on the blood, kidneys, and nervous, immune, and cardiovascular systems noted. Reproductive effects, such as decreased sperm count in men and spontaneous abortions in women, have been associated with lead exposure. The developing fetus is at particular risk from maternal lead exposure, with low birth weight and slowed postnatal neurobehavioral development noted. The inhalation value used in this assessment is the National Ambient Air Quality Standard ( quarterly average) for lead. This summary is based on IRIS ( USEPA 2003) and the ATSDR profile for lead ( ATSDR 1999b). Manganese The EPA has classified manganese as group D, not classifiable as to carcinogenicity in humans. No information is available about the cancer effects in humans from inhaling or ingesting manganese. Studies of animals ingesting high levels of manganese report mixed results, with several studies reporting no cancer effects and one study showing an increased in the occurrence of pancreatic tumors. Long term inhalation exposure of humans to high levels of manganese may result in a syndrome called manganism, characterized primarily by effects to the central nervous system. These effects typically begin with feelings of weakness and lethargy and progress to other symptoms such as speech disturbances, a mask like face, tremors, and psychological disturbances. Other effects from inhaling manganese over a long period of time include increased incidence of cough and bronchitis and an increased susceptibility to infectious lung disease. Reproductive effects, such as impotence and loss of libido, have been noted in male workers afflicted with manganism attributed to occupational exposure to high levels of manganese by inhalation. Animal studies have reported degenerative changes in the seminiferous tubules leading to sterility from intratracheal instillation of high doses of manganese ( experimentally delivering the manganese directly to the trachea). In young animals exposed to manganese orally, decreased testosterone production and retarded growth of the testes were reported. The RfC from IRIS, based on impairment of neuro behavioral function in humans was used in this assessment. This summary is based on IRIS ( USEPA, 2003) and the ATSDR profile for manganese ( ATSDR, 2000b).

4,4' Methylenediphenyl diisocyanate ( MDI) Acute ( short term) inhalation of high concentrations of MDI may cause sensitization and asthma in humans. MDI has been observed to irritate the skin and eyes of rabbits. Chronic ( long term) inhalation exposure to MDI may cause asthma, dyspnea, and other respiratory impairments in workers. EPA has classified MDI within Group D, not classifiable as to human carcinogenicity.

Mercury Mercury exists in three forms: elemental mercury, inorganic mercury compounds ( primarily mercuric chloride), and organic mercury compounds ( primarily methylmercury). Each form exhibits different health effects. Brick, structural clay products, and clay ceramics manufacturing may release elemental or inorganic mercury, but not methylmercury. However, elemental and inorganic mercury are deposited on surface water, where they are converted to methylmercury, an important food contaminant.

Acute ( short term) exposure to high levels of elemental mercury in humans results in central nervous system ( CNS) effects such as tremors, mood changes, and slowed sensory and motor nerve function. High inhalation exposures can also cause kidney damage and effects on the gastrointestinal tract and respiratory system. Chronic ( long term) inhalationexposure to elemental mercury in humans also affects the CNS, with effects such as increased excitability, irritability, excessive shyness, and tremors. Data on toxic effects of oral exposure to elemental mercury are sparse. We have not classified elemental mercury for carcinogenicity.

Acute exposure to inorganic mercury by the oral route may result in effects such as nausea, vomiting, and severe abdominal pain. The major effect from chronic exposure, either oral or inhalation, to inorganic mercury is kidney damage. Reproductive and developmental animal studies have reported effects such as alterations in testicular tissue, increased embryo resorption rates, and abnormalities of development. Mercuric chloride ( an inorganic mercury compound) exposure has been shown to result in forestomach, thyroid, and renal tumors in experimental animals. We have classified mercuric chloride as a Group C, possible human carcinogen.

Both acute and chronic oral exposure to methylmercury have been found to cause developmental damage to the central nervous system in fetuses and children, with effects including mental retardation, deafness, blindness, and cerebral palsy. Lower exposures may cause developmental delays and abnormal reflexes. The most important source of methylmercury exposure for most people is eating fish. Although fish is an important part of a balanced died, federal and state fish advisories recommend limiting intake of certain fish that contain elevated methylmercury levels.

Nickel subsulfide Human studies have reported an increased risk of lung and nasal cancers among nickel refinery workers exposed to nickel refinery dust. Nickel refinery dust is a mixture of many nickel compounds, with nickel subsulfide being the major constituent. Animal studies have also reported lung tumors from inhalation exposure to nickel refinery dusts and to nickel subsulfide." EPA has classified nickel refinery dust and nickel subsulfide in Group A, Human Carcinogens. EPA has derived an inhalation cancer unit risk estimate for nickel refinery dust and nickel subsulfide. There is some uncertainty regarding the form of nickel present in air impacted by coke oven emissions. Recognizing this, nickel subsulfide was consider less relevant to the nickel associated with coke oven emissions than was nickel refinery dust. The EPA inhalation unit risk estimate for nickel refinery dust was used in this inhalation assessment.

Phenol Phenol is highly irritating to the skin, eyes, and mucous membranes in humans after acute ( short term) inhalation or dermal exposures. Phenol is considered to be quite toxic to humans via oral exposure. Anorexia, progressive weight loss, diarrhea, vertigo, salivation, a dark coloration of the urine, and blood and liver effects have been reported in chronically ( long term) exposed humans. Animal studies have reported reduced fetal body weights, growth retardation, and abnormal development in the offspring of animals exposed to phenol by the oral route. EPA has not established a Reference Concentration ( RfC) for phenol. The California EPA REL based on twitching, muscle tremors, and neurological impairment, as well as elevated serum liver enzymes in rats was used in this assessment. EPA has characterized phenol as Group D, not classifiable as to human carcinogenicity, under the 1986 Guidelines for Carcinogen Risk Assessment. Under the draft interim Guidelines ( U. S. EPA, 1999), the data regarding the carcinogenicity of phenol via the oral, inhalation, and dermal exposure routes are considered inadequate for an assessment of human carcinogenic potential. This summary is based on the IRIS file and background document ( USEPA, 2003), and the ATSDR profile for phenol ( ATSDR 1998b).