**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  1



## Deliberative Draft Document for EPA Internal Review **Draft Residual Risk As**  **sessm ent for the Primary Aluminum**  **Pro duction**  **Source Category**

**by EPA’s Office of Air Quality Planning and Standards** 

**Office of Air and Radiation November**  **October 2011** **Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  2 

### Table of Contents 1 Introduction ................................ ................................ ................................ ................ 4 4 4 2 Methods ................................ ................................ ................................ ..................... 4 4 4 2.1 Emissions and source data ................................ ................................ ................... 4 4 4 2.2 Dispersion modeling for inhalation exposure assessment ................................ ..... 5 5 5 2.3 Estimating chronic human inhalation exposure ................................ .................... 8 7 8 2.4 Screening for potential acute impacts of concern ................................ .................. 9 8 8 2.5 Multipathway human health and environmental risk screening ......................... 10 9 10 2.6 Dose
- response assessment ................................ ................................ ............. 11 11 11 2.6.1 Sources of chronic dose
- response information ................................ ........ 11 11 11 2.6.2 Sources of acute dose
- response information ................................ ............ 15 15 15 2.7 Risk characterization ................................ ................................ ...................... 17 17 17 2.7.1 General ................................ ................................ ................................ ... 17 17 17 2.7.2 Mixtures ................................ ................................ ................................ . 19 19 19 2.7.3 Facility
- wide risks ................................ ................................ .................. 20 20 20 3 Risk results for the primar y a luminum production source categor y ................... 20 20 20 3.1 Source categor y d escription and results ................................ .......................... 20 20 20 3.2 Baseline risk characterization ................................ ................................ ......... 21 21 21 3.3 Post
- control risk characterization ................................ ................................ ... 25 25 25 4 General dis cussion of uncertainties and how they have been addressed ................ 26 26 26 4.1 Exposure modeling uncertainties ................................ ................................ .... 26 26 26 4.2 Uncertainties in the dose
- response relationships ................................ ............. 27 27 27 5 References ................................ ................................ ................................ ........... 35 35 35 **Index of Tables** Table 2.2
- 1 AERMOD version 09292 model options for RTR modeling ........................... 6 6 6 Table 2.6
- 1 (a) Dose
- Response Values for Chronic Inhalation Exposure to Carcinogens

................................ ................................ ................................ ................................ .... 14 13 14 Table 2.6
- 1 (b) Dose
- Response Values for Chronic Oral Exposure to Carcinogens .... 14 14 14 Table 2.6
- 1 (c) Dose
- Response Values for Chronic Inhalation Exposure to Noncarcinogens

................................ ................................ ................................ ................................ .... 15 15 15 Table 2.6
- 2 Dose
- Response Values for Acute Exposure ................................ .............. 17 17 17 Table 3.1
- 1 Summar y of Emissions from the Primary Aluminum Production Source Categor y and Availability of Dose
- Response Values ................................ ................................ ... 21 21 21 Table 3.2
- 1 Summar y of Sour ce Categor y L evel Inhalation Risks for Primary Aluminum Production ................................ ................................ ................................ ................... 23 23 23 Table 3.2
- 2 Summar y of Ref ined Acute Results for Secondary Aluminum Production Facilities ................................ ................................ ................................ ...................... 24 24 24 **Appendices** Appendix 1 Technical Support Document for HEM
- AERMOD Modeling Appendix 2 Meteorological Data for HEM
- AERMOD Modeling **Field Code**  **Changed** ... [1] **Field Code**  **Changed** ... [2] **Field Code**  **Changed** ... [3] **Field Code**  **Changed** ... [4] **Field Code**  **Changed** ... [5] **Field Code**  **Changed** ... [6] **Field Code**  **Changed** ... [7] **Field Code**  **Changed** ... [8] **Field Code**  **Changed** ... [9] **Field Code**  **Changed** ... [10] **Field Code**  **Changed** ... [11] **Field Code**  **Changed** ... [12] **Field Code**  **Changed** ... [13] **Field Code**  **Changed** ... [14] **Field Code**  **Changed** ... [15] **Field Code**  **Changed** ... [16] **Field Code**  **Changed** ... [17] **Field Code**  **Changed** ... [18] **Field Code**  **Changed** ... [19] **Field Code**  **Changed** ... [20] **Field Code**  **Changed** ... [21] **Field Code**  **Changed** ... [22] **Field Code**  **Changed** ... [23] **Field Code**  **Changed** ... [24] **Field Code**  **Changed** ... [25] **Field Code**  **Changed** ... [26] **Field Code**  **Changed** ... [27] **Field Code**  **Changed** ... [28] **Field Code**  **Changed** ... [29] **Field Code**  **Changed** ... [30]**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  3 Appendix 3 Analy sis of data on short
- term emission rates relative to long
- term emission

rates Appendix 4 Technical Support Document for TRIM
- Based Multipathway Screening

Scenario for RTR: Summary of Approach and Evaluation Appendix 5 Draft Detailed Risk Modeling Results Appendix 6 Acute Impacts Refined Analy sis Fi gures Appendix 7 Development of the Chronic Screening Lev el for Carbon yl Sulfide **Index of Acronyms** AERMOD American Meteorological Society /EPA Regulatory Model AEGL Acute exposure guideline level ASTDR US Agency for Toxic Substances and Disease Registr y CalEPA California Environmental Agency CTE Central Tendency Estimate ERPG Emergency Response Planning Guideline HAP Hazardous Air Pollutant HEM Human Exposure Model HI Hazard index HQ Hazard quotient IRIS Integrated Risk Information System MACT Maximum Achievable Control Technology MIR Maximum Individual Risk MOA Mode of action NAC National Advisor y C ommittee NAAQS National Ambient Air Quality Standards NATA National Air Toxics Assessment NEI National Emissions Inventor y NPRM Notice of Proposed Rulemaking PB
- HAP Persistent and Bioaccumulative
- HAP POM Polycyclic organic matter REL Reference exposure level RfC Reference concentration RfD Reference dose RME Reasonable Maximum Exposure RTR R isk and Technology TOSHI Target
- organ - specific hazard index URE Unit risk estimate**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  4 

### 1 **Introduction** Section 112 of the Clean Air Act (CAA) establishes a two
- stage regulatory process for addressing emissions of hazardous air pollutants (HAPs) from stationary sources. In the first stage, section 112(d) requires the Environmental Protection Agency (EPA, or the Agency) to develop technology
- based standards for categories of sources (e.g., petroleum refineries, pulp and paper mills, etc.) [ 1 ]. EPA has largely completed the initial Maximum Achievable Control Technology ( MACT ) standards as required under this provision. Under section 112(d)(6), EPA must review each of these technology
- based standards at least every eight ye ars and revise a standard, as necessary , “taking into account developments in practices, processe s and control technologies.” In the secon d stage, EPA is required under section 112(f)(2) to assess the health and environmental risks that remain after implementation of the MACT standards. If additional risk reductions are necessary to protect public health with an ample margin of safety or to prevent an adverse environmental effect, EPA must develop standards to address these remaining risks. This second stage of the regulator y p rocess is known as the residual risk stage. For each source categor y f or which EPA issued MACT standards, the resi dual risk stage must be completed within eight y ears of promulgation of the initial technology
- based standard. In December of 2006 we consulted with a panel from the EPA's Science Advisor y B oard (SAB) on the “Risk and Technology Review (RTR) Assessment Pl an , ” and in June of 2007, we received a letter with the results of that consultation. Subsequent to the consultation, in June of 2009 , a meeting was held with an SAB panel for a formal peer review of the “Risk and Technology Review (RTR) Assessment Methodologies” [ 2 ]. We received the final SAB report on this review in May of 2010 [ 3 ]. Where appropriate, we have responded to the ke y mes sages from this review in developing our current risk assessment s and we will be continuing our efforts to improve our assessments by incorporating updates based on the SAB recommendations as they are developed and become available . Our responses to the k ey recommendations of the SAB are outlined in a memo entitled, “EPA’s Actions in Response to Key Recommendations of the SAB Review of RTR R isk Assessment Methodologies” [ 4 ]. This document contains the methods and the results of baseline risk assessments p erformed for the Primary Aluminum Pro duction source categor y. The methods discussion includes descriptions of the methods used to screen for acute health risks, chronic non
- inhalation health risks, and adverse environmental effects, as well as description s of the methods used to develop refined estimates of chronic inhalation exposures and human health risks for cancer and noncancer endpoints. 

### 2 **Me thods**  **2.1 Emissions and source data**  The preli minary dataset was based on information in the 2005 National Air Toxic s Assessment (NATA) Inventory . This information was then supplemented with te st data and other information through an Information Collection Request (ICR), received in April 2011, from 11 of the 15 facilities in the source category. These ICR data were th en used along with the 2005 NATA inventory data to develop the emissions dataset for this source categor y . We**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  5 then performed an engineering review of the information using EPA engineers to identify readily apparent limitations and issues with the emissions data . Notably , one facility in this source categor y, Columbia Falls, has not been fully operational since 1999 and has been completely closedbeen idle for 2 approximately 4 years and therefore we did not receive recent emissions data to calculate risks based on actual emissions. However, we did estimate risks based on estimates of MACT allowable emissions for this one facility to provide an indication of what risks it might pose if it were to re
- open . Details on the development of the emissions and source data for this source categor y , including the estimation of allowable emissions from the Columbia Falls facility , are discussed in : Draft Summar y P rimary Aluminum RTR Modeling File Development , availabl e in the docket for this rulemaking . Section 3 below provides a summary of the emissions. 

### 2.2 **Dispersion modeling for inhalation exposure assessment** Both long
- and short
- term inhalation exposure concentrations and associated health risk from each facility in the source category of interest were estimated using the Human Exposure Model in combination with the American Meteorological Society/EPA Regulatory Mo del dispersion modeling sy stem (HEM
- AERMOD). The approach used in applying this modeling sy stem is outlined below, and further details are provided in Appendix 1 . HEM
- AERMOD performs three main operations: atmospheric dispersion modeling, estimation of individual human exposures and health risks, and estimation of population risks. This section focuses on the dispersion modeling component. The exp osure and risk characterization components are discussed in other subsections of Sections 2 and 3. The dispersion model in the HEM
- AERMOD system, AERMOD version 09292, is a state
- of
the
- science Gaussian plume dispersion model that is preferred by EPA for modeling point, area, and volume sources of continuous air emissions from facility applications [ 5 ]. Further details on AERMOD can be found in the AERMOD Users Guide [ 6]. The model is used to develop annual average ambient concentrations through the simulation of hour
- by
- hour dispersion from the emission sources into the surrounding atmosphere. Hourly emission rates used for this simulation are generated by ev enly di viding the total annual emission rate from the inventory into the 8,760 hours of the year . The first step in the application of the HEM
- AERMOD modeling sy stem is to predict ambient concentrations at locations of interest. The AERMOD model options employed are summarized in Table 2.2
- 1 and are discussed further below.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  6 **Table 2.2**  **- 1**  **AERMOD version 09292 mo del options for RTR**  **mo deling**  Modeling Option Selected Parameter for chronic exposure Type of calculations Hourly Ambient Concentration Source type Point, area represented as pseudo point source Receptor orientation Polar (13 rings and 16 radials) Discrete (census block centroids) Terrain characterization Actual from USGS 1
- degree DEM data Building downwash Not Included Plume deposition/depletion Not Included Urban source option No Meteorology 1 year representative NWS from nearest site (158 stations) In HEM
- AERMOD, meteorological data are ordinarily selected from a list of 158 National Weather Service (NWS) surface observation stations across the continental United States, Alaska, Hawaii, and Puerto Rico. In most cases the nearest station is selected as representative of the conditions at the subject facility . Ideally , when considering off
- site meteorological data most site specific dispersion modeling efforts will employ up to f ive ye ars of data to capture variability in weather patterns from ye ar to year. However, to minimize data processing time and resources for this assessment , we modeled only a single ye ar, typically 1991. While the selection of a single year may result in under
- prediction of long
- term ambient levels at some locations, likewise it may result in over
- prediction at others. For each facility identified by its characteristic latitude and longitude coordinates, the closest meteorological station was used in the dispersion modeling. The average distance between a modeled facility and the applicable meteorological station was 40 miles (72 km). Appendix 2 (Meteorological Data Processing Using AERMET for HEM
- AERMOD) provides a complete listing of stations and assu mptions along with further details used in processing the data through AERMET. The sensitivity of model results to the selection of the nearest weather station and the use of one year of meteorological data is discussed in “ Risk and Technology Review (RTR ) Risk Assessment Methodologies ” [ 2 ]. The HEM
- AERMOD system estimates ambient concentrations at the geographic centroids of census blocks (using the 2000 Census) and at other receptor locations that can be specified by the user. The model accounts for th e impacts of multiple facilities when estimating concentration impacts at each block centroid. Typically we combined only the impacts of facilities within the same source categor y, and assessed chronic exposure and risk onl y f or census blocks with at leas t one resident (i.e., locations where people may reasonably be assumed to reside rather than receptor points at the fenceline of a facility). Chronic ambient concentrations were calculated as the annual average of all estimated short
- term (one
- hour) conce ntrations at each block centroid. Possible future residential use of currently uninhabited areas was not considered. Census blocks, the finest resolution available in the census data, are ty pically comprised of approximately 40 people or about ten househ olds.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  7 In contrast to the development of ambient concentrations for evaluating long
- term exposures, which was performed only for occupied census blocks, worst
- case short
- term (one
- hour) concentrations were estimated both at the census block centroids and at point s nearer the facility that represent locations where people may be present for short periods, but generally no nearer than 100 meters from the center of the facility (note that for large facilities, this 100
- meter ring could still contain locations inside the facility property). Since short
- term emission rates were needed to screen for the potential for hazard via acute exposures, and since the NEI contains onl y annual emission totals, we ty pica lly appl ied the general assumption to all source categories th at the maximum one
- hour emission rate from any source w as ten times the average annual hourly emission rate for that source (s ee Appendix 3) 1

. Howe ver, for this source categor y, an engineering analy sis demonstrated that peak 1
- hour emissions are approximately 5 times average hourly emissions, and thus a factor of 5, rather than the default factor of 10 was used in the acute risk assessment . 2 3

. However, for this source categor y, an engineering analysis demonstrated that peak 1
- hour emissions are approximately 5 times average hourly emissions, and thus a factor of 5, rather than the default factor of 10 was used in the acute risk assessment . 4 Th e average hourly emissions rate is defined as the total emissions for a year divided by the total number of operating hours in the ye ar. This choice of a factor of ten for screening was originally based on engineering judgment . To develop a more robust p eak
- to - mean emissions factor, and in response to one of the ke y messages from the SAB consultation on our RTR Assessment Plan, we performed an analy sis using a short
- term emissions data set from all the major HAP
- emitting source s located in an area of Texas near Houston (originally reported on by Allen et al. 2004)[ 7]. In that report, the Texas Environmental Research Consortium Project compared hourly and annual emissions data for volatile organic compound s for all facilities in a heavily
industrialized 4
- county area (Harris, Galveston, Chambers, and Brazoria Counties , TX) over an eleven
- month time period in 2001 . We obtained the dataset and performed our own analysis, focusing that analy sis on sources whic h reported emitting high quantities of HAP over short periods of time (see Appendix 3 , “Analysis of data on short
- term emission rates relative to long
- term emission rates”). Most peak emission events were less than twice the annual average, and the highes t was a factor of 11 times the annual average . Based on these results, we chose the factor of ten for all initial screening; it is intended to cover routinely
variable emissions. While there have been some documented emission excursions above this level, our analysis of the data from the Texas Environmental Research Consortium suggests that this factor should cover more than 99% of the short
- term peak gaseous or volatile HAP emissions from typical industrial sources . We have no data relating specifically to peak short
1 In situations where we have information on hourly emissions, we will take this into account when evaluatin g acute risks. 2 Justification for applying an acute factor of 5 rather than the default value of 10 can be found in the memo “Acute Risk Modeling of Primary Aluminum Potroom Emissions” which is located in the docket supporting the proposed rulemaking . 3 In situations where we have information on hourly emissions, we will take this into account when evaluating acute risks. 4 Justification for applying an acute factor of 5 rather than the default value of 10 can be found in the memo “Acute Risk Modeling of Primary Aluminum Potroom Emissions” which is located in the docket supporting the proposed rulemaking .**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  8 term emissions of particulate HAP. In the absence of source categor y - specific data, we use this same default approach for particulate emissions as well. Census block elevations for HEM
- AERMOD modeling were determined nationally from the US Geological Service 1
- degree digital elevation model (DEM) data files, which have a spatial resolution of about 90 meters. Elevations of polar grid points used in estimating short
and long
- term ambient concentrations were assumed to be equal to the highest elevation of any census block falling within the polar grid sector corresponding to the grid point. If a sector does not contain an y b lo cks, the model defaults the elevation to that of the nearest block. If an elevation is not provided for the emiss ion source, the model uses the average elevation of all sectors within the innermost model ring. In addition to using receptor elevation to determine plume height, AERMOD adjusts the plume’s flow if nearby elevated hills are expected to influence the wind patterns. For details on how hill heights were estimated and used in the AERMOD modeling see Appendix 1 . 

### 2.3 **Estimating chronic**  **human inhalation exposure** We used the annual average ambient air concentration of each HAP at each census block centroid as a surrogate for the lifetime inhalation exposure concentration of all the people who reside in the census block. That is, the risk analysis did not consider either the short
- te rm or long
- term behavior (mobility) of the exposed populations and its potential influence on their exposure. We did not address short
- term human activity for two reasons. First, our experience with the 1996, 1999, 2002, and 2005 NATA assessments (which modeled daily activit y u sing EPA’s HAPEM model) suggests that, given our curre nt understanding of microenvironment concentrations and daily activities, modeling short
- term activity would, on average, reduce risk estimates about 25% for particulate HAPs; it will also reduce risk estimates for gaseous HAP s, but ty

pically by much less. Second, basing exposure estimates on average ambient concentrations at census block centroids may underestimate or overestimate actual exposure concentrations at some residences. Further reducing exposure estimates for the most highly exposed residents by modeling their short
- term behavior could add a sy stematic low bias to these results. We did not address long
- term migration nor population growth or decrease over 70 years, instead basing the assessment on the assumption that each person’s predicted exposure is constant over the course of their lifetime which is assumed to be 70 years. In assessing cancer risk, we generally estimated three metrics : the maximum individual risk (MIR), which is defined as the risk associated with a lifetime of exposure at the highest concentration (note that the MIR can be estimated for each source as well as for the entire source categor y) ; the population risk distribution; and the cancer incidence. The assumption of not considering short or long
- term population mobility does not bias the estimate of the MIR nor does it affect the estimate of cancer incidence since the total population number remains the same. It does, howe ver, affect the shape of the distribution of individual risks across the affected population, shifting it toward higher estimated individual risks at the upper end and reducing the number of people estimated to be at lower risks, thereby biasing the risk estimates high.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  9 When screening for potentially significant acute exposures, we used an estimate o f the highest hourly ambient concentration at any off
- site location as the surrogate for the maximum potential acute exposure concentration for any individual. 

### 2.4 **Screening for potential acute impacts of concern** In establishing a scientifically defensible approach for the assessment of potential health risks due to acute exposures to HAP, we f ollowed the same general approach that has been used for developing chronic health risk assessments for other rules under the residual risk program. That is, we develope d a tiered, iterative approach. This approach to risk assessment was endorsed by the National Academy of Sciences in its 1993 publication “Science and Judgment in Risk Assessment” and subsequently was adopted in the EPA’s “Residual Risk Report to Congress ” in 1999. With respect to screening for potential acute health risk s , the assessment methodology is designed to eliminate from further consideration those facilities for which we have confidence that no acute adverse health effects of concern will occur. To do so, we use what is called a tiered , iterative approach to the asse ssment. This means that we began with a screening assessment, which relies on readily available data and uses conservative assumptions that in combination approximate a worst
- case exposure . The result of this screening process is that either the facility being assessed poses no potential acute health risks (i.e., it “screens out”), or that it requires further , more refined assessment with respect to potential acute exposure s f rom emitted HAP . A mor e refined acute assessment could u s e industry
- or site
- specific data on the temporal pattern of emissions, the layout of emission points at the facility , the boundaries of the facility , and/or the local meteorology. In some cases, all of these site
- specific data are used to refine the assessment; in others, lesser amount s of site
- specific data can be used to determine that acute exposures are not a concern, and significant additional data collection is not necessary . Acute health risk screening was performed for each facility as the first step. We used conservative assumptions for emission rates, meteorology , and exposure location. We used the following worst
- case assumptions in our screening approach:

• Peak 1
- hour emissions were assumed to equal 5 times the average 1
- hour emission rates except in the case of fugitive dust (see section 2.2) • For facilities with multiple emission points, peak 1
- hour emissions were assumed to occur at all emission points at the same time. • For facilities with multiple emission points, 1
- hour concentrations at each receptor were assumed to be the sum of the maximum concentrations due to each emission point, regardless of whether those maximum concentrations occurred during the same hour. • Worst
- case meteorology (from one year at the nearest NWS site ) was assumed to occur at the same time the peak emission rates occur. The recommended EPA local
scale dispersion model, AERMOD, wa s used for simulating atmospheric dispersion during this worst
- case hour .**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  10

• A person was assumed to be located downwind at the point of maximum modeled impact during this same worst - case 1
- hour period, but no nearer to the source than 100 meters. As a result, the maximum modeled 1
- hour off
- site concentration equals the worst - case acute exposure concentration. • The maximum impact was compared to multiple short
- term health benchmarks for the HAP being assessed to determine whether a possible acute health risk might exist. These benchmarks are described in section 2.6 of t his report. As mentioned above, when we identify acute impacts which exceed their relevant benchmarks, we pursue refining our acute screening estimates to the extent possible . In some cases, this ma y include the use of a facility
- specific emissions multi plier to estimate the peak hourly emission rates from the average rates (rather than the default factor of 10, as is the case for this source categor y, see section 3.2 ) . In other cases, this may entail determining the actual physical layout and boundaries of a facility to more accurately gauge where people mi ght reasonably be exposed for an hour. 

### 2.5 **Multipathway human health**  **and environmental**  **risk screening** The potential for significant human health risks and adverse environmental impacts due to exposures vi a routes other than inhalation (i.e., multipathway exposures) was screened by first determining whether any sources emitted any hazardous air pollutants known to be persistent and bioaccumulative in the environment (PB
- HAP). The P B
- HAP compounds or compou nd classes are identified for the screening from the EPA’s Air Toxics Risk Assessment L ibrary [ 8 ], and they are cadmium compounds, chlordane, chlorinated dibenzodioxins and furans, DDE, heptachlor, hexachlorobenzene, hexachlorocyclohexane, lead compounds, mercury compounds, methoxychlor, polychlorinated biphenyls, pol yc yc lic organic matter (POM) , toxaphene, and trifluralin . With respect to PB
- HAP other than lead, emissions were evaluated for potential non
inhalation risks and adverse environmental impact s using our recently
- developed screening scenario which was developed for use with the TRIM.FaTE 5 model. This screening scenario uses environmental media outputs from the peer
- reviewed TRIM.FaTE to estimate the maximum potential ingestion risks for any sp ecified emission scenario by using a generic farming/fishing exposure scenario that simulates a subsistence environment. The screening scenario retains many of the ingestion and scenario inputs developed for EPA’s Human Health Risk Assessment Protocols (H HRAP) for hazardous waste combustion facilities. 6 In the development of the screening scenario a sensitivit y analy sis was conducted to ensure that its key design parameters were established such that environmental media concentrations were not underestimated, and to also minimize the occurrence of false positives for human health endpoints. See Appendix 4 for a complete discussion of the development and testing of the screening scenario, as well as for the values of facility
- level screening de minimis emis sion rates developed for screening potentially significant multi
- pathway im pacts. In general, f or the purpose of developing emission rates for our multi
- pathway screening, we
5 EPA’s Total Risk Integrated Methodology (General Information) http://epa.gov/ttn/fera/trim_gen.html 6 EPA’s Human Health Risk A sse ssment Protocol (HHRAP) for Hazardous Waste Combustion Facilities; http://www.epa.gov/epaoswer/hazwaste/combust/riskvol.htm#volume1**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  11 derived emission levels for each PB HAP at which the maximum human health risk w ould be 1 in a million for lifetime cancer risk or a hazard quotient of 1.0 for noncancer impacts. In evaluating the potential multi
- pathway risks from emissions of lead compounds, rather than developing a screening emission rate, we generally com pare maximum estimated chronic (3
- month average) atmospheric concentrations with the current primar y N ational Ambient Air Quality Standard (NAAQS) for lead. Values below the NAAQS are considered to have a low potential for multi
- pathway risks. Notabl y, for this source categor y, POM was the only PB
HAP identified in the emissions inv entor y. We also evaluated the potential for significant direct environmental exposures to HAP by evaluating the potential for exceedances of chronic human health inhalation reference value s in the ambient air near these facilities. Human health dose
- response reference values are generally derived from studies conducted on laboratory animals (such as rodents) and developed with the inclusions of uncertainty factors that could be as high as 3000. As a result, these human reference values are often significantly lo wer than the level expected to cause an adverse effect in an exposed rodent. It should be noted that there is a scarcity of data on the direct atmospheric impact of these HAP on other receptors, such as plants, birds, and wildlife. Thus, if the maximum inhalation hazard in an ecosy stem is below the level of concern for humans (i.e. , is below the human health reference value which is itself a lower reference value than would be expected for an ecologic effect) , we have generally concluded that mammalian receptors should be at no risk of adverse effects due to inhalation exposures from non
- PB
- HAP, and have assurance that other ecological receptors are also not at any si gnificant risk from direct atmospheric impact. In some isolated cases where we have data indicating potential adverse impacts on plants, birds, or other wildlife due to the direct atmospheric impacts of specific HAP, we note that as an uncertainty and, wh ere possible, refine our analysis by comparing our modeled impacts to available reference values from the scientific literature. 

### 2.6 **Dose -**  **r esponse**  **a ssessment**  **2.6.1 Sources of chronic dose**  **- response information**  Dose
- response assessment (carcinogenic and non
- carcinog enic) for chronic exposure (either by inhalation or ingestion) for the HAP reported in the emissions inventory for the Primary Aluminum Pro duction sources were based on the EPA Office of Air Quality Planning and Standards’ (OAQPS) existing recommendations for HAP [ 9 ], also used for NATA 1999, 2002, and 2005 [ 10 ]. This information has been obtained from various sources and prioritized according to (1) conceptual consistency with EPA risk assessment guidelines and (2) level of peer review received. The prioritization process was aimed at incorporating into our assessments the best available science with respect to dose
- response information. The recommendations are based on the following sources, in order of priority : 1) US Environmental Protection Agency (EPA ). EPA has developed dose
- response assessments for chronic exposure for many of the pollutants in this study . These**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  12 assessments ty

pically provide a qualitative statement regarding the strength of scientific data and specif

y a reference concentration (RfC , for inhalation) or reference dose (RfD, for ingestion) to protect against effects other than cancer and/or a unit risk estimate (URE, for inhalation) or slope factor (SF, for ingestion) to estimate the probability of developing cancer. The RfC is defined 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 l ifetime. ” The URE is defined as “ the upper
- bound excess cancer risk estimated to result from continuous lifetime exposure to an agent at a concentration of 1 μg/m 3 in air. ” The SF is “an upper bound, approximating a 95% confidence limit, on the increased cancer risk from a lifetim e exposure to an agent. This estimate, [is] usually expressed in units of proportion (of a population) affected per mg/kg
- day ...” EPA disseminates dose
response assessment information in several forms, based on the level of review . The Integrated Risk Information System (IRIS) [ 11 ] is an EPA database that contains scientific health assessment information, including dose
- response information. All IRIS assessments since 1996 have also undergone independent external peer review. The current IRIS process includes review by EPA scientists, interagency reviewers from other federal agencies, and the public, and peer review by independent scientists external to EPA. New IR IS values are developed and old IRIS values are updated as new heal th effects data become available. Refer to the “IRIS Track” website for detailed information on status and scheduling of current individual IRIS assessments and updates ( http://cfpub.epa.gov/ncea/iristrac/index.cfm)
. EPA’s science policy approach , under the current carcinogen guidelines, is to use linear low
- dose extrapolation as a default option for carcinogens for which the mode of action (MOA) has not been identified. We expect future EPA dose
- response assessments to identify nonlinear MOAs where appropriate, and we will use those analy ses (once they are peer reviewed) in our risk assessments. At this time, however, there are no available carcinogen dose
- response assessments for inhalation exp osure that are based on a nonlinear MOA . 2) US Agency for Toxic Substances and Disease Registr y ( ATSDR). ATSDR, which is part of the US Department of Health and Human Services, develops and publishes Minimum Risk Levels (MRLs) [ 12 ] for inhalation and oral exposure to man y toxic substances. As stated on the ATSDR web site: “ Following discussions with scientists within the Department of Health and Human Services (HHS) and the EPA, ATSDR chose to adopt a practice similar to that of the EP A's Reference Dose (R fD) and Reference Concentration (RfC) for deriving substance specific health guidance levels for non neoplastic endpoints .” The MRL is defined as “an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adver se effects (other than cancer) over a specified duration of exposure.” ATSDR describes MRLs as substance
- specific estimates to be used by health assessors to select environmental contaminants for further evaluation. Exposures above an MRL do not necessarily represent a threat, and MRLs are therefore not intended for use as predictors of adverse health effects or for setting cleanup levels. 3) California Environmental Protection Agency (CalEPA). The CalEPA Office of Environmental Health Hazard Assessment ha s developed dose
- response assessments for many substances, based both on carcinogenicity and health effects other than cancer. The**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  13 process for developing these assessments is similar to that used by EPA to develop IRIS values and incorporates significant external scientific peer review. As cited in the CalEPA Technical Support Document for developing their chronic assessments 7 : “The guidelines for developing chronic inhalation exposure levels incorporate many recommendations of the U.S. EPA [ 13 ] and NAS [ 14 ]. ” The non
- cancer information includes available inhalation health risk guidance values expressed as chronic inhalation reference exposure levels (RELs) [ 15 ]. CalEPA defines the REL as “the concentration level at or below which no health effects are anti cipated in the general human population.” CalEPA's quantitative dose
- response information on carcinogenicity by inhalation exposure is expressed in terms of the URE [ 16], defined similarly to EPA's URE. In developing chronic risk estimates, we adjusted dose
- response values for some HAPs based on professional judgment, as follows: 1) In the case of HAP categories such as glycol ethers and cyanide compounds, the most conservative dose
- response value of the chemical categor y i s used as a surrogate for other compounds in the group f or which dose
- response values are not available. This i s done in order to examine, under conservative assumptions, whether these HAPs that lack dose
response values ma y p ose an unacceptable risk and require further examination, or screen out from further assessment. 2) Where possible for emissions of unspecified mixtures of HAP categories such as POM (see Tables 2.6
- 1 (a) to 2.6
- 1 (c) , we apply category - specific chemical speciation profiles appropriate to the source categor y t o deve lop a composite dose
- response value for the category . 3) Emissions from Primary Aluminum Pro duction facilities include POM. A substantial proportion of POM reported to EPA’s national emission inventory (NEI) are not s pe ciated int o individual compounds. As a result, it is necessary to apply the same s implifying a ssumptions to assessments that were used for the 1999 NATA study [ 17]. The NATA approach partitions POM into eight different non - overlapping “groups” that are modeled as separate pollutants. Each P OM group comprises POM species of similar carcinogenic potenc y, for which we can apply the same URE. 4) A chronic screening level of 163 ug/m 3 was developed for carbonyl sulfide (COS) from a No Observed Adverse Effects Level (NOAEL) of 200 ppm based on brai n lesions and neuroph ys iological alterations in rodents. A more detailed discussion of the studies used to develop the COS chronic screening level is provided in Appendix 7 . 8. The screening level includes a total uncertainty factor (UF) of 3,000: 10x for extrapolation for interspecies differences, 10x for consideration of intraspecies variability , 10x for extrapolation from subchronic to chronic duration, and 3x for database insufficiencies.

7 Air T oxics Hot Spots Program, Risk Assessment Guidelines, Part III
- Te chnical Support Document for the Determination o f Non
- cancer Chronic Reference Exposure Levels. Air Toxicology and Epidemiology Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. February 2000 ( http://www.oehha.ca.gov/air/chronic_rels/pdf/relsP32k.pd f )**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  14 See section 5 of this document for a detailed discussion of exp osure modeling uncertainties. The chronic screening level for COS is used only as a screening level assessment to identify areas with significant inhalation risk potential. A high COS chronic risk based on the screening level does not necessarily indic ate that further action is required. The emissions inventory for the Primary Aluminum Pro duction source categor y i ncludes emissions of HAP with availab le chr onic quantitative inhalation dose
- response values. These HAP, their dose
- response values, and t he source of the values are listed in Tables 2.6
- 1 (a) through (c). **Table 2.6 -**  **1 (a) Dose -**  **Response Values for Chronic Inhalation Exposure to Carcinogens**  URE (unit risk estimate for cancer) 8 = cancer risk per •g/m 3 of average lifetime exposure. Sources: IRIS = EPA Integrated Risk Information System, CAL = California EPA Office of Env iro nmental Health Hazard Assessm e nt, EPA/OAQPS = interim value recommended by the EPA Office of Air Quality Planning and Standards. EPA ORD = EPA Office of Research a nd Development **Pollutant CAS Number**  **9 URE**  **5 (1/•g/m**  **3 )**  **Source** Naphthalene 91203 0.000034 CAL Polycyclic Organic Matter 10 (POM) (as Benzo [a] pyrene toxic equivalent) 50328 0.0016 CAL
**Table 2.6**  **- 1 (b)**  **Dose -**  **Response Values for Chronic Oral Exposure to Carcinogens**  SF (oral slope factor for cancer) = cancer risk per mg/kg/d of average lifetime exposure. So urces : IRIS = EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Health Hazard Assessment, EPA/OAQPS = interim value recommended by the EPA Office of Air Quality Planning and Standards. **Pollutant CAS Number**  10 **SF (1/mg/kg/d)**  **Source** P OM (as Benzo [a] py

rene toxic equivalent) 50328 10 CAL

8 The URE is the upper
- bound excess cancer risk estimated to result from continuous lifetime exposure to an agent at a concentration of 1 •g/m 3 in air. URE’s are considered upper bound estimates meaning they represent a plausible upper limit to the tru e value. 9 Chemical Abstract Services identification number. For groups of compounds that lack a CAS number we have used a surrogate 3
- digit identifier corresponding to the group’s position on the CAA list of HAPs. 10 Assigned the URE associated with a mi xture of POM compounds having a similar potency. Details of this method, also used in the 1999 National Air Toxics Assessment, are available at http://www.epa.gov/ttn/atw/nata1999 /99pdfs/pomapproachjan.pdf**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  15
**Table 2.6**  **- 1 (c) Dose**  **- Response Values for Chronic Inhalation Exposure**  **to Noncarcinogens** RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an order of ma gnitude) 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. Sources: IRIS = EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Human Health Assessm ent, ATSDR = US Agency for Toxic Substances Disease Registry. **Pollutant CAS Number**  **6 RfC**  **(mg/m3) Source**  **11** Carbonyl sulfide 463581 0.163 ORD Screening Value Hydrofluoric acid 766439 3 0.014 CAL Naphthalene 91203 0.003 IRIS
- M **2.6.2 Sources of acute dose**  **- response information**  Hazard identification and dose
- response assessment information for preliminary acute inhalation exposure assessments is based on the existing recommendations of OAQPS for HAP s [ 18 ] . Depending on availability , the results from screening acute assessments are compared to both “no effects” reference levels for the general public, such as the California Reference Exposure Levels (RELs), as well as emergency response levels, such as Acute Exposure Guideline Lev els (AEGLs) and Emergency Response Planning Guidelines (ERPGs), with the recognition that the ultimate interpretation o f any potential risks associated with an estimated exceedance of a particular reference level depends on the definition of that level and any limitations expressed therein. Comparisons among different available inhalation health effect reference values (b oth acute and chronic) for selected HAPs can be found in an EPA document . 12 **California Acute Reference Exposure Levels (RELs ).**  The California Environmental Protection Agency (CalEPA) has developed acute dose
- response reference values for many substances, expressing the results as Acute inhalation Reference Exposure Levels (RELs). The acute REL ( http://www.oehha.ca.gov/air/pdf/acuterel.pdf ) is defined by CalEPA as “ the concentration level at or below which no adverse health effects are anticipated for a specified exposure duration . [ 19 ] . RE Ls are based on the most sensitive, relevant, adverse health effect reported in the medical and toxicological literature. REL s are designed to protect the mos t sensitive individuals in the population by the inclusion of margins of safety . Since margins of safety are incorporated to address data gaps and uncertainties, exceeding the REL does not automatically indicate an adverse health impact. ” Acute RELs are developed for 1
- hour (and 8
- hour) exposures. The values incorporate uncertainty factors similar to those used in deriving EPA’s Inhalation

11 The descriptors L (low), M (medium), and H (high) have been added for IRIS RfC values to indicate the overall level of confidence in the RfC value, as reported in the IRIS file. 12 See : U.S. EPA. Graphical Arrays of Chemical
- Specific Health Effect Reference Values for Inhalation Exposures [Final Report]. (U.S. Environmental Protection Agency, Washington, D.C., EPA/600/R
- 09/061, 2009. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003.)**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  16 Reference Concentrations (RfCs) for chronic exposures (and, in fact, California also has developed chronic RELs). **Ac ute Exposure Guideline Levels (AEGLs**  ). AEGL s are developed by the National Advisor y Committee (NAC) on Acute Exposure Guideline Lev els (NAC/AEGL) f or Hazardous Substances , and then reviewed and published by the National Research Council . A s described in the Committee’s “Standing Operating Procedures (SOP) ” ( http://www.epa.gov/opptintr/aegl/pubs/sop.pdf ), AEGLs “represent threshold exposure limits for the general public and are applicable to emergency exposures ranging from 10 min to 8 h.” Their intended application is “for conducting risk assessments to aid in the development of emergency preparedness and prevention plans, as well as real time emergency response act ions, for accidental chemi cal releases at fixed facilities and from transport carriers.” The document states : “the primary purpose of the AEGL program and the NAC/AEGL Committee is to develop guideline levels for once - in
- a - lifetime , short
- term exposures to airborne concentrations of acutely toxic, high
- priority chemicals.” In detailing the intended application of AEGL values, the document states that , “ It is anticipated that the AEGL values will be used for regulatory and nonregulatory purposes b y U.S. Federal and State agencies, and possibl y the international community in conjunction with chemical emergency response, planning, and prevention programs. More specifically, the AEGL values will be used for conducting various risk assessments to aid in the development of emergency preparedness and prevention plans, as well as real
- time emergency response actions, for accidental chemical releases at fixed facilities and from transport carriers.” The NAC/AEGL defines AEGL
- 1 and AEGL
- 2 as:

“ AEGL
- 1 is the airborne concentration (expresse d as ppm or mg/m 3 ) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic nonsensor y e ffects. However, the effects are not disabli ng and are transient and reversible upon cessation of exposure. ”

“ AEGL
- 2 is the airborne concentration (expressed as ppm or mg/m 3 ) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long
- lasting adverse health effects or an impaired ability to escape. ”

“ Airborne concentrations below AEGL
- 1 represent exposure levels that can produce mild and progressively increasing but transient and nondisabling odor, taste, and sensory irritation or certain asymptomatic, nonsensory effects. With increasing airborne concentrations above each AEGL, there is a progressive increase in the likelihood of occurrence and the severity of effects described for each correspondin g AEGL. Although the AEGL values represent threshold levels for the general public, including susceptible subpopulations, such as infants, children, the elderly , persons with asthma, and those with other illnesses, it is recognized that individuals, subje ct to unique or idiosyncratic responses, could experience the effects described at concentration s below the corresponding AEGL.”**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  17 **Em ergency Response Planning Guidelines (ERPGs).**  The American Industrial Hygiene Association (AIHA) has developed Emergency Re sponse Planning Guidelines (ERPGs) [ 20 ] for acute exposures at three different levels of severity . These guidelines represent concentrations for exposure of the general population (but not particularly sensitive persons) for up to 1 hour associated with ef fects expected to be mild or transient (ERPG
- 1), irreversible or serious (ERPG
- 2), and potentially life
- threatening (ERPG
- 3). ERPG values ( http://www.aiha.org/1documents/Committees/ERP
- erpglevels.pdf ) are described in their supporting documentation as follows: “ Emergency Response Planning Guidelines (ERPGs) were developed for emergency planning and are intended as health based guideline conce ntrations for single exposures to chemicals. These guidelines (i.e., the ERPG Documents and ERPG values) are intended for use as planning tools for assessing the adequacy of accident prevention and emergency response plans, including transportation emerge ncy planning and for developing comm unity emergency response plans. The emphasis is on ERPGs as planning values: When an actual chemical emergency occurs there is seldom time to measure airborne concentrations and then to take action. ” ERPG
- 1 and ERPG
- 2 values are defined by AIHA as follows:

“ ERPG
- 1 is the maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing other than mild transient adverse health effects or without perceiving a clearly defined, objectionable odor. ”

“ ERPG
- 2 is the maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing or developing irreversible or other serious he alth effects or symptoms which could impair an individual's ability to take protective action. ” The emissions inventory for the Primary Aluminum Pro duction source categor y i ncludes emissions of two HAP with relevant and available quantitative acute dose
- response threshold values. These HAPs, their acute threshold values, and the source of the value are listed below in Table 2.6
- 2.

**Table 2.6 -**  **2 Dose -**  **Response Values for Acute Exposure**
**Pollutant CAS**  **Number AEGL**  **- 1**  **(1 -**  **hr )**  **(mg/m 3**  **) AEGL**  **- 2** 

**(1 -**  **hr )**  **(mg/m 3**  **) ERPG**  **- 1** 

**(mg/m 3**  **) ERPG**  **- 2** 

**(mg/m 3**  **) REL**  Carbonyl sulfide 463581 140 Hydrofluoric acid 766439 3 0.82 20 1.6 20 0.24 

### 2.7 **Risk c**  **haracterization 2.7.1**  **Ge neral**  The final product of the risk assessment is the risk characterization, in which the information**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  18 from the previous steps is integrated and an overall conclusion about risk is synthesized that is complete, informative, and useful for decision makers. In gen eral, the nature of this risk characterization depends on the information available, the application of the risk information and the resources available. In all cases, major issues associated with determining the nature and extent of the risk are identifi ed and discussed. Further, the EPA Administrator’s March 1995 Policy for Risk Characterization [ 21 ] specifies that a risk characterization “be prepared in a manner that is clear, transparent, reasonable, and consistent with other risk characterizations of similar scope prepared across programs in the Agency .” These principles of transparency and consistency have been reinforced by the Agency’s Risk Characterization Handbook [ 22 ], in 2002 by the Agency ’s information quality guidelines [ 23 ], and in the OMB/OST P September 2007 Memorandum on Updated Principles for Risk Analysis 13 , and are incorporated in these assessments. Estimates of health risk are presented in the context of uncertainties and limitations in the data and methodology . Through our tiered, iterative analytical approach, we have attempted to reduce both uncertainty an d bias to the greatest degree possible in these assessments, within the limitations of available time and resources. We provide summaries of risk metrics (including maximum indi vidual cancer risks and noncancer hazards, as well as cancer incidence estimates) along with a discussion of the major uncertainties associated with their derivation to provide decision makers with the fullest picture of the assessment and its limitations. For each carcinogenic HAP included in an assessment that has a potency estimate available, individu al and population cancer risks we re calculated by multipl yi ng the corresponding lifetime average exposure estimate by the appropriate URE. This calculated cancer risk is defined as the upper
- bound probability of developing cancer over a 70
- y r period (i.e., the assumed human lifespan) at that exposure. Because UREs for most HAPs are upper
- bound estimates, actual risks at a given exposure level may be lower than predicted, and could be zero. For EPA’s list of carcinogenic HAPs that act by a mutagenic mode
- of
- action [ 24 ], we applied EPA’s Supplemental Guidance for Assessing Susceptibility from Early
- Life Exposure to Carcinogens [ 25 ] . This guidance has the effe ct of adjusting the URE by factors of 10 (for children aged 0
- 1), 3 (for children aged 2
- 15), or 1.6 (for 70 years of exposure beginning at birth), as needed in risk assessments . In this case, this has the effect of increasing the estimated life time risk s for these pollutants by a factor of 1.6. In addition, although onl y a small fraction of the total POM emissions may be reported as individual compounds, EPA expresses carcinogenic potenc y f or compounds in this group in terms of benzo[a]py rene equivalence, based on evidence that carcinogenic POM have the same mutagenic mechanism of action as does benzo[a]pyrene. For this reason , EPA implementation policy [ 26] recommends applyi ng the Supplemental Guidance to all carcinogenic PAHs for which risk e stimates are based on relative potency . Accordingl y, we applied the Supplemental Guidance

13 Memorandum f

or the Heads o f Exe cutive Departments and Agencies
- Updated Principles for Risk Analysis ( September 19, 2007 ), From Susan E. Dudley, Administrator, Office of Information and Regulatory Affairs, Office of Management and Budget; and Sharon L. Hays, Associate Director and De puty Director for Science, Office of Science and Technology Policy ( http://www.whitehouse.gov/omb/memoranda/fy2007/m07
- 24.pdf )**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  19 to all unspeciated POM mixtures. Increased cancer incidence for the entire receptor population within the area of analysis wa s estimated by multiplying the estimate d lifetime cancer risk for each census block by the number of people residing in that block, then summing the results for the entire modeled domain. This lifetime population incidence estimate wa s divided by 70 years to obtain an estimate of the number of cancer cases per y ear. Unlike linear dose
- response assessments for cancer, noncancer health hazards generally are not expressed as a probability of an adverse occurrence. Instead, “risk” for noncancer effects is expressed by comparing an exposure to a reference level as a ratio. The “hazard quotient” (HQ) is the estimated exposure divided by a reference level (e.g., the RfC). For a given HAP, exposures at or below the reference level (HQ •1) are not likely to cause adverse health effects. As exposures increase above the reference level (HQs increasingly greater than 1), the potential for adverse effects increases. For exposures predicted to be above the RfC, the risk characterization includes the degree of confidence ascribed to the RfC values for the compound(s) of concern (i.e., high, medium, or low confidence) and discusses the impact of this on possible health interpretations. The risk characterization for chronic effects other than cancer is expressed in terms of the HQ for inhalation, calculated for each HAP at each census block centroid. As discussed above, RfCs incorporate generally conservative uncertainty factors in the face of uncertain extrapolations, such that an HQ greater than one does not necessarily suggest the onset of adverse effect s. The HQ cannot be translated to a probability that adverse effects will occur, and is unlikely to be proportional to adverse health effect outcomes in a population . Screening for potentially significant acute inhalation exposures also followed the HQ approach. We divided the maximum estimated acute exposure by each available short
- term threshold value to develop an array of HQ values relative to the various acute endpoints and thresholds. In general, when none of these HQ values are greater than one, there is no potential for acute risk. In those cases where HQ values above one are seen, additional information is used to determine whether there is a potential for significant acute risks. **2.7.2 Mixtures**  Since most or all receptors in these assessments recei ve exposures to multiple pollutants rather than a single pollutant, we estimated the aggregate health risks associated with all the exposures from a particular source categor y c ombined. To combine risks across multiple carcinogens, our assessments use the mixtures guidelines’ [ 27, 28 ] default assumption of additivity of effects, and combine risks by summing them using the independence formula in the mixtures guidelines. In assessing noncancer hazard from chronic exposures, in cases where different pollutants cause adverse health effects via completely different modes of action, it may be inappropriate to aggregate HQs. In consideration of these mode
- of
- action differences, the mixtures**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  20 guidelines support aggregating effects of different substances in specific and limited way s. Consistent with these guidelines, we aggregated non
- cancer HQs of HAP s that act by similar toxic modes of action, or (where this information is absent) that affect the same target organ. This process creates, for each target organ, a target - organ - specific hazard index (TOSHI), defined as the sum of hazard quotients for individual HAPs that affect the same organ or organ sy stem. A ll TOSHI calculations presented here were based exclusively on effects occurring at the “ critical dose” (i.e ., the lowest dose that produces adverse health effects). Although HQs associated with some pollutants have been aggregated into more than one TOSHI, this has been done only in cases where the critical dose affects more than one target organ . Because imp acts on organs or sy stems that occur above the critical dose have not been included in the TOSHI calculations, some TOSHIs may have been underestimated. As with the HQ, the TOSHI should not be interpreted as a probability of adverse effects, or as strict delineation of “safe” and “unsafe” levels. Rather, the TOSHI is another measure of the potential for adverse health outcomes associated with pollutant exposure, and needs to be interpreted carefully by health scientists and risk managers. Because of the conservative nature of the acute inhalation screening and the variable nature of emissions and potential exposures, acute impacts were screened on an individual pollutant basis, not using the TOSHI approach. **2.7.3 Facility**  **- wi**  **de r**  **isks** To help place the source categor y r isks in context, we ty picall y e xamine “facility
- wide” risks using facility
- wide and source categor y d ata files developed by EPA thr ough emission data updates from industry and refined EPA profiles for the source categor y. For this source categor y we did not receive facility
- wide emissions, and therefore, a facility
- wide assessment was not performed. However, most all primar y a luminum production facilities are co
- located with secondary aluminum production facilities and a facility
- wide analy sis wil l be part of the risk assessment that is currently being done for the secondary aluminum source category 14

. 

### 3 **Risk r**  **esults for the primary a**  **luminum production**  **s ource**  **c ategory**  **3.1 Source**  **c ategory**  **d escription and**  **r esults**  The Primary Aluminum Production source categor y c onsists of facilities that produce aluminum from refined ore (alumina) using a reduction process whereby the alumina is dissolved in an electrolytic bath in reduction cells which are connected electrically in series to form “potlines” in the pres ence of fluoride. The main raw materials in this process are alumina (Al 2 O 3 ), coke, pitch, and fluoride. The process of aluminum reduction includes passing a high electrical direct current from a carbon anode to a carbon cathode which results in purified molten aluminum sinking to the bottom of the reduction cell, beneath the electrolytic bath.

14 The results of this analysis will be available in the docket for the secondary aluminum source category.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  21 There are currently 1 4 secondary aluminum smelters operating in the U.S. The NP RM data set for the Primar y A luminum Pro duction category contains 1 4 facilities identified with a Primary Aluminum Reduction MACT code in the 2005 National
- Scale Air Toxics Assessment (NATA) National Emissions Inventory (NEI), September 2010 version. All 1 4 of these facilities are identified as major sources in the NEI. The emissions in the Primary Aluminum Pro duction source categor y NPRM data set (of 1 5 facilities) are summarized in Table 3.1
- 1. The total HAP emissions for the source categor y are approximately 6,000 tons per year. Air emissions from Primar y A luminum Production facilities include 4 MACT regulated toxic air pollutan ts : p olyc yc lic organic matter (POM) , carbon yl sulfide , hy drofluoric acid, and naphthalene. **Table 3.1**  **- 1**  **Summary of Em issions from the**  **Primary Aluminum Production Source Category and**  **Availability of Dose -**  **Response Values**

**HAP a**  **Em ission** 

**Estimates (tpy)**  **Number of**

**Facilities where HAP**  **Repor ted or**  **Estimated (**  **1 4**  **fac ilities**  **in NP**  **RM data set)**  **Prioritized Inhalation Dose -**  **Response Value Identified by OAQPS**  **b PB**  **** **HAP? Unit Risk**  **Estimate for Cancer?**  **Ref**

**erence Concentration**  **for Chronic**  **Noncancer? Health** 

**Benchmark Values for Acute**  **Noncancer?** Carbonyl sulfide 4,564 13 Υ c Υ Hydrofluoric acid 1 , 351 13 Υ Υ P OM 91 14 Υ Υ Naphthalene 0.72 14 Υ Υ

a Notes f or how HAP were speciated for risk assessm ent: • There were 15 total facilities, but actual emission estimates were not provided for the Columbia Falls facility. • For emissions of a ny c he micals or chemical groups classified as polycyclic organic m atter (POM), emissions were grouped into POM su

bgroups as found on EPA’s Technology Transfer Network website for the 2002 National
- Sc ale Air Toxics Assess me nt at http://www.epa.gov/nata2002/m ethods.html#pom . (

Approach to Modeling P OM ). For thi s source category, all POMs are PAHs. b Specific dose
- response values for each che mic al are identified on EPA’s Technology Transfer Network website for air toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html . C The chronic, noncancer health effects benchmark value for carbonyl sulfide is an ORD screening value. 

### 3.2 **Baseline r**  **isk c**  **haracterization** This section presents the results of the risk assessment for the Primary Aluminum Pro duction source categor y based on the modeling methods described in the previous sections . All baseline risk results are developed using the best estimates of actual and MACT
- allowable HAP emissions. The basic chronic inhalation risk e stimates presented here are the maximum individual lifetime cancer risk, the maximum target organ specific chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening assessments in the form of maximu m hazard quotients, as well as the results of our screen for potential non
- inhalation risks from PB HAP. Also presented are the HAP “drivers,” which are the HAP that collectively co ntribute 90 percent of the maximum cancer risk or maximum**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  22 hazard at the hi ghest exposure location . A detailed summary of the facility
- specific risk assessment results is available in Appendix 5 . Table s 3 .2
- 1 and 3. 2
- 2 summarize the preliminary chronic and acute inhalation risk results for this source categor y . The results of the chronic inhalation cancer risk assessment indicate that the maximum lifetime individual cancer risk , consi dering actual emissions , could be up to as high as 30 in a million , driven by POM emissions primarily from pot line roof vents and anode bake furnaces . The maximum cancer risks for this source categor y e xceeded a cancer risk of 1 in a million at 12 of 14 f acilities. The total estimated cancer incidence from this source categor y b ased on actual emission levels is 0. 005 excess cancer cases per year, or one excess case in every 200 ye ars. Approximately 900 people were estimated to have cancer risks above 10 in a million and approximately 41,000 people were estimated to have cancer risks above 1 in a million considering a ll facilities in this source categor y . Based on engineering judgment, MACT
- allowable emissions for this source categor y c ould be up to as high as 1.5 times actual emissions; thus c onsidering MACT allowable emissions, the MIR could be up to as high as 50
- in a million for the facilities presented in Table 3.2
- 1. In addition to the facilities presented in Table 3.2
- 1, we also estimated cancer risks for the Columbia Falls facility which has not been fully operational since 1999 and has been completely closed for 2 4 ye ars, and thus, did not report actual emissions for the year 2010. For this facility , we calculated an estimate of allowable emissions to approximate the cancer risk should this facility resume its primary aluminum production operations. 15 The results of this assessment indicated that should this plant resume its operations, cancer risk could be as high as 100
- in a million , resulting predominantly from pot line roof vent emissions of POM. With respect to chronic inhalation non cancer risk, we estimate a maximum TOSHI value of 0. 4 for the Primary A luminum source categor y, with pot line vent emissions of HF dominating those impacts. C onsidering MACT
- allowable emissions, this maximum TOSHI value is estimated to be 0.6 . With respec t to Columb ia Falls , should this facility resume its primary aluminum production operations , we estimate a maximum TOSHI value of 0.2 primarily from emissions of HF from pot line roof vents .

15 S ee the emissions chapter of the TSD document for a discussion of how emis sions were calculated for the Columbia Falls facility (available in the docket for th e proposed rulemaking ).**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  23
**Table 3.2 -**  **1 Summary of Source Category Level Inhalation Risks f**  **or Prim** **ary Aluminum**  **Production Result**  **HAP “Drivers” Facilities in Source Category**  Number of Facilities Estimated to be i n Source Category 15 n/a Number of Facilities Identified in NEI and Modeled in Preliminary Risk Assessment 14 16 n/a **Cancer Risks** Maximum Individual Lifetime Cancer Risk (in 1 million) 30 POM Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a Greater than or equal to 10 in 1 million 2 POM Greater than or equal to 1 in 1 million 12 POM **Ch ron** **ic Noncancer Risks** Maximum Developmental Hazard Index 0.4 hydrofluoric acid Num ber of Facilities with Maximum Developmental Hazard Index: Greater than 1 0 n/a **Refined Acute Noncancer Results**  Maximum Acute Hazard Quotient 10 4 2 hydrofluoric acid (REL)

hydrofluoric acid (AEGL
- 1) hydrofluoric acid (ERPG
- 1) Number of Facilities With Potential for Acute Effects 8 hydrofluoric acid **Population Exposure** Number of People Living Within 50 Kilometers of Facilities Modeled 3,300,000 n/a Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a Greater than or equal to 10 in 1 million 900 n/a Greater than or equal to 1 in 1 million 41,200 n/a Number of People Exposed to Noncancer Developmental Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.005 n/a Contribution of HAP to Cancer Incidence

PO M 9 9 % 90 % n/a

16 The Columbia Falls facility has not been fully oper ational since 1999 and has been completely closed for 2 operated in approximately 4 years and therefore, EPA did not generate risk estimates based on actual emissions for this facility. However, as seen below, EPA did estimate risk based on MACT allowable emissions for this facility.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  24
**Table 3.2 -**  **2 Summary of Refined Acute Results for Secondary Aluminum Production**  **Facilities**

**Refined Results MAXIMUM ACUTE HAZARD**  **QUOTIENTS ACUTE DOSE**  **- RESPONSE**  **VALUES** Based on REL Based on

AEGL
- 1 Based on

ERPG
- 1 REL

(mg/m 3 ) AEGL
- 1

(1
- hr) (mg/m 3 ) ERPG
- 1

(mg/m 3 ) HAP Ma x. 1
- hr. Air

Conc. (mg/m 3 ) hydrofluoric acid 3.0 10 4 2 0.24 0.82 1.6 Notes on Refined Process: 1) The screening was performed for all e mitted HAP with available acute dose
- re sponse values. Only those pollutants whose screening HQs were greater than 1 for at least on e acute threshold value are shown in the table. 2) HAP with available acute dose
- response values which are not in the table do not carry any potential for posing acute heal th risks, based on an analysis of currently available e miss ions data. Notes on Acute Dose
- Response Values:

REL

– California EPA reference exposure level for no adverse effects. Most, but not all, RELs are for 1
- hour exposures. AEGL

– Ac ute exposure guideline lev el s represent em ergenc y e xposu

re (1
- hour) limits for the general public. AEGL
- 1 i s the exposure lev el above which it is predicted that th e general population, includ in g s usceptible individuals, could experience effects that are notable di scomfort, but which are transient and reversible upon cessation of exposure. AEGL
- 2 i s the exposure level above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long
- lasting adverse health effects of an im paired ability to escape. EPRG

– Em

ergency Re mo va l Pr og

ram guidelines represent em ergency exposure (1
- hour) limits for the general public. ERPG
- 1 is the maximum le ve l below which it is believed that nearly all ind iv iduals could be exposed for up to 1 hour without experiencing other than mild, transient adver se health effects. ERPG
- 2 is the maximum exposure below which it i s believ ed that nearly all individuals could be exposed for up to 1 hour without experiencing or developing irreversible or other serious health effects or sym ptoms which could impair an individual’s ability to take protective action . For this source categor y, there were two pollutants that had relevant acute health effect screening values: carbonyl sulfide and hydrofluoric acid. With respect to carbonyl sulfide , we did not find any pote ntial for acute health concern s f or the 14 operational facilities based on their actual emissions . Howe ver, hydrofluoric acid emissions did not screen out. Our screening analy sis showed that worst - case screening
- level acute HQ values for hydrofluoric aci d could exceed a value of 1 (based on the REL, AEGL
- 1, or ERPG
- 1) at 9 of the 14 facilities . We refin ed our acute screening val ues somewhat by t aking into account whether acute screening value location s identified in the initial screen were within a facility’s boundar y (they must be off
- site to represent a potential exposure to the general public , see Appendix 5 and Appendix 6 ) . Considering th is refinement , the highest HQ for hydrofluoric acid based on a REL is 10, based on an AEGL
- 1 is 4, and based on an ERPG
- 1 is 2 (see Table 3.2
- 2). Moreover, after refinement , 8 of the 14 operational facilities show the potential for worst - case acute HQ values greater than 1 based on the REL, 4 of 14 facilities show the potential for worst- case acute HQ values gre ater than 1 based on the AE GL
- 1 and 4 5 of 14 facilities show the potential for worst - case acute HQ values greater than or equal to 1 based**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  25
on the ERPG
- 1. 17 AEGL
- 1 and 4 of 14 facilities show s the potential for worst - case acute HQ values greater than or equal to 1 based on the ERPG
- 1 18

. Notably in humans, concentrations above the AEGL
- 1 or at or above the AEGL
- 1 and/or ERPG
- 1 for hydrofluoric acid are associated with reversible minor irritation of the skin and ey es, as well an increase in pulmonary inflammatio n. That being said, we note again that this is still a conservative, worst - case screen with built
- in assumptions that bias the results high. As a result , there is considerable uncertainty as to whether concentrations of hydr ofluoric acid above at the AEGL
- 1 or at or above the ERPG
- 1 benchmark value could actually occur near some of these facilities . Thus, these results only indicate that there may be some potential for acute health effects from emissions of hydrofluoric acid from facilities in this source categor y ; they do not indicate that effects are actually occurring . In addition to the analy ses presented above, to screen for potential multipathwa y e ffects from emissions of PAHs, we compared actual PAH emission rates from 14 facilities in thi s source categor y t o the screening value for PAHs described in section 2.5 (also see Appendix 4 3 for a more detailed discussion of screening emission rates). Results of this worst
- case screen estimate that actual PAH emissions from all facilities exceed the PAH screening emission rate by as much as approximately 7,000 times . With respect to the se exceedence s of the worst
case multipat

hway screening level for PAHs , we note that this only indicates the potential for multipathway
- related cancer risks of concern f rom PAHs . That is, while in general, emission rates below the worst
- case multipathway screening level indicate no significant potential for multipathway related health effects, emission levels above this worst
- case screening level only indicate the potential for multipathway
- related health risks of concern based on a worst
case scenario. Due to data limitations, we were not able to refine our multi
- pathway analy sis bey ond the worst
- case screening assessment. Thus, we note that these results are biased high for purposes of screening and are therefore subject to significant uncertainties. As a result, we cannot say whether multi
- pathway risks ma y b e a concern . concern; we can only say that we cannot rule them out. With respe ct to the potential for significant and widespread environmental effects from non PB
- HAP, and in particular hydrofluoric acid which can potentially have adverse effects on vegetation, we note that all chronic non
- cancer HQ values for all pollutants considering actual emissions are well below 1 using human health reference values. Thus, we believe that it is unlikely that adverse environmental effects would occur at the actual HAP concentrations estimated in our human health risk assessment. 

### 3.3 **Post -**  **c ontrol**  **r isk**  **c haracterization**  The proposed changes to the current NESHAP (see discussion in the proposed rule) will have negligible effect on all the estimated risks associated with all the currently operating facilities

17 Indivi dual facility acute HQ values for all facilities can be found in Appendix 5, Table 4, of this document . Acute HQ values exceeding a value of 1 based on the REL were as follows: 10, 10, 9, 9, 5, 3, 2 and 2. Acute HQ values greater than a value of 1 based on the AEGL
- 1 were as follows: 4, 4, 3 and 3. Acute HQ values greater than or equal to a value of 1 based on the ERPG
- 1 were as follows: 2, 2, 1 and 1. 18**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  26 in the Primary Aluminum categor y. For the one f acility which is currently not operational ( the Columbia Falls facility) , however, the c ancer MIR under MACT
- allowable emissions would be reduced from 10 0 in a million to approximately 7 0 in a million , effectively capping the potential cancer risks from th is facility should it resume operations 19

. 

### 4 **General d**  **iscussion of u**  **ncertainties and h**  **ow t**  **hey h**  **ave b**  **een a**  **ddressed 4.1**  **E xposure**  **m odeling**  **u ncertainties**  Although every effort has been made to identify all the relevant facilities and emission points, as well as to develop accurate estimates of the annual emission rates for all relevant HAP, the uncertainties in our emission inventor y l ikely dominate the uncertainties in our exposure modeling estimates. The chronic exposure modeling uncertainties are considered rel atively small in comparison, since we are using EPA’s refined local dispersion model with site
specific parameters and reasonably representative meteorology. If any thing, the population exposure estimates are biased high by not accounting for short
- or lo ng - term population mobility , and by neglecting processes like deposition, plume depletion, and atmospheric degradation. Additionally, estimates of the maximum individual risk (MIR) contain uncertainty , because they are deriv ed at census block centroid locations rather than actual residences. This uncertainty is known to create potential underestimates and overestimates of the actual MIR values for individual facilities, but, overall, it is not thought to have a significant i mpact on the estimated MIR for a source categor y. Finally , we did not factor in the possibility of a source closure occurring during the 70
- ye ar chronic exposure period, leading to a potential upward bias in both the MIR and population risk estimates; nor did we factor in the possibility of population growth during the 70
- ye ar chronic exposure period, leading to a potential downward bias in both the MIR and population risk estimates. A sensitivity analy sis performed for the 1999 NATA found that the selection of the meteorology dataset location could result in a range of chronic ambient concentrations which varied from as much as 17% below the predicted value to as much as 84% higher than the predicted value. This variability translates directly to the pre dicted exposures and risks in our assessment, indicating that the actual risks could vary from 17% lower to 84% higher than the predicted values. We have purposely biased the acute screening results high, considering that they depend upon the joint occurrence of independent factors, such as hourly emissions rates, meteorology and human activity patterns. Howe ver, we note that there is an unquantified level of uncertainty regarding the emission estimates and the nature of the worst
- case conditions for esti mating the worst - case impacts of acute emissions of fugitive dusts. The current set of assumptions used in deriving the estimate assumes the average hourly emission level (annual emissions divided by 8760 hours per year) to occur at the default worst
- case meteorological conditions (low
19 EPA is also proposing to lower the POM limit for existing pitch storage tanks, but we do not anticipa te that this will have an appreciable effect on the risk estimates presented above since pitch storage tanks are not a significant driver of risk.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  27 winds with a stable atmosphere). The actual risks ma y b e higher or lower than the estimates based upon the current set of assumptions. In cases where multiple acute threshold values are considered scientifically acceptable w e have chosen the most conservative of these threshold values , erring on the side of overestimating potential health risks from acute exposures. In the cases where these results indicated the potential for exceeding short
- term health thresholds post - contr ols , we refined our assessment by developing a better understanding of the geograph y o f the facility relative to potential exposure locations. 

### 4.2 **Uncertainties in the**  **d ose**  **- r**  **esponse r**  **elationships** In the sections that follow, separate discussions are provided on uncertainty associated with cancer potency factors and for noncancer reference values. Cancer potency values are derived for chronic (lifetime) exposures. Noncancer reference values are generally derived for chronic exposures (up to a lifetime), bu t ma y a lso be derived for acute ( •<24 hours), short
- term (>24 hours up to 30 day s), and subchronic (>30 days up to 10% of lifetime) exposure durations, all of which are derived based on an assumption of continuous exposure throughout the duration spe cified. For the purposes of assessing all potential health risks associated with the emissions included in an assessment, we rely on both chronic (cancer and noncancer) and acute (noncancer) benchmarks, which are described in more detail below. Although every effort is made to identify peer - review ed dose
- response values for all HAPs emitted by the source category included in an assessment, some HAP have no peer
- reviewed cancer potency values or reference values for chronic non
- cancer or acute effects (inhalation or ingestion) . Since exposures to these pollutants cannot be included in a quantitative risk estimate, an understatement of risk for these pollutants at environmental exposure levels is possible. Additionall y, chronic dose
- response values for ce rtain compounds included in the assessment ma y be under EPA IRIS review and revised assessments may determine that these pollutants are more or less potent than currently thought. We will re
- evaluate risks if, as a result of these reviews, a dose
- response metric changes enough to indicate that the risk assessment may significantly mischaracterize human health risk **Cancer assessm ent**  The discussion of dose
- response uncertainties in the estimation of cancer risk below focuses on the uncertainties associated with the specific approach currently used by the EPA to develop cancer potency factors. In general, these same uncertainties attend the development of cancer potency factors by CalEPA, the source of peer
- reviewed cancer potency factors used where EPA
- dev eloped values are not yet available. To place this discussion in context, we provide a quote from the EPA’s Guidelines for Carcinogen Risk Assessment [ 29 ] (herein referred to as Cancer Guidelines ). “The primary goal of EPA actions is protection of human health; accordingl y, as an Agency policy , risk assessment procedures, including default options that are used in the absence of scientific data to the contrary , should be health**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  28 protective.” The approach adopted in this document is consistent with this approach as described in the Cancer Guidelines . For cancer endpoints EPA usually derives an oral slope factor for ingestion and a unit risk value for inhalation exposures. These values allow estim ation of a lifetime probability of developing cancer given long
- term exposures to the pollutant. Depending on the pollutant being evaluated, EPA relies on both animal bioassay and epidemiological studies to characterize cancer risk. As a science policy approach, consistent with the Cancer Guidelines , EPA uses animal cancer bioassay s as indicators of potential human health risk when other human cancer risk data are unavailable. Extrapolation of study data to estimate potential risks to human population s is based upon EPA’s assessment of the scientific database for a pollutant using EPA’s guidance documents and other peer
- reviewed methodologies. The EPA Cancer Guidelines describes the Agency ’s recommendations for methodologies for cancer risk assessment . EPA believes that cancer risk estimates developed following the procedures described in the Cancer Guidelines and outlined below generally provide an upper bound estimate of risk. That is, EPA’s upper bound estimates represent a “plausible upper limit to the true value of a quantity” (although this is usually not a true statistical confidence limit). 20 In some circumstances, the true risk could be as low as zero; however, in other circumstances the risk could also be greater. 21 When developing an upper bound estimate of risk and to provide risk values that do not underestimate risk, EPA generally relies on conservative default approaches. 22 EP A also uses the upper bound (rather than lower bound or central) estimates in its assessments, although it is no ted that this approach can have limitations for some uses (e.g. priority setting, expected benefits analy sis). Such health risk assessments have associated uncertainties, some which may be considered quantitatively , and others which generally are expresse d qualitatively . Uncertainties may vary substantially among cancer risk assessments associated with exposures to different pollutants, since the assessments employ different databases with different strengths and limitations and the procedures employed ma y d iffer in how well they represent actual biological processes for the assessed substance. EPA’s Risk Characterization Handbook also recommends that risk characterizations present estimates demonstrating the impact on the assessment of alternative

20 IRIS glossary (www.epa.gov/NCEA/iris/help_gloss.htm). 21 The exception to this is the URE for benzene, whic h is considered to cover a range of values, each end of which is considered to be equally plausible, and which is based on maximum likelihood estimates. 22 According to the NRC report Science and Judgment in Risk Assessment (NRC, 1994) “[Default] options are generic approaches, based on general scientific knowledge and policy judgment, that are applied to various elements of the risk
- assessment process when the correct scientific model is unknown or uncertain.” The 1983 NRC report Risk Assessment in the F ederal Government: Managing the Process defined default option as “the option chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to the contrary” (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the agency may depart from them in evaluating the risks posed by a specific substance when it believes this to be appropriate. In keeping with EPA’s goal of protecting public health and the environment, default assumpti ons are used to ensure that risk to chemicals is not underestimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An Examination of EPA Risk Assessment Principles and Practices, EPA/100/B
- 04/001 available at: http://www.ep a.gov/osa/pdfs/ratf
- final.pdf.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  29 choice s, data, models and assumptions [ 30 ]. Some of the major sources of uncertainty and variability in deriving cancer risk values are described more fully below. (1) The qualitative similarities or differences between tumor responses observed in experimental animal bioassays and those which would occur in humans are a source of uncertainty in cancer risk assessment. In general, EPA does not assume that tumor sites observed in an experimental animal bioassay are necessarily predictive of the sites at which tumors would occur in humans. 23 However, unless scientific support is available to show otherwise, EPA assumes that tumors in animals are relevant in humans, regardless of target organ concordance. For a specific pollutant, qualitative differences in speci es responses can lead to either under
- estimation or over
- estimation of human cancer risks. (2) Uncertainties regarding the most appropriate dose metric for an assessment can also lead to differences in risk predictions. For example, the measure of dose is commonl y e xpressed in units of mg/kg/d ingested or the inhaled concentration of the pollutant. However, data may support development of a pharmacokinetic model for the absorption, distribution, metabolism and excretion of an agent, which may result in improved dose metrics (e.g., average blood concentration of the pollutant or the quantity of agent metabolized in the body). Quantitative uncertainties result when the appropriate choice of a dose metric is uncertain or when dose metric estimates are thems elves uncertain (e.g., as can occur when alternative pharmacokinetic models are available for a compound). Uncertainty in dose estimates may lead to either over or underestimation of risk. (3) For the quantitative extrapolation of cancer risk estimates from experimental animals to humans, EPA uses scaling methodologies (relating expected response to differences in phy sical size of the species), which introduce another source of uncertainty . These methodologies are based on both biological data on differences in rates of process according to species size and empirical comparisons of toxicity between experimental animals and humans. For a particular pollutant, the quantitative difference in cancer potency between experimental animals and humans may be ei ther greater than or less than that estimated by baseline scientific scaling predictions due to uncertainties associated with limitations in the test data and the correctness of scaled estimates. (4) EPA cancer risk estimates, whether based on epidemiol ogical or experimental animal data, are generally de veloped using a benchmark dose (BMD) analysis to estimate a dose at which there is a specified excess risk of cancer, which is used as the point of departure (or POD) for the remainder of the calculation . Statistical uncertainty in developing a POD using a benchmark dose (BMD) approach is generally addressed though use of the 95% lower confidence limit on the dose at which the specified excess risk occurs (the BMDL), decreasing the likelihood of understating risk. EPA has generally utilized the multistage model for estimation of the BMDL using cancer bioassay data (see further discussion below).

23 Per the EPA Cancer Guidelines: “The default option is that positive effects in animal cancer studies indicate that the agent under study can have carcinogenic potential in humans.” and “Target organ concordance is not a prerequisite for evaluating the implications of animal study results for humans.”**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  30 (5) Extrapolation from high to low doses is an important, and potentially large, source of uncertainty in cancer risk assessment. EPA uses different approaches to low dose risk assessment (i.e., developing estimates of risk for exposures to environmental doses of an agent from observations in experimental or epidemiological studies at higher dose) depending on the available data and understanding of a pollutant’s mode of action (i.e., the manner in which a pollutant causes cancer). EPA’s Cancer Guidelines express a preference for the use of reliable, compound
- specific, biologically
- based risk models when feasible; however, such models are rarely av ailable. The mode of action for a pollutant (i.e., the manner in which a pollutant causes cancer) is a ke y c o nsideration in determining how risks should be estimated for low
- dose exposure. A reference value is calculated when the available mode of action data show the response to be nonlinear (e.g., as in a threshold response). A linear low
- dose (straight line from POD) approach is used when available mode of action data support a linear (e.g., nonthreshold response) or as the most common default approach when a compound’s mode of action is unknown. L inear extrapolation can be supported by both pollutant
- specif ic data and broader scientific considerations. For example, EPA’s Cancer Guidelines generally consider a linear dose
- response to be appropriate for pollutants that interact with DNA and induce mutations. Pollutants whose effects are additive to backgroun d biological processes in cancer development can also be predicted to have low
- dose linear responses, although the slope of this relationship may not be the same as the slope estimated by the straight line appro ach. EPA most frequently utilizes a linear low
- dose extrapolation approach as a baseline science
policy choice (a “default”) when available data do not allow a compound
- specific determination. This approach is designed to not underestimate risk in the face of uncertainty and variability . EPA bel ie ves that linear dose
- response models, when appropriately applied as part of EPA’s cancer risk assessment process, provide an upper bound estimate of risk and generally provide a health protective approach. Note that another source of uncertainty is the characterization of low
- dose nonlinear, non
- threshold relationships. The National Academy of Sciences has encouraged the exploration of sigmoidal type functions (e.g., log
- probit models) in representing dose response relationships due to the variability i n response within human populations. Another National Research Council (NRC) report [ 31 ] suggests that models based on distributions of individual thresholds are likely to lead to sigmoidal
- shaped dose
- response functions for a population. This report note s sources of variability in the human population: “One might expect these individual tolerances to vary extensively in humans depending on genetics, coincident exposures, nutritional status, and various other susceptibility factors...” Thus, if a distribution of thresholds approach is considered for a carcinogen risk assessment, application would depend on ability of modeling to reflect the degree of variability in response in human populations (as opposed to responses in bioassays with genetically more uniform rodents). Note also that low dose linearity in risk can arise for reasons separate from population variability: due to the nature of a mode of action and additivity of a chemical’s effect on top of background chemical exposures and biological proc esses. As noted above, EPA’s current approach to cancer risk assessment ty pically utilizes a straight line approach from the BMDL. This is equivalent to using an upper confidence limit on the slope of the straight line extrapolation. The impact of the c hoice of the BMDL on bottom line**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  31 risk estimates can be quantified by comparing risk estimates using the BMDL va lue to central estimate BMD values, although these differences are generally not a large contributor to uncertainty in risk assessment (Subramani am et. al., 2006) [ 32 ]. It is important to note that earlier EPA assessments, including the majority of those for which risk values exist today , were generally developed using the multistage model to extrapolate down to environmental dose levels and did no t involve the use of a POD. Subramaniam et ., al. (2006) also provide comparisons indicating that slopes based on straight line extrapolation from a POD do not show large differences from those based on the upper confidence limit of the multistage model. ( 6) Cancer risk estimates do not generally make specific adjustments to reflect the variability in response within the human population

— resulting in another source of uncertainty in assessments. In the diverse human population, some individuals are likel y t o be more sensitive to the action of a carcinogen than the ty pical individual, although compound
- specific data to evaluate this variability are generally not available. There may also be important life stage differences in the quantitative potency of c arcinogens and, with the exception of the recommendations in EPA’s Supplemental Cancer Guidance for carcinogens with a mutagenic mode of action, risk assessments do not generally quantitatively address life stage differences. Howe ver, one approach used co mmonly in EPA assessments that may help address variability in response is to extrapolate human response from results observed in the most sensitive species and sex tested, resulting ty pically in the highest URE which can be supported by reliab le data, thu s supporting estimates that are designed not to underestimate risk in the face of uncertainty and variability . **Chronic noncancer assessment** Chronic noncancer reference values represent chronic exposure levels that are intended to be health
- protective. Th at is, EPA and other organizations which develop noncancer reference values (e.g., the Agency for Toxic Substances and Disease Registry

– ATSDR) utilize an appro ach that is intended not to underestimate risk in the face of uncertainty and variability . Whe n there are gaps in the available information, uncertainty factors (UFs) are applied to derive reference values that are intended to be protective against appreciable risk of deleterious effects . Uncertainty factors are commonl y d efault values 24 e.g., fact ors of 10 or 3, used in the absence of compound
- specific data; where data are available, uncertainty factors ma y a lso be developed using compound
- specific information. When data are limited, more
24 According to the NRC report Science and Judgment in Risk Assessment (NRC, 1994) “[Default] options are generic approaches, based on general scientific knowledge and policy j udgment, that are applied to various elements of the risk
- assessment process when the correct scientific model is unknown or uncertain.” The 1983 NRC report Risk Assessment in the Federal Government: Managing the Process defined de fault option as “the opt ion chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to the contrary” (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the agency may depart from them in eval uating the risks posed by a specific substance when it believes this to be appropriate. In keeping with EPA’s goal of protecting public health and the environment, default assumptions are used to ensure that risk to chemicals is not underestimated (althou gh defaults are not intended to overtly overestimate risk). See EPA 2004 An examination of EPA Risk Assessment Principles and Practices, EPA/100/B
- 04/001 available at: http://www.epa.gov/osa/pdfs/ratf
- final.pdf.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  32 assumptions are needed and more default factors are used. Thus there may be a greater tendency to overestimate risk

— in the sense that further study mi ght support development of reference values that are higher (i.e., less potent) because fewer default assumptions are needed. However, for some pollutants it is po ssible that risks may be underestimated. For non - cancer endpoints related to chronic exposures, EPA derives a Reference Dose (RfD) for exposures via ingestion, and a Reference Concentration (RfC) for inhalation exposures. These values provide an estimate (with uncertainty spanning perhaps an order of magnitude) of daily oral exposure (RfD) or a continuous inhalation exposure (RfC) to the human population (including sensitive subgroups) that is likely to be without an appreciable risk o f deleterious effects during a lifetime. 25 To derive values that are intended to be “without appreciable risk,” EPA’s methodology relies upon an uncertainty factor (UF) approach (U.S. EPA, 1993, 1994) which includes consideration of both uncertainty and variability . EPA begins by evaluating all of the available peer
- reviewed literature to determine non
cancer endpoints of concern, evaluating the quality , strengths and limitations of the available studies. EPA typically chooses the relevant endpoint that occurs at the lowest dose, often using statistical modeling of the available data, and then determines the appropriate point of departure (POD) for derivation of the reference value. A POD is determined by (in order of preference): (1) a statistical estimation using the benchmark dose (BMD) approach; (2) use of the dose or concentration at which the toxic response was not significantly elevated (no observed adverse effect level

— NOAEL); or (3) use of the lowest observed adverse effect level (LOAEL). A s eries of downward adjustments using default UFs is then applied to the POD to estimate the reference value (U.S. EPA 1994, 2002). While collectively termed “UFs”, these factors account for a number of different quantitative considerations when utilizing observed animal (usually rodent) or human toxicity data in a risk assessment. The UFs are intended to account for: (1) variation in susceptibility among the members of the human population (i.e., inter
individual variability); (2) uncertainty in extrapolating from experimental animal data to humans (i.e., interspecies differences); (3) uncertainty in extrapolating from data obtained in a stud y w ith less
- than
- lifetime exposure (i.e., extrapolating from subchronic to chronic exposure); (4) uncertainty in extr apolating from a LOAEL in the absence of a NOAEL ; and (5) uncertainty when the database is incomplete or there are problems with applicability of available studies . When scientifically sound, peer
- reviewed assessment
- specific data are not available, defau lt adjustment values are selected for the individual UFs. For each type of uncertainty (when relevant to the assessment) , EPA typically applies an UF value of 10 or 3 with the cumulative UF value leading to a downward adjustment of 10
- 3000 fold from the se lected POD. An UF of 3 is used when the data do not support the use of a 10
- fold factor. If an extrapolation step or adjustment is not relevant to an assessment (e.g., if apply ing human toxicit y d ata and an interspecies extrapolation is not required) the associated UF is not used. The major adjustment steps are described more fully below. 1) Heterogeneity among humans is a key source of variability as well as uncertainty . Uncertainty related to human variation is considered in extrapolating doses from a subset or
25 See IRIS glossary**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  33 smaller
- sized population, often of one sex or of a narrow range of life stages (ty pical of occupational epidemiologic studies), to a larger, more diverse population. In the absence of pollutant
- specific data on human variation, a 10
- fold UF i s used to account for uncertainty associated with human variation. Human variation may be larger or smaller; however, data to examine the potential magnitude of human variability are often unavailable. In some situations, a smaller UF of 3 may be applied to reflect a known lack of significant variability among humans. 2) Extrapolation from results of studies in experimental animals to humans is a necessary step for the majority of chemical risk assessments . When interpreting animal data, the concentration at the POD (e.g. NOAEL , BMDL) in an animal model (e.g. rodents) is extrapolated to estimate the human response. While there is long
- standing scientific support for the use of animal studies as indicators of potential toxicity to humans , there are uncertainties in such extrapolations. In the absence of data to the contrar y, the ty pical appro ach is to use the most relevant endpoint from the most sensitive species and the most sensitive sex in assessing risks to the average human. Typicall y , compound sp ecific data to evaluate relative sensitivity in humans versus rodents are lacking, thus leading to uncertainty in this extrapolation. Size
- related differences (allometric relationships) indicate that ty pically humans are more sensitive than rodents when c ompared on a mg/kg/da y b asis. The default choice of 10 for the interspecies UF is consistent with these differences. For a s pecific chemical, differences in species responses may be greater or less than this value . Pharmacokinetic models are useful to e xamine species differences in pharmacokinetic processing and associated uncertainties; however, such dosimetric adjustments are not always possible. Information may not be available to quantitatively assess toxicokinetic or toxicodynamic differences betwe en animals and humans, and in many cases a 10
- fold UF (with separate factors of 3 for toxicokinetic and toxicodynamic components) is used to account for expected species differences and associated uncertainty in extrapolating from laboratory animals to hum ans in the derivation of a reference value. If information on one or the other of these components is available and accounted for in the cross
- species extrapolation, a UF of 3 ma y b e used for the remaining component. 3) In the case of reference values for chronic exposures where onl y d ata from shorter durations are available (e.g., 90
- day subchronic studies in rodents) or when such data are judged more appropriate for development of an RfC, an additional UF of 3 or 10
- fold is ty pically applied unless th e available scientific information supports use of a different value. 4) Toxicity data are ty

pically limited as to the dose or exposure levels that have been tested in individual studies; in an animal study, for example, treatment groups may differ in exp osure by up to an order of magnitude. The preferred approach to arrive at a POD is to use BMD analy sis; however, this approach requires adequate quantitative results for a meaningful analysis, which is not always possible. Use of a NOAEL is the next pref erred approach after BMD analy sis in determining a POD for deriving a health effect reference value. However, man y s tudies lack a dose or exposure level at which an adverse effect is not observed (i.e., a NOAEL is not identified). When using data limited to a LOAE L, a UF of 10 or 3
- fold is often applied.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  34 5) The database UF is intended to account for the potential for deriving an underprotective RfD/RfC due to a data gap preventing complete characterization of the chemical’s toxicity . In the absence of studies for a known or suspected endpoint of concern, a UF of 10 or 3
- fold is ty

pically applied. **Acute noncancer assessment** Many of the UFs used to account for variability and uncertainty in the development of acute reference values are quite similar to those developed for chronic durations, but more often using individual UF values that may be less than 10. UFs are applied based on chemical
specific or health effect
- specific information (e.g., simple irritation effects do not var y appreciably between human individuals, hence a value of 3 is ty pically used), or based on the purpose for the reference value (see the following paragraph). The UFs applied in acute reference value derivation include: 1) heterogeneity among humans; 2) uncertainty in extrapol ating from animals to humans; 3) uncertaint y i n LOAE L to NOAEL adjustments; and 4) uncertainty in accounting for an incomplete database on toxic effects of potential concern. Additional adjustments are often applied to account for uncertainty in extrapolation from observations at one exposure duration (e.g., 4 hours) to arrive at a POD for derivation of an acute reference value at another exposure duration (e.g., 1 hour). Not all acute reference values are developed for the same purpose and care must be taken when interpreting the results of an acute assessment of human health effects relative to the reference value or values being exceeded. Where relevant to the estimated exposures, the lack of threshold values at different levels of severity should be factored into the risk characterization as potential uncertainties.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  35 

### 5 **Re ferences**  1 . US EPA. National Emission Standards for Hazardous Air Pollutants . http://www.epa.gov/ttn/atw/mactfnlalph.html . 2 US EPA, 2009. Risk and Technology Review (RTR) Risk Assessment Methodologies: For Review by th e EPA’s Science Advisory Bo ard with Case Studies

– MACT I Petroleum Refining Sources and Portland Cement Manufacturing . EPA
- 452/R
- 09
- 006. http://www.epa.gov/ttn/atw/rrisk/rtrpg.html. 3 . US EPA, 2010. SAB’s Response to EPA’s RTR Risk Assessment Methodologies. http://yosemite.epa.gov/sab/sabproduct.nsf/4AB3966E263D 943A8525771F00668381/$File/EP A
- SAB
- 10
- 007
- unsigned.pdf 4 . US EPA, 2010. Memorandum from Dave Guinnup to RTR Wood Furniture Docket, entitled, “EPA’s Actions in Response to Key Recommendations of the SAB Review of RTR Risk Assessment Methodologies. 5 . US EPA, 2005. Revision to the Guideline on Air Quality Models: Adoption of a Preferred General Purpose (Flat and Complex Terrain) Dispersion Model and Other Revisions; Final Rule. 40 CFR Part 51. http://www.epa.gov/EPA
- AIR/2005/November/Day
- 09/a21627.htm 6 . US EPA, 2004. Users’ guide for the AMS/EPA regulatory model

– AERMOD. EPA
- 454/B
03
- 001 . http://www.epa.g ov/scram001/7thconf/aermod/aermodugb.pdf . 7 . Allen , D. , C . Murphy, Y . Kimura, W . Vizuete, T . Edgar , H . Jeffries, B . - U . Kim, M . Webster , and M . Symons , 2004. Variable industrial VOC emissions and their impact on ozone formation in the Houston Galveston Area. Final Report: Texas Environmental Research Consortium Project H
- 13. http://files.harc.edu/Projects/AirQuality/Projects/H013.2003/H13FinalReport.pdf 8 . US EPA, 2004. Air Toxics Risk Assessment Reference Library, Volume 1. EPA
- 453
- K
- 04
- 001A. http://www.epa.gov/ttn/fera/risk_atra_vol1.html. 9 . US EPA, 2005. Table 1. Prioritized Chronic Dose
- Response Values (2/28/05). Office of Air Quality Pl anning and Standards. http://www.epa.gov/ttn/atw/toxsource/table1.pdf 10 . US EPA, 2005. 1999 National Air Toxics Risk Assessment. http://www.epa.gov/ttn/atw/nata1999 11 . US EPA, 2006. Integrated Risk Information System. http://www.epa.gov/iris/index.html . 12 . US Agency for Toxic Substances and Disease Registry . 2006. Minimum Risk Levels (MRLs) for Hazardous Substances. http://www.atsdr.cdc.gov/mrls/index.html . 13 . US EPA, 1994 . US Environmental Protection Agency . Methods for Derivation of Inhalation Reference Concentrations and Application of Inhalation Dosimetry . EPA/600/8
- 90/066F. Office of Research and Development. Washington, DC: U.S.EPA. 14 . NRC, 1994. National Research Council. Science and Judgment in Risk Assessment. Washington, DC: National Academy Press.**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  36

15. CA Office of Environmental Health Hazard Assessment, 2005. Chronic Reference Exposure Levels Adopted by OEHHA as of December 2008. http://www.oehha.ca.gov/air/chronic_rels/AllChrels.html . 16 . CA Office of Environmental Health Hazard Assessment, 2005. Te chnical Support Document for Describing Available Cancer Potenc y Factors, May 2005 . http://www.oehha.ca.gov/air/hot_spots/may2005tsd.html . 17. US EPA, 2006. Approach for modeling POM. Technical support information for the 1999 National Air Toxics Assessment. http://www.epa.gov/ttn/atw/nata1999/99pdfs/pomapproachjan.pdf . 18 . US EPA, 2005. Table 2. Acute Dose
- Response Values for Screening Risk Assessments (6/02/2005). Office of Air Quality Planning and Standards. http://www.epa.gov/ttn/atw/toxsource/table2.pdf 19 . CA Office of Environmental Health Hazard Assessment, 2000. All Acute Reference Exposure Levels de ve loped by OEHHA as of May 2000. http://www.oehha.ca.gov/air/acute_rels/allAcRELs.html 20 . American Industrial Hygiene Association , 2009. Current AIHA ERPG Values. http://www.aiha.org/insideaiha/volunteergroups/Documents/ERP
- erpglevels.pdf . 21 . US EPA, 1995. Guidance for Risk Characterization. Science Policy Council. http://www.epa.gov/OSA/spc/pdfs/rcguide.pdf . 22 . US EPA, 2000. Risk Characterization Handbook. EPA 100
- B
- 00
- 002. 23 . US EPA, 2002. EPA’s Guidelines for Ensuring and Maximizing the Quality, Objectivity, Utility, and Integrity of Information Disseminated by the Environmental Protection Agency . EPA Office of Environmental Information. EPA /260R
- 02
- 008 . http://www.epa.gov/quality/informationguidelines/documents/EPA_InfoQualityGuidelines.pdf 24 . US EPA, 2006. Performing risk assessments that include carcinogens described in the Supplemental Guidance as having a mutagenic mode of action. Science Policy C ouncil Cancer Guidelines Implementation Workgroup Communication II: Memo from W.H. Farland dated 14 June 2006. http://www.epa.gov/osa/spc/pdfs/CGIWGCommunication_II.pdf 25 . US EPA, 200 5. Supplemental guidance for assessing early
- life exposure to carcinogens. EPA/630/R
- 03003F. http://www.epa.gov/ttn/atw/childrens_supplement_final.pdf. 26 . US EPA, 2005. Science P olicy Council Cancer Guidelines Implementation Workgroup Communication I: Memo from W.H. Farland dated 4 October 2005 to Science Policy Council. http://www.epa.gov/osa/s pc/pdfs/canguid1.pdf 27. US EPA, 1986. Guidelines for the Health Risk Assessment of Chemical Mixtures. EPA
- 630
- R
- 98
- 002. http://www.epa.gov/NCEA/raf/pdfs/chem_mix/chemmix_1986.pdf**Draft Risk Assessment for the Primary Aluminum Production Source Category**  **--**

**FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  37
28 . US EPA, 2000. Supplementary Guidance for Conducting Health Risk Assessment of Chemical Mixtures. EPA
- 630/R
- 00
- 002. http://www.epa.gov/ncea/raf/pdfs/chem_mix/chem_mix_08_2001.pdf . 29 . US EPA, 2005. Guidelines for Carcinogen Risk Assessment (2005). U.S. Environmental Protection Agency, Washington, DC, EPA/630/P
- 03/001F, 2005. http://cfpub.epa.gov/ncea/raf/recordisplay .cfm?deid=116283 30 . US EPA, 2000 . Risk Characterization Handbook. EPA 100
- B
- 00
- 002. 31 . NRC (National Research Council) 2006. Assessing the Human Health Risks of Trichloroethy

lene. Nat ional Academies Press, Washington DC . 32 . R.P. Subramaniam, P. White and V.J. Cogliano. 2006. Comparison of cancer slope factors using different statistical approaches, Risk Anal. Vol 26, p. 825

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