**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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## Draft Residual Risk Assessment for **7 Source Categories:** 

**Pesticide Active Ingredient Manufacturing Polyether Polyols**  **Production Polymers and Resins IV**  **-- Styrene Acrylonitrile**  **Polymers and Resins IV --**  **Polystyrene Polymers and Resins IV** 
**– Polyethylene**  **Ter e**  **phthalate Polymers and Resins IV**  **-- Methyl Methacrylate**  **- Butadiene Styrene**  **Polymers and Resins IV --**  **Acrylic Butadiene Styrene**

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

**Office of Air and Radiation November**  **2011 Draft Risk Ass**  **essment for 7 Chemical Sector Source Categories**

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### Table **of Contents** 1. Introduction
................................ ................................ ................................ ............................. 6 2. Methods
................................ ................................ ................................ ................................ ... 7 2.1. Emissions and source data
................................ ................................ ........................... 7 2.2. Dispersion modeling for inhalation exposure assessment
................................ ........... 7 2.3. Estimating chronic human inhalation exposure
................................ ........................ 10 2.4. Acute Risk Screening and Refined Assessments
................................ ...................... 11 2.5. Multipathway

human health and environmental risk screen ing
................................ 12 2.6. Dose - Response Assessment ................................ ................................ ...................... 14 2.6.1. Sources of chronic dose
- response information
................................ .................. 14 2.6.2. Sources of acute dose
- response information
................................ ...................... 23 2.7. Risk Characterization
................................ ................................ ................................ 28 2.7.1. General
................................ ................................ ................................ ............... 28 2.7.2. Mixtures
................................ ................................ ................................ ............. 30 2.7.3. Facilit y - wide Risks
................................ ................................ ............................ 30 2.7.4. MACT
- Allowable Risks
................................ ................................ .................... 31 3. Risk Results for Pesticide Active Ingredient Manufacturing
................................ ................ 31 3.1 Source Category

Description and Results
................................ ................................ . 31 3.2 Risk Characterization
................................ ................................ ................................ 34 4. Risk Results for the Poly ether Polyols Production Source Category
................................ ... 39 4.1 Source Category

Description and Results
................................ ................................ . 39 4.2 Risk Characterization
................................ ................................ ................................ 44 5. Risk Results for the P&V IV Sty rene Acrylonitrile Source Category
................................ .. 48 5.1 Source Category

Description and Results
................................ ................................ . 48 5.2 Risk Characterization
................................ ................................ ................................ 49 6. Ris k Results for the P&R IV Poly st yrene Production Source Category
............................... 52 6.1 Source Category

Description and Results
................................ ................................ . 52 6.2 Risk Characterization
................................ ................................ ................................ 53 7. Risk Results for the P&R IV Poly eth yl ene Terephthalate Source Category
........................ 56 7.1 Source Category Description and Results
................................ ................................ . 56 7.2 Risk Characterization
................................ ................................ ................................ 59 8. Risk Results for the P&R IV Meth yl Methacrylate
- Butadiene
- Sty rene Source Category ... 63 8.1 Source Category

Description and Results
................................ ................................ . 63 8.2 Risk Characterization
................................ ................................ ................................ 64 9. Risk Results for the P&R IV Acrylonitrile
- Butadiene
- Sty rene Source Category ................ 68 9.1 Source Category

Description and Results
................................ ................................ . 68 9.2 Risk Characterization
................................ ................................ ................................ 70 10. General Discussion of Uncertainties and How They Have Been Addressed
........................ 73 10.1 Exposure Modeling Uncertainties
................................ ................................ ......... 73 10.2 Uncertainties i n the Dose
- Response Relationships
................................ ............... 74 11 References
................................ ................................ ................................ ............................. 82 **Index of Tables** Table 2.2
- 1 AERMOD version 11103 model options for RTR modeling
................................ 8**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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3 Table 2.6
- 1 (a) Dose
- Response Values for Chronic Inhalation Exposure to Carcinogens
.... 18 Table 2.6
- 1 (b) Dose
- Response Values for Chronic Inhalation Exposure to Noncarcinogens

................................ ................................ ................................ ................................ .................. 20 Table 2.6
- 2 Dose - Response Values for Acute Exposure
................................ ........................ 26 Table 3.1
- 1 Summary of Emissions from the Pesticide Active In gredients Source Category and Availability

of Dose
- Response Values
................................ .............................. 32 Table 3.2
- 1 Summary of Source Category

L evel Risks for Pesti cide Active Ingredient Production 37 Table 3.2
- 2 Summary of Refined Acute Results for Pesticide Active Ingredient Production Facili ties
................................ ................................ ................................ ................ 38 Table 3.2
- 3 Source Category Contribution to Facility
- Wide Cancer Risks

– Pesticide Active Ingredient
................................ ................................ ................................ ...................... 39 Table 4.1
- 1 Summary of Emissions from the Poly ether Polyols Production Source Category and Availability

of Dose
- Response Values
................................ .............................. 41 Table 4.2
- 1 Summary of Source Category

L evel Inhalation Risks for Polyether Polyols Production 46 Table 4.2
- 2 Summary of Acute Refined Results for Poly ether Polyols Production Facilities 47 Table 4.2
- 3 Source Category Contribution to Facility
- Wide Cancer Risks

– Poly ether Polyols Production
................................ ................................ ................................ ................... 48 Table 5.1
- 1 Summary of Emissions from the Sty rene - Acrylonitrile Production Source Category and Availability

of Dose
- Response Values
................................ .............................. 49 Table 5.2
- 1 Summary of Source Category

L evel Risks for Sty

re ne - Acrylonitrile Production 51 Table 5.2
- 2 Source Category Contribution to Facility
- Wide Cancer Risks

– Sty rene Acrylonitrile Production
................................ ................................ ................................ ........... 52 Table 6.1
- 1 Summary of Emissions from the Poly sty rene Production Source Category and Availability

of Dose
- Response Values
................................ ................................ .................... 53 Table 6.2
- 1 Summary of Source Category

L evel Risks for Poly sty

rene Production
........ 55 Table 6.2
- 2 Source Category Contribution to Facility
- Wide Cancer Risks

– Poly st yr ene Production 56 Table 7.1
- 1 Summary of Emissions from the Poly eth yl ene Terephthalate Production Source Category

and Availability

of Dose
- Response Values
................................ .................. 57 Table 7.2
- 1 Summary of Source Category

L evel Risks for Poly ethylene Terephthalate Production 61 Table 7.2
- 2 Summary of Acute Refined Results for Poly eth yl ene Terephthalate Production 62 Table 7.2
- 3 Source Category Contribution to Facility
- Wide Cancer Risks

– Poly eth yl ene Terephthalate Production
................................ ................................ ................................ ......... 63 Table 8.1
- 1 Summary of Emissions from the Methyl Methacrylate
- Butadiene
- Sty rene Production Source Category and Availability

of Dose
- Response Values
............................... 64 Table 8.2
- 1 Summary of Source Category

L evel Risks for Methyl Methacrylate
Butadiene
- Sty

rene Production
................................ ................................ ................................ . 66 Table 8.2
- 2 Summary of Acute Refined Results for Methyl Methacrylate
- Butadiene
Sty rene Production Facilities
................................ ................................ ................................ ... 67**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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4 Table 8.2
- 3 Source Category Contribution to Facility
- Wide Cancer Risks

– Meth yl Methacrylate
- Butadiene
- Sty rene Production
................................ ................................ ........... 67 Table 9.1
- 1 Summary of Emissions from the Acrylonitrile
- Butadiene
- Sty rene Production Source Category

and Availability

of Dose
- Response Values
................................ .................. 69 Table 9.2
- 1 Summary of Source Category

L evel Risks for Acrylonitrile
- Butadiene
Sty rene Production
................................ ................................ ................................ .................. 71 Table 9.2
- 2 Summary of Acute Refined Results for Acrylonitrile
- Butadiene
- Sty rene Production 72 Table 9.2
- 3 Source Category Contribution to Facility
- Wide Cancer Risks

– Acrylonitrile
Butadiene
- Sty

rene Production
................................ ................................ ................................ . 73 **Appendices** Appendix 1 Technical Support Document for HEM3 Modeling Appendix 2 Meteorological Data for HEM3 Modeling Appendix 3 Analy sis of data on short
- term emission rates relative to long
- term emission

rates Appendix 4 Detailed Risk Modeling Results Appendix 5 Technical Support Document for TRIM
- Based Multipathway Screening Scenario for RTR: Summary of Approach and Evaluation Appendix 6 Acute Impacts Refined Analy sis Appendix 7 Disper sion Model Receptor Revisions and Additions **Index of Acronyms** AERMOD American Meteorological Society /EPA Regulatory

Model AEGL Acute exposure guideline level ASTDR US Agency for Toxic Substances and Disease Registry CalEPA California Environmental Agen cy ERPG Emergency Response Planning Guideline HAP Hazardous Air Pollutant HEM Human Exposure Model HI Hazard index HQ Hazard quotient IR IS Integrated Risk Information Sy stem MACT Maximum Achievable Control Technology MIR Maximum Individual Risk MOA Mode of action NAC National Advisory Committee NATA National Air Toxics Assessment NEI National Emissions Inventory NPRM Notice of Proposed Rulemaking PB - HAP Persistent and Bioaccumulative
- HAP POM Polycyclic organic matter**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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5 REL Reference exposure level RfC Reference concentration RfD Reference dose RTR Risk and Technology TOSHI Target - organ - specific hazard index URE Unit risk estimate**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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6 

### 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 largel y 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 safet y or to prevent an adverse environmental effect, EPA must develop standards to address these remaining risks. This second stage of the regulatory process is known as the residual risk stage. For each source category for which EPA issued MACT standards, the resi dual risk stage must be completed within eight years of promulgation of the initial technology
- based standard. In December of 2006 we consulted with a panel from the EPA's Science Advisory Board (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 July of 2009 a meeting was held with an SAB panel for a formal peer review of the “Risk and Technology

Review (RTR) Assessment Methodol ogies” [ 2 ]. We received the final SAB report on this review in May of 2010 [ 3 ]. Where appropriate, we have responded to the key messages from this review in developing our current risk assessment s and we will be continuing our efforts to improve our asse ssments by incorporating updates based on the SAB recommendations as they are developed and become available . Our responses to the key recommendations of the SAB are outlined in the me mo entitled, “EPA’s Actions in Response to Key Recommendations from the SAB Review of RTR R isk Assessment Methodologies” [ 4 ]. This document contains the methods and the results of baseline risk assessments (i.e., after the implementation of the respective MACT standards) performed for seven chemical industry source categories. Five of the source categories were originall y addressed under the Polymers and Resins IV MACT. The seven source categories are: Pesticide Active Ingredient Manufacturing , Poly ether Pol yols Production , Poly mers and Resins IV
-- Sty rene Acrylonitri le, Poly mers and Resins IV
-- Poly sty rene , Poly mers and Resins IV
-- Poly eth yl ene Ter ephthalate , Poly mers and Resins IV
-- Methyl Methacrylate
- Butadiene Sty rene , and Poly mers and Resins IV
-- Acrylic Butadiene Sty rene . The methods discussion includes descriptions of the methods used to develop refined estimates of chronic inhalation exposures and human health risks for cancer and noncancer**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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7 endpoints, as well as descriptions of the methods used to screen for acute health risks, chronic non - inhalation health risks, and adverse e nvironmental effects. Since the screening assessments indicated low potential for chronic non
- inhalation health effects or environmental impacts, including effects to threatened and endangered speci es, no further refinement of these assessments was performed. 

### 2. **Methods 2.1.**  **Emissions and source data** The 200 5 Nat ional Emissions Inventory (NEI) that was used in the 2005 National
- scale Air Toxics Assessment (NATA) 1 served as the starting point for th ese asse ssments . The 2005 NEI contains information on actual emissions during the entire 2005 base year. Using the process MACT code, 2 we developed a subset of the NEI that contain s facility , process, and emissions data for each facility in the se seven source categories. Next, we performed an engineering review of the information using EPA engineers who were directly involved in the development of the MACT standards for these source categories, and/or who have extensive knowledge of the characteristics of this industry . The goal of the engineering review was to identify readil y - apparent limitations and issues with the emissions data (particularly those that would have the potential to influence risk estimates) and to make changes to the data set where possible to address these issues and decrease the uncertainties associated with the assessments. Industry

trade groups then reviewed the data set to provide input on facility names, source classification codes, and MACT codes. Industry also provided revisions to emissions, stack parameters, and location coordinates. Finall y, EPA engineers reviewed the suggested industry

revisions and performed a comprehensive review of the location coordinates. These data underwent an extensive QA/QC procedure, and revisions we re made to the dataset as necessary . The emissions data and modifications made to the NEI data are discussed in the memo entitled “ Emissions Data Used in Residual Risk Modeling: Pesticide Active Ingredient Manufacturing, Poly ether Polyols Production, and Poly mers and Resins IV ” available in the docket for this action
. 

### 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 Model (AERMOD) dispersion modeling s ys tem (HEM 3 ). The approach used in applying this modeling s ys tem is outlined below, and further details are provided in Appendix 1 . The HEM 3 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 modeli ng component. The exposure and risk characterization components are discussed in other subsections of Sections 2 and 3.
1 http://www.epa.gov/ttn/atw/nata2005/ 2 Assigning data with MACT codes allow s EPA to determine reductions attributable to the MACT program. The NEI associates MACT codes corresponding to MACT source categories with stationary major and area source data.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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8 The dispersion model in the HEM3 sy stem, AERMOD version 11103 , is a state
- of
- the
science Gaussian plume dispersion model that is prefe rred b y 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. Hourl y emission rates used for this simulation are generated b y evenl y dividing the total annual emission rate from the inventory into the 8,760 h ours of the ye ar. The first step in the application of the HEM3 modeling s ys tem is to estimate ambient concentrations at locations of interest. The AERMOD model options employed are summarized in Table 2.2
- 1 and are discussed further below. **Table 2.2**  **- 1**  **AERMOD version 11103**  **mo del options for RTR**  **modeling** 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) and user
- supplied receptors 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 ( over 200 stations) In HEM3 , meteorological data are ordinaril y selected from a list of over 200 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
. Ideall y, when considering off
- site meteorological data , most site
- specific dispersi on modeling efforts will employ up to five ye ars of data to capture variability in weather patterns from ye ar to ye ar. However, because we had an insufficient number of appropriatel y formatted model input files derived from available meteorological data, we modeled only a single y ear, t ypicall y 1991. While the selection of a single ye ar may result in under
- estimation of long
- term ambient levels at some locations, likewise it may result in over
- estimation at others. For each facility identified b y 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 (Meteorolog ical Data Processing Using AERMET for HEM3 ) provides a complete listing of stations and**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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9 assumptions 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 ye ar of meteorological data is discussed in “ Risk and Technology Review (RTR) Risk Assessment Methodologies ” [ 2 ]. The HEM3 sy stem estimates ambient concentrations at the geographic centroids of census blocks (using the 2000 Census), and at other receptor locations that can be specified b y the user. The model accounts for the effects of multiple facilities when estimating concentration impacts at each block centroid. Ty pically we combined only

the impacts of facilities within the same source category, and assessed chronic exposure and risk onl y for census blocks with at least 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) concentrations at each block centroid. Possible future residential use of currentl y uninhabited areas was not considered. Census blocks, the finest resolution available in the census data, are typically comprised of approximately 40 people or about ten households. For each facility in these source categories census block locations were care fully evaluated for proximity

to each facility’s propert y line (see Appendix 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 generall y 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 facilit y property). Since short
- term emission rates were needed to screen for the potential for hazard via acute exposures, and since the NEI contains only annual emission totals, we generall y appl y the assumption to all source categories that the max imum one
- hour emission rate from an y source is ten times the average annual hourl y emission rate for that source. 3 The average hourly

emissions rate is defined as the total emissions for a year divided by the total number of operating hours in the year. The choice of a factor of ten for acute screening was originally based on engineering judgment
. To develop a more robust peak
- to - mean emissions factor, and in response to one of the key messages from the SAB consultation on our RTR Assessment Plan, we per formed an anal ysis using a short
- term emissions data set from a number of source s located in Texas (originally reported on b y 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 anal ys is, focus ing that analy sis on sources which reported emitting high quantities of HAP over short periods of time (see Appendix 3 , “Analy sis of data on short
- term emission rates relative to long
- term emission rates”). Most peak emission events were less than twice the annual average, the highest was a factor of 74 times the annual average , and the 99 th

3 In situations where we have information on hourly emissions, we will take this into account when evaluating acute risks.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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10 percentile ratio of peak hourly emission rate to the annual hourl y emission rate was 9 . Based on these results, we chose a factor of ten for the initial screening , except for several source categories where a factor of 2 was applied for certain situations (see source category risk characterization sections) . These factors are intended to cover all possible hourly peaks associated with routinel y - variable emissions. While there have been some documented emission excursions above this level, our anal ys is of the data from the Texas Environmental Research Consortium suggests that th ese factor s should cover more than 99% of the short
term peak gaseous or volatile HAP emis sions from ty pical industrial sources
. We have no data relating specificall y to peak short
- term emissions of particulate HAP. In the absence of source category - specific data, we use this same default approach for particulate emissions as well. A list of facilities where we used the factor of two instead of ten is provided in Appendix 6 . Census block elevations for HEM3 modeling were determined nationally from the US Geological S urvey 1 - degree digital elevation model (DEM) data files, which have a spat ial 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. I f a sector does not contain an y blocks, the model defaults the elevation to that of the nearest block. If an elevation is not provided for the emission 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 nearb y el evated hills are expected to influence the wind patterns. For details on how hill heights were estimated and used in the AERMOD modelin g , see Appendix 1 . 

### 2.3. **Estimating chronic**  **human inhalation exposure** We used the estimated 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 peopl e who reside in the census block. That is, the risk anal ys is did not consider either the short
- term 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 NATA assessments (which modeled dail y activity using EPA’s HAPEM model) suggests that, given our current understanding of microenvironment concentrations and daily activities, modeling short
- term activity w ould, on average, reduce risk estimates about 25% for particulate HAPs; it w ould also reduce risk estimates for gaseous HAPs, but ty picall y b y much less. Second, basing exposure estimates on average ambient concentrations at census block centroids may

und erestimate or overestimate actual exposure concentrations at some residences. Further reducing exposure estimates for the most highl y exposed residents b y 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 estimated exposure is**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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11 constant over the course of their lifetime which is assumed to be 70 years. In assessing can cer risk, we generall y estimated three metrics; the maximum individual risk (MIR), which is defined as the risk associated with a lifetime of exposure at the highest concentration; 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 theoretical MIR nor does it affect the estimate of cancer incidence since the total population number remains the same. It does, however, 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, thereb y increasing the estimated number of people at sp ecific risk levels
. When screening for potentially significant acute exposures, we used an estimate of the highest hourly ambient concentration at any off
- site location as the surrogate for the maximum potential acute exposure concentration for an y indi vidual. 

### 2.4. **Ac ute Risk Screening and Refined A** **ssessments** 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 c hronic health risk assessments under the residual risk program. That is, we developed a tiered, iterative approach. This approach to risk assessment was endorsed b y the National Academ y of Sciences in its 1993 publication “Science and Judgment in Risk As sessment” and subsequently was adopted in the EPA’s “Residual Risk Report to Congress” in 1999. The assessment methodology is designed to eliminate from further consideration those facilities for which we have confidence that no acute adverse health eff ects of concern will occur. To do so, we use what is called a tiered, iterative approach to the asse ssment. This means that we begin with a screening assessment, which relies on readil y 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. A refined 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 facilit y, and /or the local meteorology . In some cases, all of these site
- specific dat a would be needed to refine the assessment; in others, lesser amount s of site
- specific data c an be used to determine that acute exposures are not a concern, and significant additional data collection is not necessary . Acute health risk screening was per formed 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 10 times the average 1
- hour emission rates.  For facilities with multiple emission points, peak 1
- hour emissions were assumed to occur at all emission points at the same time.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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12  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.  Wor st - case meteorology (from one ye ar of local meteorology) was assumed to occur at the same time the peak emission rates occur. The recommended EPA local
- scale dispersion model, AERMOD, is used for simulating atmospheric dispersion.  A person was assumed to be located downwind at the point of maximum impact during this same 1
- hour period, but no nearer to the source than 100 meters.  The maximum impact was compared to multiple short
- term health benchmarks for the chemical being assessed to determine if a possi ble acute health risk might exist. These benchmarks are described in section 2.6 of this report. As mentioned above, when we identify acute impacts which exceed their relevant benchmarks, we pursue refining our acute screening estimates to the extent pos sible
. Insome cases, this includes the use of a refined emissions multiplier to estimate the peak hourl y emission rates from the average rates (rather than the default factor of 10) . For the source categories in th is document, we conducted a review of the layout of emission points at the facilities with the facilit y boundaries to determine the maximum off
- site acute impact for the facilities that did not screen out during the initial model run. Refer to Appendix 6 for the detailed results for these site s. 

### 2.5. **Multipathway human health**  **and env**  **ironmental risk screening**  The potential for significant human health risks due to exposures via routes other than inhalation (i.e., multipathway exposures) was screened b y first determining whether an y sources emitted any

hazardous air pollutants known to be persistent and bioaccumulative in the environment (PB
- HAP) 4 . The PB
- HAP compounds or compound classes are identified for the screening from the EPA’s Air Toxics Risk Assessment L ibrary [ 8 ]. Examples of PB
HAP are cadmium compounds, chlordane, chlorinated dibenzodioxins and furans, DDE, heptachlor, hexachlorobenzene, hexachlorocyclohexane, lead compounds, mercury compounds, methoxychlor, polychlorinated biphenyls, pol yc yclic organic matter (POM) , toxaphene, and trif

luralin
. There were PB
- HAP emission s identified for three of the source categories addressed in this risk document. F or the poly eth yl ene terephthalate production source category , we identified emissions of cadmium compounds, polycyclic organic matter (POM), and lead compounds . For the pesticide active ingredient production source category , we identified emissions of lead compounds and polychlorinated biphenyls (PCBs). F or the p oly ether polyols production s ource category , we identified emissions of POM, lead compounds, and hexachlorobenzene
. These PB - HAP emissions were evaluated for potential non
- inhalation risks and adverse environmental impacts using our recentl y - developed screening scenario which was dev eloped
4 Although the two - letter chemical symbol for lead is Pb, in this assessment PB
- HAP refers to the many air pollutants known to be pers istent and bioaccumulative in the environment. In instances where the report is specifically referring to lead, it is spelled out (i.e., the two
- letter chemical symbol for lead is not used in this document).**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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13 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 an y specified 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 (HHRAP) for hazardous waste combustion facilities. 6 In the devel opment of the screening scenario , a sensitivity

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 fo r human health endpoints. See Appendix 5 for a complete discussion of the development and testing of the screening scenario, as well as for the values of facility
- level emission rates developed for screening potentially significant multi
- pathway

impacts. For the purpose of developing emission rates for our multi
- pathway screening, we derived emission levels for each PB - HAP (other than lead) at which the maximum human health risk would 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 for them , we compared maximum estimated chronic atmospheric concentrations with the current Nationa l Ambient Air Quality Standard (NAAQS) for lead. Values below the NAAQS were considered to have a low potential for multi
- pathway

risks. Additionally , we evaluated the potential for significant ecological exposures to non PB
- HAP from exceedances of chron ic human health inhalation thresholds in the ambient air near these facilities. Human health dose
- response threshold values are generall y 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 threshold values are often significantl y lower than the level expected to cause an adverse effect in an exposed rodent. It should be noted that there is a scarcit y of data on the direct atmospheric impact of these HAPs 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, we have generall y 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 an y significant risk from direct atmospheric impact. In some isolated cases where we have data indicating potential adv erse impacts on plants, birds, or other wildlife due to the direct atmospheric impacts of specific HAP, we note that as an uncertainty and, where possible, refine our anal ysis by comparing our modeled impacts to available threshold values from the scientif

ic literature.

5 EPA’s Total Risk Integrated Methodology (Gen eral Information) http://epa.gov/ttn/fera/trim_gen.html 6 EPA’s Human Health Risk Assessment Protocol (HHRAP) for Hazardous Waste Combustion Facilities; http://www.epa.gov/epaoswer/hazwaste/combust/riskvol.htm#volume1**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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14 

### 2.6. **Dose -**  **Response A ssessment**  **2.6.1. Sources of chronic dose**  **- response information**  Dose - response assessment (carcinogenic and non
- carcinogenic) for chronic exposure (either by inhalation or ingestion) for the HAPs reported in the emissions inventories for the source categories in this document were based on the EPA Office of Air Quality Planning and Standards’ existing recommendations for HAPs [ 9 ], also used for NATA [ 10 ]. This information has been obtained from various sources and prioritized accordin g 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. Th e 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 assessments ty

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

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 uncertaint y spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (in cluding sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. ” The RfD is “an estimate (with uncertaint y spanning perhaps an order of magnitude) of a daily

oral exposure to the human population (in cluding sensitive subgroups) that is likely

to be without an appreciable risk of deleterious effects during a lifetime. ” The URE is defined as “ the upper
- bound excess cancer risk estimated to result from continuous lifetime exposure to an agent at a conc entration 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 lifetime exposure to an agent. This estimate, [is] usually expressed in units of proportion (of a population) affected per m g/kg
- day ...” EPA disseminates dose
- response assessment information in several forms, based on the level of review. The Integrated Risk Information Sy stem (IRI S) [ 11 ] is an EPA database that contains scientific health assessment information, including dose
- r esponse information. All IRI S assessments since 1996 have also undergone independent external peer review. The current IRI S process includes review b y EPA scientists, interagency reviewers from other federal agencies, and the public, and peer review by in dependent scientists external to EPA. New IRI S values are developed and old IR IS values are updated as new health effects data become available. Refer to the “IRI S Track” website for detailed information on status and scheduling of current individual IRI S 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 exposure that are based on a nonlinear MOA
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15 2) US Agency

for Toxic Substances and Disease Registry (ATSDR). ATSDR, which is part of the US Department of Health and Human Services, develops and publishes Minimum Risk L evels (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 Hea lth and Human Services (HHS) and the EPA, ATSDR chose to adopt a practice similar to that of the EPA's Reference Dose (RfD) and Reference Concentration (RfC) for deriving substance specific health guidance levels for non neoplastic endpoints .” The MRLis defined as “an estimate of dail y human exposure to a substance that is likely to be without an appreciable risk of adverse effects (other than cancer) over a specified duration of exposure.” ATSDR describes MRL s 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 level s. 3) California Environmental Protection Agency (CalEPA). The CalEPA Office of Environmental Health Hazard Assessment has developed dose
- response assessments for many substances, based both on carcinogenicity and health effects other than cancer. The 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 (REL s) [ 15 ]. CalEPA defines the RELas “the concentratio n level at or below which no health effects are anticipated 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 HAP based on professional judgment, as follows: 1) In the case of HAP categories such as gl ycol ethers and cyanide compounds, the most conservative dose
- response value of the chemical category 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 may

pose an un acceptable risk and require further examination, or screen out from further assessment. 2) Where possible , for emissions of unspecified mixtures of HAP categories such as met al compounds and POM, we appl y category - specific chemical speciation profiles appro priate to the source category

to develop a composite dose
- response value for the category
.
7 Air Toxics Hot Spots Program, Risk A ssessment Guidelines, Part III
- Technical Support Document for the Determination of Non
- cancer Chronic Reference Exposure Levels. Air Toxicology and Epidemiology Section, Office of Environmental Health Hazard Assessment, California Environmental Protecti on Agency. February 2000 ( http://www.oehha.ca.gov/air/chronic_rels/pdf/relsP32k.pdf )**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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16 3) In 2004, the EPA determined that the Chemical Industry Institute of Toxicology

(CIIT) cancer dose
- response value for formaldehyde (5.5 x 10 - 9 per μg/m 3 ) was based on better science than the IRIS cancer dose
- response value (1.3 x 10 - 5 per μg/m 3 ), and we switched from using the IR IS value to the CIIT value in risk assessments supporting regulatory actions. Subsequent research published by EPA suggested th at the CIIT model was not appropriate and in 2010 EPA returned to using 1991 IRI S value. EPA has been working on revising the formaldehyde IR IS assessment and the National Academ y of Sciences (NAS) completed its review of the EPA’s draft assessment in April of 2011. 8 EPA will follow the NAS Report recommendations and will present results obtained by implementing the biologically
- based dose
- response ( BBDR) model for formaldehyde. EPA will compare these estimates with those currently presented in the Exter

nal Review draft of the assessment and will discuss their strengths and weaknesses. As recommended by the NAS committee, appropriate sensitivity and uncertaint y analyses will be an integral component of implementing the BBDR model. Inthe interim, we wil l present findings using the 1991 IRIS value as a primary estimate, and EPA may

also consider other information as the science evolves. 4) A substantial proportion of POM emissions reported to EPA’s N ati onal E mission Inventory (NE I) are not speciated into in dividua l compounds. As a result, it i s necessary to apply the same simplifyingassumptions to assessment s that are used in NATA. [ 17] The NATA approach partitions POM into eight different non - overlapping “groups” that are modeled as separate pollutants. E ach POM group comprises POM species of similar carcinogenic potency , for which we can appl y the same URE. 5) In the case of nickel compounds, to provide a health
- protective estimate of potential cancer risks, we used the IRIS URE value for nickel subsulfid e in this assessment. Based on past scientific and technical considerations, the determination of the percent of nickel subsulfide was considered a major factor for estimating the extent and magnitude of the risks of cancer due to nickel
- containing emissi ons. Nickel speciation information for some of the largest nickel
- emitting sources (including oil combustion, coal combustion, and others) suggested that at least 35 percent of total nickel emissions may be soluble compounds and that the URE for the mixture of inhaled nickel compounds (based on nickel subsulfide, and representative of pure insoluble cry stalline nickel) could be derived to reflect the assumption that 65 percent of the total mass of nickel may be carcinogenic. Based on consistent views of m ajor scientific bodies (i.e., National Toxicology Program (NTP) in their 12 th Report of the Carcinogens (ROC) 9 , International Agency for Research on Cancer (IARC) 10 , and other international agencies) 11 that consider all nickel

8 http://www.nap.edu/catalog.php?record_id=13142 9 National Toxicology Program (NTP), 2011. Report on carcinogens. 12 th ed. Research Triangle Park, NC: US Department of Health and Human Services (DHHS), Public Health Service. Available online at http://ntp.niehs.nih.gov/ntp/roc/tw elfth/roc12.pdf 10 International Agency for Research on Cancer (IARC), 1990. IARC monographs on the evaluation of carcinogenic r isks to humans. Chromium, nickel, and welding. Vol. 49. Lyons, France: International Agency for Research on Cancer, World Health Organization Vol. 49:256. 11 World Health Organization (WHO, 1991) and the Europea n Union’s Scientific Committee o n Health and Environmental Risks (SCHER, 2006)
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17 compounds to be carcinogenic, we currently consider all nickel compounds to have the potential of being carcinogenic to humans. The 12th Report of the Carcinogens states that the “combined results of epidemiological studies, mechanistic studies, and carci nogenic studies in rodents support the concept that nickel compounds generate nickel ions in target cells at sites critical for carcinogenesis, thus allowing consideration and evaluation of these compounds as a single group.” Although the precise nickel c ompound (or compounds) responsible for the carcinogenic effects in humans is not always clear, studies indicate that nickel sulfate and the combinations of nickel sulfides and oxides encountered in the nickel refining industries cause cancer in humans (the se studies are summarized in a review b y Grimsrud et al., 2010 12 ). The major scientific bodies mentioned above have also recognized that there are differences in toxicity and/or carcinogenic potential across the different nickel compounds. In this inhalat ion risk assessment, to take a conservative approach, we have considered all nickel compounds to be as carcinogenic as nickel subsulfide and have applied the IRIS URE for nickel subsulfide without a factor to reflect the assumption that 100 percent of the total mass of nickel may be as carcinogenic as pure nickel subsulfide. In addition, given that there are two additional URE values 13 derived for exposure to mixtures of nickel compounds, as a group, that are 2
- 3 fold lower than the IR IS URE for nickel subs ulfide, the EPA also considers it reasonable to use a value that is 50 percent of the IRIS URE for nickel subsulfide for providing an estimate of the lower end of the plausible range of cancer potency values for different mixtures of nickel compounds. 6) 

### For 3 carcinogenic substances, ( captan, i sophorone and p ropylene dichloride ) that lack inhalation assessments from the sources evaluated in this document , oral carcinogenic potency

estimates were converted to inhalation UREs. The conversion from oral risk (pe r mg/kg/d oral intake) to inhalation risk ( per μ g/m 3 

### inhaled) was based on EPA’s standard assumptions of a 70
- kg body m ass and 20 m 3 

### /d inhalation rate, as follows:

Where: URE = Unit risk estimate for inhalation (risk per μ g/m 3 

### )

CPS = Carcinogenic potency slope for ingestion (risk per mg oral intake per kg body

mass per day) EPA understands that conversion of oral dose
- response information to inhalation exposure ma y add significant uncertainty to the resulting risk estimates
. However,

12 Grim srud TK and Andersen A. Evidence of carcinogenicity in humans of water
- soluble nickel salts. J Occup Med Toxicol 2010, 5:1
- 7. Available online at http://www.ossup
- med.com/content/5/1/7. 13 Two UREs (other than the current IRIS values) have been derived for nickel compounds as a group : one developed by the California Department of Health Services ( http://www.arb.ca.gov/toxics/id/summary/nickel_tech_b.pdf ) and the other by the Texas Commission on Environmental Q uality ( http://www.epa.gov/ttn/atw/nata1999/99pdfs/healtheffectsinfo.pdf ). 

##                             

        

 g mg d m kg d kg mg CPS m g URE   1000 1 20 70 1 3 1 1 3**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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18 

### the alternative to this would have been to omit these substances from quantitative inhalation risk estimates altogether, thereby making a de facto assumption of zero carcinogenic potency
. For the purposes of the residual risk assessment, EPA prefers to use the approach described above to screen these carcinogens for their potential contributions to risk. If a substance is determined to be a potentially important contributor to risk, it wil l be prioritized for further dose
- response development through EPA’s IRIS process
. The emissions inventory

for the source categories in this risk document includes emissions of HAP with available chronic quantitative inhalation dose
- response values. Th ese HAP, their dose
- response values, and the source of the values are listed in Tables 2.6
- 1 (a) and (b ). **Table 2.6 -**  **1 (a) Dose -**  **Response Values for Chronic Inhalation Exposure to Carcinogens**  URE (unit risk estimate for cancer) 14 = cancer risk per μg/m 3 of average lifetime exposure. Sources: IRI S = EPA Integrated Risk Information Sy stem, EPA OAQPS = interim value recommended b y the EPA Office of Air Quality Planning & Standards, CAL= California EPA Office of Environmental Health Hazard Assessment , Conv . Oral = Oral unit risk converted to inhalation. **Pollutant CAS**  **Number 15**  **URE 7** 

**(1/μg/m 3**  **) Source**  1,1,2 - Trichloroethane 79005 0.000016 IRIS 1,3 - Butadiene 106990 0.00003 IRIS 1,3 - Dichloropropene 542756 0.000004 IRIS 1,4 - Dichlorobenzene 106467 0.000011 CAL 1,4 - Dioxane 123911 0.0000077 CAL 2,4,6 - Trichlorophenol 88062 0.0000031 IRIS 2,4 - T oluene diisocyanate 584849 0.000011 CAL 4,4'
- Methylenedianiline 101779 0.00046 CAL Acetaldehyde 75070 0.0000022 IRIS Acrylonitrile 107131 0.000068 IRIS Aniline 62533 0.0000016 CAL Arsenic compounds 7440382 0.0043 IRIS Benzene 16 71432 0.0000078 IRIS Benzyl c hloride 100447 0.0 00049 CAL

14 The URE is 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. URE’s are considered upper bound estimates meaning they represent a plausible upper limit to the true value. 15 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. 16 The EPA IRIS assessment for benzene provides a range of plausible UREs. This assessment used the highest value in that range, 7.8E
- 06 per ug/m 3 . The low end of the range is 2.2E
- 06 per ug/m 3

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19 **Table 2.6 -**  **1 (a) Dose -**  **Response Values for Chronic Inhalation Exposure to Carcinogens**  URE (unit risk estimate for cancer) 14 = cancer risk per μg/m 3 of average lifetime exposure. Sources: IRI S = EPA Integrated Risk Information Sy stem, EPA OAQPS = interim value recommended b y the EPA Office of Air Quality Planning & Standards, CAL= California EPA Office of Environmental Health Hazard Assessment , Conv . Oral = Oral unit risk converted to inhalation. **Pollutant CAS**  **Number 15**  **URE 7** 

**(1/μg/m 3**  **) Source**  Beryllium compounds 7440417 0.0024 IRIS Bis(2
- ethylhexyl)phthalate 117817 0.0000024 CAL Bromoform 75252 0.0000011 IRIS Cadmium compounds 7440439 0.0018 IRIS Captan 133062 0.000001 Conv. Oral Carbon t etrachloride 56235 0.000006 IRIS Chromium (VI) compounds 18540299 0.012 IRIS Dichloroethyl e ther 111444 0.00033 IRIS Epichlorohydrin (1
- Chloro
- 2,3 - e poxypropane) 106898 0.0000012 IRIS Ethyl b enzene 100414 0.0000025 CAL Ethylene dichloride 107062 0.000026 IRIS Ethylene o xide 75218 0.000088 CAL Formaldehyde 17 50000 0.000013 IRIS Hexachlorobenzene 118741 0.00046 IRIS Hexachloroethane 67721 0.000004 IRIS Hydrazine 302012 0.0049 IRIS Isophorone 18 7859 1 0.00000027 Conv. Oral Methyl tert
-butyl e ther 1634044 0.00000026 CAL Methylene c hloride 75092 0.00000047 IRIS Naphthalene 91203 0.000034 CAL Nickel compounds 7440020 0.00048 EPA OAQPS o - Toluidine 95534 0.000051 CAL Polychlorinated b iphenyls 1336363 0.0001 IR IS Polycyclic Organic Matter 19 (POM) 2 - Methylnaphthalene 91576 0.000088 CAL Fluoranthene 206440 0.000088 CAL Fluorene 86737 0.000088 CAL Phenanthrene 85018 0.000088 CAL Pyrene 129000 0.000088 CAL

17 The EPA has used the CII T URE value, 5.5X10 - 9 per mg/m 3 , to characterize formaldehyde cancer risk in some instances. 18 No inhalation unit risk estimates were available for this compound. T herefore we c onverted from an IRIS oral potency slope of 0.00095 per mg/kg/d. UREs that are converted from the oral route to the inhalation route of exposure are considered highly uncertain, and are only used in cases where no other URE is available. 19 Assigned the URE associated with a mixture of POM compounds having a similar potency. Details of this method, also used in the National Air Toxics Assessments, are available at http://www.epa.gov/nata2002/methods.html#pom**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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20 **Table 2.6 -**  **1 (a) Dose -**  **Response Values for Chronic Inhalation Exposure to Carcinogens**  URE (unit risk estimate for cancer) 14 = cancer risk per μg/m 3 of average lifetime exposure. Sources: IRI S = EPA Integrated Risk Information Sy stem, EPA OAQPS = interim value recommended b y the EPA Office of Air Quality Planning & Standards, CAL= California EPA Office of Environmental Health Hazard Assessment , Conv . Oral = Oral unit risk converted to inhalation. **Pollutant CAS**  **Number 15**  **URE 7** 

**(1/μg/m 3**  **) Source**  Propylene d ichloride 20 78875 0.000019 Conv. Oral Propylene oxide 75569 0.0000037 IR IS Tetrachloroethylene 127184 0.0000059 CAL Trichloroethylene 79016 0.000002 CAL Vinyl c hloride 75014 0.0000088 IRIS **Table 2.6 -**  **1 (b) Dose -**  **Response Values for Chronic Inhalation Exposure to Noncarcinogens**  RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRI S = EPA Integrated Risk Information Sy stem, CAL= California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry , HEAST = EPA Health Effects Assess ment Tables , EPA OAQPS = EPA Office of Air Quality Planning & Standards **Pollutant CAS Number**  **8 RfC**  **(mg/m 3**  **) Source**  **21** 1,1,1 - Trichloroethane (methyl chloroform) 71556 5 IRIS
- M 1,2 - Epoxybutane 10688 7 0.02 IRIS
- M 1,3 - Butadiene 106990 0.002 IRIS
- M 1,3 - Dichloropropene 54275 6 0.02 IRIS
- H 1,4 - Dichlorobenzene 106467 0.8 IRIS
- M 1,4 - Dioxane 12391 1 3.6 ATSDR 2,4 - Toluene diisocyanate 58484 9 0.00007 IRIS
- M 4,4'
- Methylenedianiline 10177 9 0.02 CAL Acetaldehyde 75070 0.009 IRIS
- L Acrolein 107028 0.00002 IRIS
- M Acrylic a cid 79107 0.001 IRIS
- M

20 No inhalation unit risk estimates were available for this compound. T herefore we c onverted from a oral potency slope of 0.068 per mg/kg/d. UREs that are converted from the oral route to the inhalation route of exposure are considered highly uncertain, and are only used in cases where no other URE is av ailable. 21 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 IRIS.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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21 **Table 2.6 -**  **1 (b) Dose -**  **Response Values for Chronic Inhalation Exposure to Noncarcinogens**  RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRI S = EPA Integrated Risk Information Sy stem, CAL= California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry , HEAST = EPA Health Effects Assess ment Tables , EPA OAQPS = EPA Office of Air Quality Planning & Standards **Pollutant CAS Number**  **8 RfC**  **(mg/m 3**  **) Source**  **21** Acrylonitrile 10713 1 0.002 IRIS
- M Aniline 6253 3 0.001 IRIS
- L Antimony c om

pounds 7440360 0.0002 IRIS
- L Arsenic c ompounds 7440382 0.000015 CAL Benzene 71432 0.03 IRIS
- M Beryllium c om

pounds 7440417 0.00002 IRIS
- M Bis(2
- ethylhexyl)phthalate 11781 7 0.01 CAL Cadmium c ompounds 7440439 0.00001 ATSDR Carb on t etrachloride 56235 0.1 IRIS
- M Chlorine 7782505 0.00015 ATSDR Chlorobenzene 108907 1 CAL Chloroform 67663 0.098 ATSDR Chromium (VI) compounds 18540299 0.0001 IRIS
- M Cresol s (mixed) 1319773 0.6 CAL Cumene 98828 0.4 IRIS
- M Cyanide & Cyanide Compounds Cyanide compounds 22 57125 0.003 IRIS
- L Hydrogen cyanide 74908 0.003 IRIS
- L Diethanolamine 111422 0.003 CAL Epichlorohydrin (1
- Chloro
- 2,3 - e poxypropane ) 10689 8 0.001 IRIS
- M Ethyl b enzene 100414 1 IRIS
- L Ethyl chloride 7500 3 10 IRIS
- M Ethylene dichloride 107062 2.4 ATSDR Ethylene g lycol 107211 0.4 CAL Ethylene o xide 75218 0.03 CAL Formaldehyde 50000 0.0098 ATSDR Glycol Ethers 23 2 - (Hexyloxy)e thanol 11225 4 0.02 IRIS
- M 2 - Butoxyethyl a cetate 11207 2 0.02 IRIS
- M Butyl Carbitol a cetate 12417 4 0.02 IRIS
- M Diethylene glycol monobutyl ether 11234 5 0.02 HEAST
22 The value for hydrogen cyanide was used as a surrogate for all cyanide compounds without an RfC. 23 The RfC value for ethylene glycol methyl ether was used as a surrogate for all glycol ethers without an RfC.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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22 **Table 2.6 -**  **1 (b) Dose -**  **Response Values for Chronic Inhalation Exposure to Noncarcinogens**  RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRI S = EPA Integrated Risk Information Sy stem, CAL= California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry , HEAST = EPA Health Effects Assess ment Tables , EPA OAQPS = EPA Office of Air Quality Planning & Standards **Pollutant CAS Number**  **8 RfC**  **(mg/m 3**  **) Source**  **21** Diethylene glycol monoethyl ether 11190 0 0.02 IRIS
- M Ethoxytriglycol 11250 5 0.02 IRIS
- M Ethylene glycol ethyl ether 11080 5 0.2 IRIS
- M Ethylene glycol methyl ether 10986 4 0.02 IRIS
- M Glycol e thers 171 0.02 IRIS
- M Methoxytriglycol 11235 6 0.02 IRIS
- M Propyl c ellosolve 280730 9 0.02 IRIS
- M Triglycol monobutyl ether 14322 6 0.02 IRIS
- M Hexachlorobenzene 11874 1 0.003 CAL Hexachloroethane 67721 0.08 CAL Hexane 11054 3 0.7 IRIS
- M Hydrazine 302012 0.0002 CAL Hydrochloric a cid (hydrogen chloride) 7647010 0.02 IRIS
- L Hydrof luori c acid (hydrogen fluoride) 766439 3 0.014 CAL Isophorone 7859 1 2 CAL Lead compounds 743992 1 0.00015 EPA OAQPS Maleic anhydride 10831 6 0.0007 CAL Manganese c ompounds 7439965 0.00005 IRIS
- M Methanol 67561 4 CAL Methyl b romide 74839 0.005 IRIS
- H Methyl c hloride 74873 0.09 IRIS
- M Methyl isobutyl ketone 108101 3 IRIS
- L/M Methyl isocyanate 62483 9 0.001 CAL Methyl m ethacrylate 80626 0.7 IRIS
- M/H Methyl tert
-butyl e ther 1634044 3 IRIS
- M Methylene c hloride 75092 1 ATSDR Naphthalene 91203 0.003 IRIS
- M Nickel c ompounds 7440020 0.00009 ATSDR Phenol 108952 0.2 CAL Phosgene 7544 5 0.0003 IRIS
- M Phthalic anhydride 8544 9 0.02 CAL Propionaldehyde 123386 0.008 IRIS

– L/M Propylene d ichloride 78875 0.004 IRIS
- M**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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23 **Table 2.6 -**  **1 (b) Dose -**  **Response Values for Chronic Inhalation Exposure to Noncarcinogens**  RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRI S = EPA Integrated Risk Information Sy stem, CAL= California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry , HEAST = EPA Health Effects Assess ment Tables , EPA OAQPS = EPA Office of Air Quality Planning & Standards **Pollutant CAS Number**  **8 RfC**  **(mg/m 3**  **) Source**  **21** Propylene oxide 7556 9 0.03 IRIS
- M Selenium c ompounds 7782492 0.02 CAL Styrene 100425 1 IRIS
- M Tetrachloroethylene 12718 4 0.27 ATSDR Titanium tetrachloride 755045 0 0.0001 ATSDR Toluene 108883 5 IRIS
- H Trichloroethylene 79016 0.6 CAL Triethylamine 12144 8 0.007 IRIS
- L Vinyl a cetate 108054 0.2 IRIS
- H Vinyl c hloride 75014 0.1 IRIS
- M Xylenes (mixed) 1330207 0.1 IRIS
- M m - Xylene 1 8 108383 0.1 IRIS
- M o - Xylene 24 95476 0.1 IRIS
- M p - Xylene 1 8 106423 0.1 IRIS
- M
**2.6.2. Sources of acute dose**  **- response information**  Hazard identification and dose
- response assessment information for preliminary acute inhalation exposure assessments are based on the existing recommendations of OAQPS for HAPs [ 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 (REL s), as well as emergency respons e levels, such as Acute Exposure Guideline Levels (AEGLs) and Emergency Response Planning Guidelines (ERPGs), with the recognition that the ultimate interpretation of an y potential risks associated with an estimated exceedance of a particular reference lev el depends on the definition of that level and an y limitations expressed therein. Comparisons among different available inhalation health effect reference values (both acute and chronic) for selected HAPs can be found in an EPA document [ 19 ]. **California A cute Reference Exposure Levels (RELs**  **).** The California Environmental Protection Agency

(CalEPA) has developed acute dose
- response reference values for man y substances, expressing the results as acute inhalation Reference Exposure Levels (RELs).
24 The RfC for mixed xylene was used as a surrog ate.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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24 The acut e 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 [ 20 ] . REL s are based on the most sensitive, relevant, adverse health effect reported in the medical and toxicological literature. RELs are designed to protect the most sensitive individuals in the population by the inclusion of margins of safet y. Since margins of safet y are incorporated to address data gaps and uncertainties, exceeding the RELdoes not automatically indicate an adverse health impact. ” Acute REL s are developed for 1
- hour (and 8
- hour) exposures. The values incorporate uncertaint y factors similar to those used in deriving EPA’s Inhalation Reference Concentrations (RfCs) for chronic exposures (and, in fact, California also has developed chronic RELs). **Acute Exposure Guideline Levels (AEGLs** ). AEGL s are developed by the National Advisory Committee (NAC) on Acute Exposure Guideline Levels (NAC/AEGL) f or Hazardous Substances , and then reviewed and published b y 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 conductin g 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 document states that “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 acutel y toxic, high
- priority chemicals.” In detailing the intended application of AEGL values, the document states , “ Itis anticipated that the AEGL values will be used for regulatory

and nonregulatory

purposes by

U.S. Federal and State agencies, and possibly the international community in conjunction with chemical emergency response, plann ing, 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 (expressed 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 asy mptomatic nonsensory

effects. However, the effects are not disabling and are transi ent 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 o ther serious, long
- lasting adverse health effects or an impaired ability to escape. ”**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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25 “ Airborne concentrations below AEGL
- 1 represent exposure levels that can produce mild and progressivel y increasing but transient and nondisabling odor, taste, and sensory irritation or certain as ymptomatic, 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 corresponding 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, subject to unique or i diosy ncratic responses, could experience the effects described at concentration s below the corresponding AEGL.” **Emergency Response Planning Guidelines (ERPGs).** The American Industrial Hygiene Association (AIHA) has developed Emergency Response Planning Guidelines (ERPGs) [ 21 ] 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 effects 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 concentrations for single exposures to chemicals. These guide lines (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 emergency planning and for developing community emergency

respo nse 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 AI HA as follows:

“ ERPG
- 1 is the maximum airborne concentration below which it is believed that nearl y 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, objectionab le odor. ”

“ ERPG
- 2 is the maximum airborne concentration below which it is believed that nearl y all individuals could be exposed for up to 1 hour without experiencing or developing irreversible or other serious health effects or s ymptoms which could impai r an individual's ability to take protective action. ” The emissions inventory

for the source categories in this risk document includes emissions of HAP with relevant and available quantitative acute dose
- response threshold values. These HAP, their acute threshold values, and the source of the value are listed below in Table 2.6 - 2.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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26

**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**

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

**(1 -**  **hr) (mg/m**  **3 )**  **REL** 1,1,1 - Trichloroethane (methyl chloroform) 7155 6 1300 3300 1900 3800 68 1,2 - Epoxybutane 10688 7 210 410 1,3 - Butadiene 10699 0 1500 12000 22 440 1,4 - Dioxane 12391 1 61 1200 3 2,4 - Toluene diisocyanate 58484 9 0.14 0.59 0.071 1.1 Acetaldehyde 75070 81 490 18 360 0.47 Acetonitrile 7505 8 22 540 Acrolein 107028 0.069 0.23 0.11 0.34 0.0025 Acrylic a cid 79107 4.4 140 3 150 6 Acrylonitrile 10713 1 10 130 22 77 Aniline 6253 3 30 46 Arsenic compounds 744038 2 0.0002 Benzene 71432 170 2600 160 480 1.3 Benzyl chloride 10044 7 5.2 52 0.24 Beryllium c om

pounds 7440417 0.025 Biphenyl 92524 61 Carbon t etrachloride 56235 280 1200 130 630 1.9 Chlorine 7782505 1.5 5.8 2.9 8.7 0.21 Chloroacetic a cid 79118 26 Chlorobenzene 108907 46 690 Chloroform 67663 310 240 0.15 Chloromethyl methyl ether 10730 2 1.6 3.3 Cumene 98828 250 1500 Hydrogen cyanide 7490 8 2.2 7.8 11 0.34 Dimethyl formamide 6812 2 270 6 300 Dimethyl sulfate 7778 1 0.12 0.62 Epichlorohydrin ( 1 - Chloro
- 2,3 - e poxypropane) 106898 22 91 19 76 1.3 Ethyl a crylate 140885 34 150 0.041 120 Ethyl b enzene 100414 140 4800 Ethylene dichloride 107062 200 810 Ethylene o xide 75218 81 90 Formaldehyde 50000 1.1 17 1.2 12 0.055 Glycol Ethers 25 2 - ( Hexyloxy)e thanol 112 25 4 0.093 2 - Butoxyethyl a cetate 11207 2 0.093
25 The acute REL for ethylene glycol methyl ether was used as a surrogate for glycol ether compounds without an acute REL.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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27

**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**

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

**(1 -**  **hr) (mg/m**  **3 )**  **REL** Butyl carbitol a cetate 12417 4 0.093 Ethoxytriglycol 11250 5 0.093 Ethylene glycol ethyl ether 11080 5 0.37 Ethylene glycol methyl ether 10986 4 0.093 Glycol ethers 171 0.093 Methoxytriglycol 11235 6 0.093 Propyl c ellosolve 280730 9 0.093 Triglycol monobutyl ether 14322 6 0.093 Hexane 110543 12000 Hydrazine 302012 0.13 17 0.65 6.5 Hydrochloric a cid 7647010 2.7 33 4.5 30 2.1 Hydrogen f

luoride 7664393 0.82 20 1.6 16 0.24 Maleic anhydride 10831 6 0.8 8 Methanol 67561 690 2700 260 1300 28 Methyl b romide 74839 820 190 3.9 Methyl c hloride 74873 1900 830 Methyl hydrazine 6034 4 3.2 Methyl isocyanate 62483 9 0.16 0.058 0.6 Methyl m ethacrylate 80626 70 490 Methyl tert
-butyl e ther 1634044 180 2100 Methylene c hloride 75092 690 1900 1000 2600 14 Nickel c ompounds 7440020 0.006 Phenol 108952 58 89 38 190 5.8 Phosgene 7544 5 1.2 2 0.004 Propionaldehyde 123386 110 620 Propylene oxide 7556 9 170 690 120 1100 3.1 Styrene 100425 85 550 210 1100 21 Tetrachloroethylene 127184 240 1600 680 1400 20 Titanium tetrachloride 755045 0 0.54 7.8 5 20 Toluene 108883 750 4500 190 1100 37 Trichloroethylene 79016 700 2400 540 2700 Triethylamine 12144 8 2.8 Vinyl a cetate 108054 24 630 18 260 Vinyl c hloride 75014 640 3100 1300 13000 180 Xylenes (mixed) 1330207 560 4000 22 m - Xylene 26 108383 22 o - Xylene 20 95476 22 p - Xylene 20 106423 22

26 The REL for mixed xylenes was used as a surrogate.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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28 

### 2.7. **Risk Characterization 2.7.1.**  **General** The final product of the risk assessment is the risk characterization, in which the information from the previous steps is integrated and an overall conclusion about risk is sy nthesized 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 [ 22 ] 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 [ 23 ], in 2002 by the Agency ’s information quality guidelines [ 24 ], and in the OMB/OST P September 2007 Memorandum on Updated Principles for Risk Analy sis 27 , 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 analy tical approach, we have attempted to reduce both uncertainty

and 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 individua l 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 multiplying the corresponding lifetime average exposure estimate by the appropriate URE. This calculated canc er 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 estimated , and could be zero. For EPA’s list of carcinogenic HAPs that act b y a mutagenic mode
- of
- action [ 25 ], we applied EPA’s Supplemental Guidance for Assessing Susceptibility from Early
- Life Exposure to Carcinogens [ 26] . This guidance has the effect of adjusting the URE by factors of 10 (for children aged 0
- 1), 3 (for children aged 2
- 15), or 1.6 (for 70 ye ars of exposure beginning at birth), as needed in risk assessments . In this case, this has the effect of increasing the

27 Memorandum f

or the Heads o f Executive Departments and Agencies
- Updated Pr inciples 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 Deputy Director for Science, Office of Science and Technology Policy ( http://www.whitehouse.gov/omb/memoranda/fy2007/m07
- 24.pdf )**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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29 estimated life time risks for these pollutants by a factor of 1.6. Inaddition, although onl y a small fraction of the total POM emissions may be reported as individual compounds, EPA expresses carcinogenic potency for 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]py rene. For this reason , EPA implem entation policy [ 27] recommends appl yi ng the Supplemental Guidance to all carcinogenic PAH s for which risk estimates are based on relative potency . Accordingl y, we applied the Supplemental Guidance to all unspeciated POM mixtures. In creased cancer incidence for the entire receptor population within the area of anal ys is wa s estimated by

multip lying the estimated 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 y ears to obtain an estimat e of the number of cancer cases per ye ar. In the case of benzene, the high end of the reported cancer URE range was used in our assessments to provide a conservative estimate of potential cancer risks. Use of the high end of the range provides risk estim ates that are approximately 3.5 times higher than use of the equally plausible low end value. If the estimated benzene

– associated risks exceed 1 in a million, we also evaluate d the impact of using the low end of the URE range on our risk results. 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 likel y to cause adverse health effects. As exposures increase above the reference lev el (HQs increasingl y greater than 1), the potential for adverse effects increases. For exposures estimated 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., hi gh, 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 blo ck 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 effects. 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 if there is a potential for significant acute risks.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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30 **2.7.2. Mixtures**  Since most or all receptors in these assessments receive exposures to multiple pollutants r ather than a single pollutant, we estimated the aggregate health risks associated with all the exposures from a particular source category combined. To combine risks across multiple carcinogens, our assessments use the mixtures guidelines’ [ 28 , 29 ] default a ssumption 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 completel y different modes of action, it may be inappropriate to aggregate HQs. In consideration of these mode
- of
- action differences, the mixtures guidelines support aggregating effects of different substances in specific and limited way s. To conform to the se guidelines, we aggregated non
- cancer HQs of HAP 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 HAP 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
. B ecause impacts 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**  **- wide Risks**  T o help place the source category risks in context, we examined “facility
- wide” risks using 2005 NEI data and modeling as described in Section 2.2. For the facilities in these source categories, we estimated the maximum inhalation cancer and chronic noncan cer risks associated with all HAP emissions sources at the facility , including emissions sources that are not part of the source categories but are located within a contiguous area and are under common control. We analyzed risks due to the inhalation of H AP for the populations residing within 50 kilometers of each facility . The results of these facility
- wide assessments are summarized below in the Risk Characterization sections of this document. The complete results of the facility
- wide assessments are p rovided in Appendix 4 .**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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31 **2.7.4. MA**  **CT -**  **Al lowable Risks**  The emissions data in the data sets for these seven source categories are estimates of actual emissions on an annual basis. The risk results presented in the following sections are based on these actual emiss ions. For these seven source categories, the MACT
- allowable emissions are estimated to be equivalent to the actual emissions except for certain emission sources
. See the memo randum titled “ MACT Allowable Emissions and Risks for the Pesticide Active In gre dient (PAI), Poly ether Polyols, and Pol ym ers and Resins IV Production Source Categories ” available in the docket for this action. Therefore, except for certain sources, the risks based on MACT
- allowable emissions would be equivalent to the actual risks pr esented below. See the source category risk characterization sections and the memorandum MACT
Allowable Emissions and Risks for the Pesticide Active Ingredient, Poly ether Polyols, and Poly mers and Resins IV Production Source Categories (available in the d ocket for this action) for details on the MACT
- allowable risk. 

### 3. **Risk Results for Pesticide A ctive Ingredient Manufacturing**  **3.1 Source Category**  **Description and Results** The pesticide active ingredient (PAI) production source category consists of major source facilities that manufacture active ingredients in insecticides, herbicides, fungicides, an d related products. The HAP emission sources at PAI production facilities include storage vessels, process vents, equipment leaks, wastewater s ys tems, heat exchange sy stems, and bag dumps and product dry ers. The primary HAP emitted by

these facilities include toluene, methanol, methylene chloride, and hydrochloric acid, but numerous other organic HAP, chlorine, cyanide compounds, metal compounds, and hydrogen fluorid e are also emitted. A complete description of the pesticide active ingredient production source category can be found in the text of the NPRM. We currentl y estimate that there are 17 pesticide active ingredient production facilities operating in the U.S. The data set contains all 17 facilities identified with a pesticide active ingredient production MACT code in the 2005 NEI . The 2005 NEI was updated for this category with more recen t data from industry and enhanced quality

assurance of facility

and emission locations. All 17 of these facilities are identified as major sources in the NEI. The emissions for the pesticide active ingredient production source category data set (of 1 7 facilities) are summarized in Table 3.1 - 1 . The total HAP emissions for the source category are approximately

350 tons per y ear. Based on these data, the HAP emitted in the largest quantities across these 17 facilities are: toluene, methanol, methylene chloride, hydrochloric acid, meth yl isobut yl ketone, ethylene gl ycol ethyl ether (a.k.a. cellosolve solvent), hexane, chlorine, formaldeh yde, tetrachloroeth yl ene, x yl enes (mixed), triethylamine, trichloroeth yl ene, and ethylene glycol. These 1 4 HAP account for 9 0 percent of the total emissions by

mass. Persistent and bioaccumulative HAP (PB
- HA P) 28 in the data set for the
28 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Volume 1, EPA
- 453K - 04 - 001A, as referenced in the ANPRM and provided on the EPA’s Technology Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html
.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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32 pesticide active ingredient production source category include lead compounds , hexachlorobenzene, and polychlorinated biphenyls (PCBs). 29 **Table 3.1 -**  **1 Summary of Emissions from the Pesticide Active Ingredients Source Category**  **and Availability of Dose -**  **Response Values**

**HAP a**  **Emissions (tpy)**  **Number of**

**Facilities Reporting**  **HAP (**  **1 7**  **facilities in data set)**  **Prioritized Inhalation Dose -**  **Response Value Identified by OAQPS**  **b PB**  **- HAP?**  **Unit Risk Estimate for**  **Cancer? Reference** 

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

**Benchm ark**  **Values for Acute Noncancer?**  Toluene 79 7   Methanol 58 12   Methylene chloride 40 5    Hydrochloric Acid 3 3 10   Methyl Isobutyl Ketone 21 3  Glycol Ethers Ethylene glycol ethyl ether (Cellosolve) 17 1   Ethylene glycol methyl ether 0.5 1   Glycol Ethers 0.01 1   Hexane 16 5   Chlorine 1 1 7   Formaldehyde 10 4    Tetrachloroethylene 6 5    Xylenes (Mixture of o, m, and p Isomers) 6 7   Triethylamine 5 5   Trichloroethylene 5 2    Ethylene Glycol 4 5  Ethylene dichloride 3 3    Phenol 3 3   Chloroform 3 6   Naphthalene 3 4   Chlorobenzene 2 4   m - Xylene 2 1   Carbon tetrachloride 2 5    o - Xylene 2 1   Ethyl Benzene 2 4    Benzene 2 6    Ethyl chloride 1 4  Phosgene 2 4 0.8 4  

29 After the risk assessment was completed, we learned that the emissions of hexachlorobenzene in the data set for polyether polyols production should have been assigned to the pesticide active ingredient MACT code. We will update the data set with this information, and any additional information received during the comment period, before the final rule.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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33 **Table 3.1 -**  **1 Summary of Emissions from the Pesticide Active Ingredients Source Category**  **and Availability of Dose -**  **Response Values**

**HAP a**  **Emissions (tpy)**  **Number of**

**Facilities Reporting**  **HAP (**  **1 7**  **facilities in data set)**  **Prioritized Inhalation Dose -**  **Response Value Identified by OAQPS**  **b PB**  **- HAP?**  **Unit Risk Estimate for**  **Cancer? Reference** 

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

**Benchm ark**  **Values for Acute Noncancer?**  Methyl bromide 0.8 2   1,4 - dioxane 0.8 1    N,N’
- dimethylaniline 0.8 1 1,3 - butadiene 0.7 2    Cy anide Compounds Hydrogen Cyanide 0.6 2   Cy anide & Compounds 0.3 2  Acetonitrile 0.5 4   Methyl Chloride 0.5 3   Captan 0.5 1  Carbaryl 0.4 1 Aniline 0.4 1    Acrylonitrile 0.2 2    Methyl isocyanate 0.2 2   Biphenyl 0.2 2  Isophorone 0.1 1   Dim ethyl formamide 0.1 2   Acetaldehyde 0.1 2    1,1,1 - Trichloroethane 0.08 2   Benzyl chloride 0.07 2   Lead & Compounds 0.04 1 c  Cumene 0.04 3   Arsenic & Compounds (Inorganic Including Arsine) 0.04 1 30    Nickel & Compounds 0.04 1    Propionaldehyde 0.04 1   Acrolein 0.03 1   Titanium tetrachloride 0.02 1   Methyl hydrazine 0.02 1  Vinyl Chloride 0.02 1    Hydrazine 0.009 1    Propoxur 0.009 1

30 After the risk assessment was completed, we learned that the arsenic emissions should not be part of the data set and that the phosgene emissions were incorrect. Additionally, we learned that the emissions of h exachlorobenzene in the data set for PEPOs production should have been assigned to the PAI MACT code. The arsenic emissions from the facility, Bayer Crop Science in WV (NEIWV0390007), are still included in the emissions summary and the emissions of hexach lorobenzene are still attributed to the PEPOs source category, but risk results have been removed from the risk summary. Also, w e learned that the emissions of phosgene were incorrect for facility NEI8596 and are much lower than in our reported data. We will update the data set with this information, and any additional information received during the comment period, before the final rule.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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34 **Table 3.1 -**  **1 Summary of Emissions from the Pesticide Active Ingredients Source Category**  **and Availability of Dose -**  **Response Values**

**HAP a**  **Emissions (tpy)**  **Number of**

**Facilities Reporting**  **HAP (**  **1 7**  **facilities in data set)**  **Prioritized Inhalation Dose -**  **Response Value Identified by OAQPS**  **b PB**  **- HAP?**  **Unit Risk Estimate for**  **Cancer? Reference** 

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

**Benchm ark**  **Values for Acute Noncancer?**  Hexachlorobenzene 2 4 0.006 2   1,3 - Dichloropropene 0.006 1   Maleic anhydride 0.00 5 1   Bromoform 0.004 1  Methyl tert
- butyl ether 0.004 1    Hexachloroethane 0.003 2   Styrene 0.002 1   Beryllium & Compounds 0.002 1    Methyl methacrylate 0.002 1   Hydrogen Fluoride 0.002 1   Vinyl acetate 0.0008 1   Polychlorinated Biphenyls 0.00004 1  

a Notes for how HAP were speciated for risk assessment:  For most metals, emissions reported as the elemental metal are combined with metal compound emissions (e.g., “cadmium” emissions modeled as “cadmium & compounds”). In the absence of speciation information, we assume the reported mass is 100 percent metal.  For emissions reported generically as “Glycol Ethers” or specific glycol ethers not found on EPA’s Technology Transfer network for air toxics (see fo otnote b), emissions will be treated as ethylene glycol methyl ether. b Specific dose
- response values for each chemical are identified on EPA’s Technology Transfer Network website for air toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html . c There is no reference concentration for lead. In considering noncancer hazards for lead in this assessment, we compared maximum annual ambi ent exposure estimates to the National Ambient Air Quality Standards (NAAQS) for lead (0.15 μg/m3 ). These NAAQS for lead were reviewed with revisions adopted in October 2008 ( http://www.epa.gov/air/lead/actions.html ). The primary (health
- based) standard is a maximum or not
- to - be
- exceeded, rolling three
- month average, measured as total suspended particles (TSP). The secondary (welfare
- based) standard is identical to the primary standard. 

### 3.2 **Risk Characterization** This section presents the results of the risk assessment for the pesticide active ingredient production source category . The basic chronic inhalation risk estimates presented here are the maximum individual lifetime ca ncer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients, as well as the results of our preliminary screen for potential non
inhalatio n risks from PB
- HAP. Also presented are the HAP “drivers,” which are the HAP that collectively

contribute 90 percent of the maximum cancer risk or maximum hazard index at the highest exposure location , as well as a summary of the results of our facility
- w ide assessments and our analy sis of risks associated with the maximum allowed emissions under the current MACT standards. A detailed summary of the facility
- specific risk assessment results is available in Appendix 4 .**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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35 Table s 3 .2 - 1 and 3.2
- 2 summarize the chronic and acute inhalation risk results for this source category . The results for the p esticide a ctive i ngredient m anufacturing source category indicate that maximum lifetime individual cancer risks could be as high as 7 in a million. The major co ntributor s to this risk are naphthalene and nickel compounds
. 31 Approximately 11,000 people (this does not reflect the updated emissions information received after the risk modeling was done) were estimated to have cancer risks above 1 in a million as a re sult of the emissions from 6 facilities . The maximum chronic non
- cancer target organ specific hazard index ( TOSHI ) value for the source category could be up to 0.7 associated with emissions of chlorine , indicating no significant potential for chronic noncancer impacts. Worst - case a cute HQs were calculated f or every emitted HAP that has an acute benchmark
. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that might occur outside facility boundaries. Anal ys is of potential off

- site impacts for the PAI source category identified four facilities with the potential to exceed the acute REL for s ix pollutants (ethylene gl ycol eth yl ether (one facility) , acrolein (one facility) , chloroform (one facility) , nickel compounds (one facility) , chlorine (one facility) , and formaldehyde (one facility) ) . One facilit y has HQs greater than 1 for three pollutants: ethylene gl yc ol ethyl ether , acrolein, and nickel compounds. Table 3.2
- 2 provides more information on the acute risk estimates for HAP that had an acute HQ greater than 1 for any benchmark. The highest refined worst
- case acute HQ value is 8 (based on the ethylene gl ycol eth yl ethe r REL). 32 All other HAP emissions at all other facilities indicated no potential to cause acute impacts of concern. While these estimated worst
- case exceedances indicate that there is some potential for such acute exposures to occur, we note that exceed ing the modeled REL value does not necessarily

indicate that adverse effects will occur, only that they cannot be ruled out. Further, in characterizing the potential for acute noncancer impacts of concern, it is important to remember the upward bias of th ese worst - case exposure estimates and to consider the results along with the rather large uncertainties related to the emissions estimates and screening methodology
. In our refined screening anal ys is we adjusted the multiplier of 10 to 2 for emissions ass ociated with equipment leaks for one facilit y (see Appendix 7 of this document and the memorandum “Emission Data and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active In gredients, Poly ether Polyols, Poly mers and Resins IV” in the docket f or this action ). W e

31 After the risk assessment was completed, we learned that the arsenic emissions from the facility, Bayer Crop Scien ce in WV (NEIWV0390007), should not have been included in the data set for PAI production. The MIR for this facility based on the incorrect emissions in the risk modeling was 20 and the acute result was 80 (REL) associated with arsenic emissions. Arsenic wa s not emitted from any other facilities in the source category. We will update the data set with this information, and any additional information received during the comment period, before the final rule. 32 Additionally, we learned that the phosgene e missions at facility 01097NEI18596 w ere incorrect. Based on the emissions as modeled this facility had an acute value for phosgene of 4 for the REL. The emissions should have been 0.02tpy. With the smaller emissions the acute value is less than 1. We will update the data set with this information, and any additional information received during the comment period, before the final rule.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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36 reviewed 2 facilities with the highest HQ values and determined equipment leaks were primarily responsible for the high acute HQ values of 4 and 8 and that they were modeled assuming that they

all emanate from a single emission locatio n rather than from numerous phy sical locations throughout the processing area. We note that this assumption further biases the HQ values high, but to an unknown extent, given that we do not know the actual size of the processing areas at each of these fac ilities. Taking all of this into consideration, these acute impact screening results indicate only the potential for acute impacts of concern, while the uncertainties and bias associated with them suggest that there may be no real acute issues at all. We conducted a screening
- level evaluation of the potential human health risks associated with emissions of PB
- HAP. Reported emissions of PB
- HAP were compared to emission thresholds established by EPA for the purposes of the RTR risk assessments. 33 The PB
- HAP emitted from this category are lead , hexachlorobenzene, and polychlorinated biphenyls (PCBs). Lead is a PB
- HAP, but the National Ambient Air Quality Standards (NAAQS) value (which was used for the chronic noncancer risk assessment) takes into account multipathway exposures, so a separate multipathway screening value was not developed. Since we did not estimate an y exceedances of the NAAQS in our chronic noncancer risk assessment, we do not expect any

significant multipathway exposure and risk due to l ead emissions from these facilities. In addition, there is currentl y not a screening value for PCBs and they were not evaluated for potential non
- inhalation risks. We do not currentl y have a multipathway screening value for hexachlorobenzne and so it was not evaluated for potential non
- inhalation risks
. As shown in Table 3.1
- 1, these HAP are not emitted in appreciable quantities. 34

33 ICF International. TRIM
-Based Multipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, R esearch Triangle Park, NC. October 2008. 34 After the risk assessment was completed, we learned that the emissions of hexachlorobenzene in the data set for polyether polyols production should have been assigned to the pesticide active ingredient MACT code.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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37 **Table 3.2 -**  **1 Summary of Source Category Level Risks for Pesticide Active Ingredient**  **Production Result**  **HAP “Drivers” Facilities in**  **Source Category** Number of Facilities Estimated to be i n Source Category 17 n/a Number of Facilities Identified in NEI and Modeled in Preliminary Risk Assessment 17 n/a **Cancer Risks** Maximum Individual Lifetime Cancer Risk (in 1 million) 35 7 naphthalene, nickel compounds 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 0 n/a Greater than or equal to 1 in 1 million 6 naphthalene, nickel compounds, ethylene dichloride, acrylonitrile, formaldehyde, hydrazine, trichloroethylene, 1,4 - dioxane, 1,3
-butadiene **Chronic Noncancer Risks** Maximum Respiratory Hazard Index 0.7 chlorine Number of Facilities with Maximum Respiratory Hazard Index: Greater than 1 0 n/a **Acute Noncancer Refined Screening**  **Results** Maximum Acute Hazard Quotient 3 5 8 4 2 2 2 2 ethylene glycol ethyl ether (REL) acrolein (REL) nickel compounds (REL) chloroform (REL) chlorine (REL) formaldehyde (REL) Number of Facilities With Potential for Acute Effects 4 ethylene glycol ethyl ether, acrolein, nickel compounds, chlorine, chloroform , formaldehyde **Population Exposure 35**  Number of People Living Within 50 Kilometers of Facilities Modeled 14,000,000 n/a

35 After the risk assessment was completed, we learned that the arsenic emissions from the facility, Bayer Crop Science in WV (NEIWV0390007), should not have been included in the data set for PAI production. The MIR for this facility based on the incorr ect emissions in the risk modeling was 20 and the acute result was 80 (REL) associated with arsenic emissions. Arsenic was not emitted from any other facilities in the source category. We also learned that the emissions of phosgene were incorrect and are muc h less than in our data. The refined screening acute risk for phosgene based on the incorrect emissions was 4, but with the adjusted emissions the acute value is below

1. The population exposed to cancer risk is less than presented in the table due to the adjusted emissions. We will update the data set with this information, and any additional information received during the comment period, before completing the final rule.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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38 **Table 3.2 -**  **1 Summary of Source Category Level Risks for Pesticide Active Ingredient**  **Production Result**  **HAP “Drivers”** 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 11,000 n/a Number of People Exposed to Noncancer Respiratory Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cases per year) 0.001 n/a Contribution of HAP to Cancer Incidence naphthalene 30% n/a formaldehyde 18% n/a methylene chloride 10% n/a tetrachloroethylene 9% n/a ethylene dichloride 6% n/a 1,3 -butadiene 5% n/a nickel compounds 4% n/a
**Table 3.2 -**  **2 Summary of Refined**  **Screening Acute Results for Pesticide Active Ingredient**  **Production Facilities**

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

**AEGL -**  **1/ ERPG**  **- 1**  **Based on**

**AEGL -**  **2/ ERPG**  **- 2**  **REL**

**(m g/m** **3 )**  **AEGL -**  **1 (1 -** 

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

**(m g/m** **3 )**  **AEGL -**  **2**

**(1 -**  **hr) (m**  **g/m 3**  **) ERPG**  **- 2** 

**(m g/m** **3 )**  **HAP** 35 **Max. 1 -**  **hr.**

**Air Conc. (m**  **g/m 3**  **)** Ethylene glycol ethyl ether 0.3 8 0.37 Acrolein 0.01 4 0.1 /0.09 0.04 /0.03 0.0025 0.069 0.11 0.23 0.34 Nickel Cpds 0.012 2 0.006 Chloroform 0.3 2 0.001 / 0.001 0.15 310 240 Chlorine 0.42 2 0.3 /0.1 0.07 /0.05 0.21 1.5 2.9 5.8 8.7 Formaldehyde 0.1 2 0.1 /0.08 0.0 06/0.008 0.055 1.1 1.2 17 12

Notes on Refined Process: 1) The screening was performed for all emitted HAP with available acute dose
- response values. Only those pollutants whose screening HQs were greater than 1 for at least one 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 health risks, based on an analysis of currently available emissions 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. AE GL

– Acute exposure guideline levels represent emergency exposure (1
- hour) limits for the general public. AE GL
- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience effects that are notable discomfort, but which are transient and reversible upon cessation of exposure.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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39

AE GL
- 2 is the exposure level above which it is predicted that the general population, including susceptible in dividuals, could experience irreversible or other serious, long
- lasting adverse health effects of an impaired ability to escape. EPRG

– Emergency Removal Program guidelines represent emergency exposure (1
- hour) limits for the general public. ERPG
- 1 is the maximum level 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. ERPG
- 2 is the maximum exposure below which it is believed that nearly all indivi duals could be exposed for up to 1 hour without experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual’s abilit y to take protective action. The facility
- wide M IR

and TOSHI , available in Appendi x 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility
- wide assessment for cancer risks are summarized in Table 3.2
- 3. The results indicate that 12 facilities with pesti cide active ingredient production processes have a facility - wide cancer MIR greater than or equal to 1 in a million. The maximum facility
- wide cancer MIR for the source category is 20 in a million , and it occurs at 2 facilities . At one of these facilit ie s , the risk is driven by eth yl ene dichloride from a mercury cell chlor
- alkali process and the PAIsource category

contributes less than one percent to the facility
- wide risk . At the other facility , the risk is almost 100 percent from an unidentified sourc e category due to arsenic emissions . The maximum facility
- wide TOSHIfor the source category is 2, driven b y emissions of chlorine from inorganic chemical manufacturing, s ynthetic organic chemical manufacturing, and mercury cell chlor
- alkali processes. T he source category contributes less than 5 percent to the facility
- wide TOSHI. **Table 3.2 -**  **3 Source Category Contribution to Facility**  **- Wide Cancer Risks** 
**– Pesticide**  **Active Ingredient Pesticide Active Ingredient**  **Manufacturing Number of Facilities Binned**  **by Facility -**  **Wide MIR (in 1 million)**  **Source Category MIR Contribution to Facility**  **- Wide MIR**  < 1 1 ≤ MIR<10 10 ≤ MIR<100 > 100 **Total** > 90% 1 3 0 0 4 50 - 90% 1 1 0 0 2 10 - 50% 2 4 0 0 6 < 10% 1 0 4 0 5 **Total** 5 8 4 0 17 

### 4. **Risk Results for the Poly ether**  **Poly ols Production Source**  **Categor y**  **4.1 Source Category**  **Description and Results** The p oly ether pol yols production source category consists of major source facilities that produce chemical products with repeating ether linkages (i.e.,
- R - O
- R - ) formed by the reaction of eth yl ene oxide, prop yl ene oxide, or other cyclic ethers with compounds having one or more reactive h ydrogens. Poly ether pol yols do not have significant uses of their own, but rather are used to mak e a variety of other products. Poly ether pol yols can be produced b y**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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40 either poly

merization of epoxides (i.e., a three
- membered cyclic ether, such as ethylene oxide or prop yl ene oxide) or tetrah ydrofuran (THF). In the produc tion of pol yether polyols, HAP are used primaril y as reactants or extraction solvents and include eth yl ene oxide, propylene oxide, h exane, toluene, and other HAP. P otential sources of emissions for this category , regardless of the specific process emplo ye d, include process vents, storage vessels, equipment leaks, wastewater operations, and heat ex changers/cooling towers . A complete description of the poly ether pol yols production source category can be found in the text of the NPRM. We currentl y estimat e that there are 2 3 pol yether polyols production facilities operating in the U.S. 36 The data set contains all 2 3 facilities identified with a poly ether pol yo ls production MACT code in the 2005 NEI. The 2005 NEI was updated for this category with more rece nt data from industry

and enhanced quality

assurance of facility

and emission locations. All 2 3 of these facilities are identified as major sources in the NEI. The emissions for the polyether pol yols production source category data set (of 2 3 facilit ies) are summarized in Table 4.1
- 1 . The total HAP emissions for the source category are approximately

440 tons per year. Based on these data, the HAP emitted in the largest quantities across these 2 3 facilities are: ethylene glycol, ethylene oxide, propylene oxide, acetaldeh yde, methanol, ethyl benzene, benzene, chlorobenzene, gl ycol ethers, hexane, propionaldeh yde, and p - dioxane. These 12 HAP account for 9 0 percent of the total emissions by mass. PB - HA P 37 reported as emissions from these facilities include POM and lead compounds. 38

36 After the risk assessment was completed, we learned that two facilities incl uded in the data set for polyether polyols production should not have been included. These facilities, Emerald Carolina Chemical (NEINC0595) and Port Neches Operations C4 Plant (NEI12483), are still included in the emissions summary, but risk results have been removed from the risk summary. We will update the data set with this information, and any additional information received during the comment period, before the final rule. 37 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Volume 1, EPA
- 453K - 04 - 001A, as referenced in the ANPRM and provided on the EPA’s Technology Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.ep a.gov/ttn/fera/risk_atra_vol1.html
. 38 After the risk assessment was completed, we learned that two facilities included in the data set for PEPOs production should not have been included. These facilities, Emerald Carolina Chemical (NEINC0595) and Port Ne ches Operations C4 Plant (NEI12483) are still included in the emissions summary. Additionally, after the risk assessment was completed, we learned that the emissions of hexachlorobenzene in the data set for polyether polyols production should have been as signed to the PAI MACT code. These emissions are still included in the emissions summary, but risk results have been removed from the risk summary. We will update the data set with this information, and any additional information received during the comm ent period, before the final rule.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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41 **Table 4.1 -**  **1 Sum**  **mary of Emissions from the Polyether Polyols Production**  **Source Category and**  **Availability of Dose -**  **Response Values**

**HAP a**  **Emissions (tpy)**  **Number**

**of Facilities**  **Reporting HAP**  **(25 facilities**  **in data set)**  **36 Prioritized**  **I nhalation Dose**  **- Response Value**  **Identified by OAQPS b**  **PB**   ** HAP?** **Unit Risk Estimate for**  **Cancer? Reference** 

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

**Benchm ark**  **Values for Acute Noncancer?**  Ethylene Glycol 17 8 9  Ethylene Oxide 57 2 5    Propylene Oxide 3 4 19    Acetaldehyde 27 12    Methanol 25 11   Ethyl Benzene 19 4    Benzene 16 8    Chlorobenzene 12 4   Glycol Ethers Glycol Ethers 9 5   2 - Butoxyethyl Acetate 2 1   Methoxytriglycol 1 2   Diethylene Glycol Monoethyl Ether 0.6 1   Ethylene glycol ethyl ether ( Cellosolve ) 0.5 1   Propyl Cellosolve 0.4 1   Ethylene Glycol Methyl Ether 0.3 1   Diethylene Glycol Monobutyl Ether 0.07 1   2 - (Hexyloxy)Ethanol 0.05 1   Butyl Carbitol Acetate 0.004 1   Ethoxytriglycol 0.0009 1   Triglycol Monobutyl Ether 0.0003 1   Hexane 6 6   Propionaldehyde 6 5   1,4 - Dioxane (p
- Dioxane) 5 7    1,3 - Butadiene 5 3    Chlorine 4 3   Styrene 4 6   Acrylic Acid 4 2   Toluene 3 7   Formaldehyde 3 1 0    Hydrochloric Acid 2 4   Vinyl Acetate 1 3   Diethanolamine 1 5 **Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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42 **Table 4.1 -**  **1 Sum**  **mary of Emissions from the Polyether Polyols Production**  **Source Category and**  **Availability of Dose -**  **Response Values**

**HAP a**  **Emissions (tpy)**  **Number**

**of Facilities**  **Reporting HAP**  **(25 facilities**  **in data set)**  **36 Prioritized**  **I nhalation Dose**  **- Response Value**  **Identified by OAQPS b**  **PB**   ** HAP?** **Unit Risk Estimate for**  **Cancer? Reference** 

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

**Benchm ark**  **Values for Acute Noncancer?**  Xylenes (Mixture of o, m, and p Isomers) 1 7   Ethyl Acrylate 1 2  Methyl Tert
- Butyl Ether 1 3    Propylene Dichloride 1 1   Acrolein 1 3   Ethyl Chloride 1 6  Ethylene Dichloride 0.9 5    Phenol 0.8 7   1,2 - Epoxybutane 0.8 2   Naphthalene 0.7 4   Acetophenone 0.6 3 Acrylonitrile 0. 2 3    Trichloroethylene 0. 2 1    Cumene 0. 2 5   Phosgene 0. 2 2   Vinyl Chloride 0.2 4    N,N - Dimethylformamide 0.1 1   2,4 - Dichlorophenoxy Acetic Acid 0.1 1 Dim ethyl Sulfate 0. 1 1  Epichlorohydrin ( 1 - Chloro
- 2,3 - Epoxypropane ) 0. 1 2    Benzyl Chloride 0. 1 2   Biphenyl 0.1 2  Isophorone 0.06 1   Aniline 0. 06 4    Methyl ene Chloride 0.04 3    Chloroacetic Acid 0.03 2  Fluoranthene 0.03 1   Chloroform 0.03 4   Triethylamine 0.02 3   Hexachlorobenzene 3 3 0.0 2 1    Methyl Isobutyl Ketone 0.02 3  m - Xylene 0.01 1   Acetonitrile 0.01 2   Diethyl Sulfate 0.0 1 1 Methyl Methacrylate 0.008 1  **Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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43 **Table 4.1 -**  **1 Sum**  **mary of Emissions from the Polyether Polyols Production**  **Source Category and**  **Availability of Dose -**  **Response Values**

**HAP a**  **Emissions (tpy)**  **Number**

**of Facilities**  **Reporting HAP**  **(25 facilities**  **in data set)**  **36 Prioritized**  **I nhalation Dose**  **- Response Value**  **Identified by OAQPS b**  **PB**   ** HAP?** **Unit Risk Estimate for**  **Cancer? Reference** 

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

**Benchm ark**  **Values for Acute Noncancer?**  Hydroquinone 0.006 1 Tetrachloroethylene 0. 00 6 1    2,4,6 - Trichlorophenol 0.006 1  Phthalic Anhydride 0.004 1  Cresol 0.003 2  1,3 - Dichloropropene 0.002 1   4,4'
- Methylenedianiline 0.001 1   Dichloroethyl Ether 0.00 1 1  p - Xylene 0.0009 1   2,4 - Toluene Diisocyanate 0.0005 1    Bis(2
- Ethylhexyl)Phthalate 0.0005 1   Dibutyl Phthalate 0.0005 1 Lead 0.0005 1 c  Quinoline 0.0005 1 o - Toluidine 0.0005 1  1,1,2 - Trichloroethane 0.0001 1   Carbon Tetrachloride 0.0001 1   

a Notes for how HAP were speciated for risk assessment:  For most metals, emissions reported as the elemental metal are combined with metal compound emissions (e.g., “cadmium” emissions modeled as “cadmium & compounds”). In the absence of speciation information, we assume the reported mass is 100 percent metal.  For emissions of any chemicals or chemical groups classified as POM, emissions were grouped into POM subgroups as found on EPA’s Technology Transfer Network website for the 200 5 National
- Scale Air Toxics Assessment at http://www.epa.gov/ttn/atw/nata2005/methods.html#pom ( Approach to Modeling POM)
. These POM subgroups (e.g., POM 7 2 002, not shown above) all have unit risk estimates for cancer, and are considered PB - HAP.  For emissions rep orted generically as “Glycol Ethers” or specific glycol ethers not found on EPA’s Technology Transfer network for air toxics (see footnote b), emissions will be treated as ethylene glycol methyl ether. b Specific dose
- response values for each chemical are identified on EPA’s Technology Transfer Network website for air toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html
. c There is no reference concentration for lead. In considering no ncancer hazards for lead in this preliminary assessment, we compared the maximum annual ambient exposure estimates to the National Ambient Air Quality Standards (NAAQS) for lead (0.15 μg/m3 ). The primary (health
- based) standard is a maximum or not
- to - be
- ex ceeded, rolling three
- month average, measured as total suspended particles (TSP). The secondary (welfare
- based) standard is identical to the primary standard. These NAAQS for lead were reviewed with revisions adopted in October 2008 (http://www.epa.gov/air/lead/actions.html ).**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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44 

### 4.2 **Risk Characterization** This section presents the results of the risk assessment for the pol yether polyols production source category . The basic chronic inha lation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients, a s well as the results of our preliminary screen for potential non
- inhalation ris ks from PB
- HAP. Also presented are the HAP “drivers,” which are the HAP that collectively

contribute 90 percent of the maximum cancer risk or maximum hazard index at the highe st exposure location , as well as a summary of the results of our facility
- wide assessments and our analy sis of risks associated with the maximum allowed emissions under the current MACT standards. A detailed summary of the facility
- specific risk assessment results is available in Appendix 4 . Table s 4.2 - 1 and 4.2
- 2 summarize the chronic and acute inhalation risk results for this source category . The results indicate that maximum lifetime individual cancer risks could be as high as 3 0 in a million, with ethylene oxide as the major contributor to the risk. The total estimated cancer incidence from the source category is 0.02 excess cancer cases per year, or one case in every

50 y ears. Approximately 6,800 people are estimated to have cancer risks at or above 10 in a million, and approximately 160,000 people are estimated to have cancer risks at or above 1 in a million as a result of the emissions from 17 facilities ; however these estimates are biased high due to the mistake s with the emissions data . The maximum chronic noncancer TOSHI value for the source category could be up to 0.8 from emissions of acrolein
. Worst - case a cute HQs were calculated f or every HAP that has an acute benchmark
. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries. Additionally , for the facility with the highest acute HQ value the multiplier of 10 was adjusted to 2 resulting in a reduction of the acute risk for one facility (see Appendix 7 of this document and the memorandum “Emission Data and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active Ingredients, Poly ether Polyols, Poly mers and Resins IV” in the docket for th is action ). T he highest acute HQ value of 6 (based on the gl yc ol ether REL) is shown in Table 4.2
- 1. Analy sis of potential off
- site acute impacts for this source category identified two facilities with the potential to exceed the acute REL for two pollutants (gl ycol e thers (1 facility) and acrolein (1 facility) ). Table 4.2
- 2 provides more information on the acute risk estimates for HAP that had an acute HQ greater than 1 for an y benchmark. The highest refined worst
- case acute HQ value is 6 (based on the REL for gl ycol ethers )
. In characterizing the potential acute noncancer risks from gl ycol ethers, it is important to consider the uncertainties related to the emission inventory as it relates to a lack of speciation data for gl ycol ethers for this source category
. A ll other HAP emissions at all other facilities indicated no potential to cause acute impacts of concern. While these estimated worst
- case exceedances indicate that there is some potential for such acute exposures to occur, we note that exceeding the mod eled REL values does not necessarily

indicate that adverse effects will occur, only that they cannot be ruled out. Further, in characterizing the potential for acute noncancer impacts of concern, it is important to remember the upward bias of these worst
- case exposure estimates and to consider the**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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45 results along with the rather large uncertainties related to the emissions estimates and screening methodology
. We reviewed the two facilities with potential off
- site acute HQ values greater than one and determi ned equipment leaks were primaril y responsible and that they were modeled assuming that they all emanate from a single emission location, rather than from numerous phy sical locations throughout the processing area. We note that this assumption further bia ses the HQ values high, but to an unknown extent, given that we do not know the actual size of the processing areas at each of these facilities. Taking all of this into consideration, these acute impact screening results indicate onl y the potential for ac ute impacts of concern, while the uncertainties and bias associated with them suggest that there may be no real acute issues at all. Nonetheless, the emission points and pollutants identified by this evaluation should be examined to see if further cost
- ef fective emission reductions are achievable. We conducted a screening
- level evaluation of the potential human health risks associated with emissions of PB
- HAP. Reported emissions of PB
- HAP w ere compared to emission thresholds established by EPA for the purposes of the RTR risk assessments. 39 The PB
- HAP emitted by

facilities in this category include POM as benzo(a)py rene T EQ ( 1 facility) and lead compounds (1 facility). 40 The one facility with POM emissions above the threshold level exceed s the screening e mission level by a factor of 4 . Lead is a PB HAP, but the NAAQS value (which was used for the chronic noncancer risk assessment) takes into account multipathway

exposures, so a separate multipathway screening value was not developed. Since we did not estimate an y exceedances of the NAAQS in our chronic noncancer risk assessment, we do not expect an y significant multipathway exposure and risk due to lead emissions from these facilities.

39 ICF International. TRIM
-Based Multipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008. 40 After the risk assessment was completed, we learned that the emissions of hexachlorobenzene in the data set for the PEPOs production should have been assigned to the PAI MACT code. These emissions are still included in the PEPOs emissions summary, but have been removed from the risk summary. We will update the data set with this information, and any additional information received during the comment period, before the final rule.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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46 **Table 4.2 -**  **1 Summary of Source Category Level Inhalation Risks for**  **Polyether Polyols Production**  **Result HAP “Drivers”**  **Facilities in Source Category** **41** Number of Facilities Estimated to be i n Source Category 2 3 n/a Number of Facilities Identified in NEI and Modeled in Preliminary Risk Assessment 25 n/a **Cancer Risks** Maximum Individual Lifetime Cancer Risk (in 1 million) 3 0 ethylene oxide 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 5 ethylene oxide, acetaldehyde, acrylonitrile, 1,3
-butadiene, benzene, 1,4 - dioxane Greater than or equal to 1 in 1 million 17 ethylene oxide, acetaldehyde, acrylonitrile, 1,3
-butadiene, benzene, 1,4
- dioxane, propylene oxide, ethyl benzene, propylene dichloride, ethylene dichloride, naphthalene, benzyl chloride **Chronic Noncancer Risks**  Maximum Respiratory Hazard Index 0.8 acrolein Number of Facilities with Maximum Respiratory Hazard Index: Greater than 1 0 n/a **Acute Noncancer Refined Screening**  **Results** Maximum Acute Hazard Quotient 6 4/0.1 g lycol ethers (REL)

acrolein (REL/AEGL
- 1) Number of Facilities With Potential for Acute Effects 3 acrolein, glycol ethers **Population Exposure 41**  Number of People Living Within 50 Kilometers of Facilities Modeled 18,000,000 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 6,800 n/a Greater than or equal to 1 in 1 million 160,000 n/a

41 After the risk assessment was completed, we learned that two facilities included in the data set for polyether polyols production sh ould not have been included. These facilities, Emerald Carolina Chemical (NEINC0595) and Port Neches Operations C4 Plant (NEI12483), are still included in the emissions summary but risk results have been removed from the risk summary. One of the faciliti es does not have any of the maximum risks. The other, is responsible for the maximum cancer risk, the maximum respiratory hazard index, and the maximum facility
- wide MIR and TOSHI. The risk results with these 2 facilities in the data set were 60 for the MIR and 1 for the maximum HI. The risks presented in the summary table represent the results based on the updated information. The population exposed to cancer risk would be less than presented in the table due to the adjusted emissions. We will update the data set with this information, and any additional information received during the comment period, before the final rule.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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47 **Table 4.2 -**  **1 Summary of Source Category Level Inhalation Risks for**  **Polyether Polyols Production**  Number of People Exposed to Noncancer Respiratory Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cases per year) 0.02 n/a Contribution of HAP to Cancer Incidence ethylene oxide 87% n/a propylene oxide 4% n/a benzene 3% n/a
**Table 4.2 -**  **2 Summary of Acute Refined**  **Sce ening**  **Results for Polyether Polyols Production**  **Facilities**

**Results MAXIMUM ACUTE HAZARD QUOTIENTS**  **ACUTE DOSE -**  **RESPONSE VALUES**

**Based on REL Based on** 

**AEGL -**  **1/ ERPG**  **- 1**  **Based on**

**AEGL -**  **2/ ERPG**  **- 2**  **REL**

**(m g/m** **3 )**  **AEGL -**  **1**

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

**(m g/m** **3 )**  **AEG**

**L -**  **2 (1**  **- hr)**  **(m g/**  **m 3**  **) ERP**  **G -**  **2 (m**  **g/ m** **3 )**  **HAP Max. 1**  **- hr.** 

**Air Conc. (m**  **g/m 3**  **)** Glycol Ethers 0.56 6 0.093 Acrolein 0.0 1 4 0.1 4 /0.09 0.04 /0.03 0.0025 0.069 0.11 0.23 0.34 Notes on Refined Process: 1) The screening was performed for all emitted HAP with available acute dose
- response values. Only those pollutants whose screening HQs were greater than 1 for at least one 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 health risks, based on an analysis of currently available emissions 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. AE GL

– Acute exposure guideline levels represent emergency exposure (1
- hour) limits for the general public. AE GL
- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience effects that are notable discomfort, but which are trans ient and reversible upon cessation of exposure. AE GL
- 2 is 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 impaired ability to escape. EPRG

– Emergency Removal Program guidelines represent emergency exposure (1
- hour) limits for the general public. ERPG
- 1 is the maximum level 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. ERPG
- 2 is the maximum exposure below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing or developing irreversible or other s erious health effects or symptoms which could impair an individual’s ability to take protective action. The facility
- wide M IR

and TOSHI , available in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identifi ed facilities. The results of the facility
- wide assessment are summarized in Table 4.2
- 3. The results indicate that 18 facilities with poly ether pol yols production processes have a facilit y - wide cancer MIR greater than or equal to 1 in a million. The maximum facility
- wide MIR is 30 in a million, with the poly ether polyol production source category contributing 100 percent of the risk, driven by emissions of ethylene oxide from proc ess vents and equipment leaks. The maximum facility
- wide TOSHI**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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48 for the so urce category

is 2 , driven b y emissions of chlorine from industrial inorganic chemical manufacturing and HON process units . T he source category contributes approximately 1 3 percent to the facility
- wide TOSHI. 42 **Table 4.2 -**  **3 Source Category Contribution t**  **o Facility -**  **Wide Cancer Risks**
**– Polyether**  **Polyols Production Polyether Polyols**  **Production Number of Facilities Binned by Facility**  **- Wide MIR**  **(in 1 million) 4**  **2 Source Category MIR**  **Contribution to Facility -**  **Wide**

**MIR** < 1 1 ≤ MIR<10 10 ≤ MIR<100 > 100 **Total**

> 90% 3 3 4 0 1 0 50 - 90% 0 3 2 0 5 10 - 50% 1 2 1 0 4 < 10% 0 2 2 0 4 **Total** 4 10 9 0 2 3 

### 5. **Risk Results for the P&V IV Sty rene A**  **cr yl**  **onitrile Source Categor** **y 5.1**  **Source Category Description and Results**  This section summary

presents the risk assessment for the sty rene - acrylonitrile (SA) resin production source category . St yrene - acrylonitrile resins are copol ym ers of sty rene and acryl onitrile. Sty

rene - acrylonitrile resins may be sy nthesized by

emulsion, suspension, and continuous mass poly

merization; howeve r, the majority of production is by

batch emulsion. In emulsion poly

merization, monomers are dispersed in water using a soap solution or an emulsifier. In suspension poly merization, the monomer is suspended in a water phase. In mass poly

merization, monome rs are reacted without the use of emulsifiers, suspending agents, salts or waters. Emission points along the SA resin production process include equipment leaks, process vents, storage vessels, and wastewater operations. Many facilities that produce Acryl onitrile
- Butadiene
- Sty rene (ABS) resins also produce SA, because much of the SA resins that are produced are used as feedstock in the production of ABS. Ty pical uses include automobile instrument panels and interior trim and housewares. A complete

42 After the risk assessment was completed, we learned that two facilities included in the data set for polyether polyols production should not have been included. These facilities, Emerald Carolina Chemical (NEINC0595) and Port Neches Operations C4 Plant (NEI12483), are still included in the emissions summary, but risk results have been removed from the risk summary . One of the fac ilities does not have any of the maximum risks. The other, is responsible for the maximum cancer risk, the maximum respiratory hazard index, and the maximum facility
- wide MIR and TOSHI. The risk results with these 2 facilities in the data set were 60 for the MIR and 1 for the maximum HI. We will update the data set with this information, and any additional information received during the comment period, before the final rule.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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49 descri ption of the st yrene - acryl onitrile production source category can be found in the text of the NPRM. We currentl y estimate that there are two st yr ene - acrylonitrile production facilities operating in the U.S. The data set contains two facilities identifi ed with a sty rene - acrylonitrile production MACT code in the 2005 NEI. The 2005 NEI was updated for this category with more recent data from industry

and enhanced quality

assurance of facility

and emission locations. Both of these facilities are identifie d as major sources in the NEI. The emissions for the styrene
- acryl onitrile production source category data set (of two facilities) are summarized in Table 5.1
- 1 . The total HAP emissions for the source category are approximately

2 tons per year. Based on these data, the HAP emitted in the largest quantities for these 2 facilities are: ethyl benzene, sty rene, methylene chloride and acrylonitrile. T hese four HAP account for 100 percent of the total emissions by mass. No PB - HA P 43 are reported in the data set for the st yr ene - acrylonitrile production source category
. **Table 5. 1**  **- 1**  **Summary of Emissions from the Styrene -**  **Acrylonitrile Production Source Category and Availability of Dose**  **- Response Values** 

**HAP Emissions**  **(tpy) Number of** 

**Facilities Reporting**  **HAP (2**  **facilities in data set)**  **Prioritized Inhalation Dose -**  **Response Value Identified by OAQPS**  **a PB**  **- HAP?**  **Unit Risk Estimate for**  **Cancer? Reference** 

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

**Benchm ark**  **Values for Acute Noncancer?**  Ethyl Benzene 1 1    Styrene 1 2   Methylene chloride 0. 4 2    Acrylonitrile 0. 04 2   

a Specific dose
- response values for each chemical are identified on EPA’s Technology Transfer Network website for air toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html
. 

### 5.2 **Risk Characterization** This section presents the results of the risk assessment for the sty rene - acrylonitrile production source category . The basic chronic inhalation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients, as well as the results of our preliminary screen for potenti al non
- inhalation risks from PB
- HAP. Also presented are the HAP “drivers,” which are the HAP that collectively

contribute 90 percent of the maxi mum cancer risk or maximum hazard index at the highest exposure location , as well as a summary of the results of our facility
- wide

43 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Volume 1, EPA
- 453K - 04 - 001A, as referenced in the ANPRM and provided on the EPA’s Technology Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.epa .gov/ttn/fera/risk_atra_vol1.html
.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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50 assessments and our analy sis of risks associated with the maximum allowed emissions under the current MACT standards. A deta iled summary of the facility
- specific risk assessment results is available in Appendix 4 . Table 5.2
- 1 summarizes the chronic and acute inhalation risk results for this source category
. The results indicate that maximum lifetime individual cancer ris ks could be as high as 0.03 in a million, with acrylonitrile and ethyl benzene as the major contributors to the risk. The total estimated cancer incidence from the source category is 0.000006 excess cancer cases per ye ar, or one case in every

167,000 y ear s. There are no people with an estimated cancer risk greater than or equal to one. The maximum chronic noncancer TOSHI value for the source category is estimated to be 0.0002 , based primaril y on emissions of acrylonitrile, indicating no significant potential for chronic noncancer impacts. Worst - case a cute HQs were calculated f or every HAP that has an acute benchmark, and the highest acute HQ value of 0.007 (based on the methylene chloride REL) is shown in Table 5.2 - 1. There were no screening acute HQs greater than 1, so further refinement was not performed. A screening
- level evaluation of the potential human health risks associated with emissions of PB
- HAP was not necessary for this source category

since no PB
- HAP are emitted
.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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51 **Table 5.2 -**  **1 Summary of Source Category Level Risks for Styrene**  **- Acrylonitrile**  **Production Result**  **HAP “Drivers” Facilities in Source Category**  Number of Facilities Estimated to be i n Source Category 2 n/a Number of Facilities Identified in NEI and Modeled in Preliminary Risk Assessment 2 n/a **Cancer Risks** Maximum Individual Lifetime Cancer Risk (in 1 million) 0.03 acrylonitrile, ethyl benzene 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 0 n/a Greater than or equal to 1 in 1 million 0 n/a **Chronic Noncancer Risks** Maximum Respiratory Hazard Index 0.0002 acrylonitrile Number of Facilities with Maximum Respiratory Hazard Index: Greater than 1 0 n/a **Acute Noncancer Screening Results** Maximum Acute Hazard Quotient 0.007 methylene chloride (REL) Number of Facilities With Potential for Acute Effects 0 n/a **Population Exposure** Number of People Living Within 50 Kilometers of Facilities Modeled 680,000 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 0 n/a Greater than or equal to 1 in 1 million 0 n/a Number of People Exposed to Noncancer Respiratory Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.000006 n/a Contribution of HAP to Cancer Incidence ethyl benzene 52% n/a acrylonitrile 44% n/a The facility
- wide M IR

and TOSHI , available in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility
- wide assessment are summarized in Table 5.2
- 2 . The results indicate that both facilities with sty

rene - acrylonitrile production processes have a facility
- wide cancer MIR**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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52 greater than or equal to 1 in a million. The maximum facility
- wide cancer MIR is 20 in a million for 1 facility . At this facility , the source category contributes less than one percent t o the facility
- wide MIR, which is driven by emissions of ethylene dichloride from a mercury cell chlor
- alkali process. The other facility has a cancer risk of 10 in a million. Again, the sty rene - acrylonitrile source category contributes less than one percent to the fa cilit y - wide MIR, which is driven by

emissions of acrylonitrile from the acrylonitrile
- butadiene
- st yrene resins production source category . The maximum facility
- wide TOSHI for the source category is 2, driven b y emissions of chlorine from inorganic chemica l manufacturing, sy nthetic organic chemical manufacturing, and mercury cell chlor
- alkali processes. The source category

contributes less than one percent to the facility
- wide TOSHI. **Table 5.2 -**  **2 Source Category Contribution to Facility**  **- Wide Cancer Risks** 
**– Styrene**  **** **Acrylonitrile Production Styrene**  **- Acrylonitrile**  **Production Number of Facilities Binned by Facility**  **- Wide**  **MIR (in 1 million) Source Category MIR Contribution**  **to Facility -**  **Wide MIR** < 1 1 ≤ MIR<10 10 ≤ MIR<100 > 100 **Total** > 90% 0 0 0 0 0 50 - 90% 0 0 0 0 0 10 - 50% 0 0 0 0 0 < 10% 0 0 2 0 2 **Total** 0 0 2 0 2 

### 6. **Risk Results for the P&R IV Poly st**  **yrene Production Source Categor** **y 6.1**  

### Source Category

**Description and Results** Poly st yr ene resins (PS) are those produced b y the poly merization of sty

rene monomer. This ty pe of resin can be produced b y three methods: (1) suspension poly merization (operated in batch mode); (2) mass (operated in a continuous mode); and (3) emulsion process (operated in a continuous mode). The mass and suspension methods are the most commerciall y significant, whereas use of the emulsion process has decreased significantly since the mid
1940s. The suspension process is a batch process that can be used to produce cry stal, impact, or expandable poly st yr ene beads. In this process, poly merization is carried out in an aqueous medium that permits the removal of heat resulting from the reaction. The poly st yrene is formed in small beads which are separated from the aqueous phase. The mass process uses no water or organi c solvents and is the simplest process for producing pol ys ty re ne. There are four major stages in the process: prepol ym erization, poly merization, devolatilization, and extrusion. The uses for poly st yrene resin include packaging and one
- time use, expandabl e poly st yrene beads, electronics, resellers and compounding, consumer and institutional products, and furniture, building, or construction uses. A wide variety of consumer and construction products are made from pol ys ty rene resins, including disposable di nnerware,**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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53 shower doors, light diffusers, soap dishes, insulation board, food containers, drain pipes, audio and video tape, picnic coolers, loose fill packaging, and tubing. A complete description of the poly st yr ene production source category can be found in the text of the NPRM. We currentl y believe that there are 11 pol ys ty rene production facilities operating in the U.S. , and the data set contains those 11 facilities identified with a poly st yr ene production MACT code in the 2005 NEI. The 2005 NEI was updated for this category with more recent data from industry

and enhanced qualit y assurance of facility and emission locations. All 11 of these facilities are identified as major sources in the NEI. The emissions for the poly sty rene production sourc e category data set (of 11 facilities) are summarized in Table 6.1 - 1 . The total HAP emissions for the source category are approximately

90 tons per y ear. Based on these data, the HAP emitted in the largest quantities for these 11 facilities is s ty rene, which accounts for 94 percent of the total emissions by mass. No PB - HA P 44 are reported in the data set for the poly sty rene production source category
. **Table 6.1 -**  **1 Summary of Emissions from the Polystyrene Production Source Category and Availability**  **of Dose**  **- Response Values** 

**HAP Emissions** 

**(tpy) Number of** 

**Facilities Reporting HAP**  **(11 facilities in data set)**  **Prioritized Inhalation Dose -**  **Response Value Identified by OAQPS**  **a PB**  **- HAP?**  **Unit Risk Estimate for**  **Cancer? Reference** 

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

**Benchm ark**  **Values for Acute Noncancer?**  Styrene 85 10   Toluene 2 5   Ethyl Benzene 1 7    Tetrachloroethylene 1 1    Xylenes (mixed) 1 5   Hydrochloric acid 0.3 1   Cumene 0.1 4   Hexane 0.1 1   Benzene 0.007 2   

a Specific dose
- response values for each chemical are identified on EPA’s Technology Transfer Network website for air toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html
. **6.2** 

### Risk Characterization This section presents the results of the risk assessment for the pol ys ty rene production source category . The basic chronic inhalation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum

44 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Volume 1, EPA
- 453K - 04 - 001A, as referenced in the NPRM and provided on the EPA’s Technology Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html
.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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54 hazard quotients. Also presented are the HAP “drivers,” which are the HAP that collectively contribute 90 percent of the maximum cancer risk or maximum hazard index at the highest exposure location , as well as a summary of the results of our facility
- wide assessments and our anal ys is o f risks associated with the maximum all owed emissions under the current MACT standards. A detailed summary of the facility
- specific risk assessment results is available in Appendix 4 . Table 6.2
- 1 summarizes the chronic and acute inhalation risk results for this source category
. The resul ts indicate that maximum lifetime individual cancer risks could be as high as 2 in a million, with tetrachloroethyl ene as the major contributor to risk. The total estimated cancer incidence from the source category is 0.00003 excess cancer cases per ye ar, or one case in every 33,000 y ears. Approximately 180 people are estimated to have cancer risks at or above 1 in a million as a result of the emissions from one facility. The maximum chronic noncancer TOSHIvalue for the source category could be up to 0. 004 from emissions of x yl enes and sty rene, indicating no significant potential for chronic noncancer impacts. Worst - case acute HQs were calculated for every HAP with an acute benchmark, and the highest acute HQ value of 0.3 (based on the sty rene REL) is shown in Table 6.2
- 1. There were no screening acute HQs greater than 1, indicating no potential concerns about acute impacts , and further refinement was not performed
. A screening
- level evaluation of the potential human health risks associated with emis sions of PB
- HAP was not necessary for this source category

since no PB
- HAP are emitted
.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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55 **Table 6.2 -**  **1 Summary of Source Category Level Risks for**  **Polystyrene Production**

**Result HAP “Drivers”**  **Facilities in Source Category** Number of Facilities Estimated to be i n Source Category 11 n/a Number of Facilities Identified in NEI and Modeled in Preliminary Risk Assessment 11 n/a **Cancer Risks** Maximum Individual Lifetime Cancer Risk (in 1 million) 2 tetrachloroethyl ene 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 0 n/a Greater than or equal to 1 in 1 million 1 tetrachloroethyl ene **Chronic Noncancer Risks** Maximum Neurological Hazard Index 0.004 xylenes (mixed), styrene Number of Facilities with Maximum Neurological Hazard Index: Greater than 1 0 n/a **Acute Noncancer Screening Results** Maximum Acute Hazard Quotient 0.3 styrene (REL) Number of Facilities With Potential for Acute Effects 0 n/a **Population Exposure** Number of People Living Within 50 Kilometers of Facilities Modeled 9,000,000 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 0 n/a Greater than or equal to 1 in 1 million 180 n/a Number of People Exposed to Noncancer Neurological Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.00003 n/a Contribution of HAP to Cancer Incidence tetrachloroethyl ene 74% n/a ethyl benzene 25% n/a The facility
- wide M IR

and TOSHI , available in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility
- wide assessment are summarized in Table 6.2
- 2. The results indicate that two facilities with poly st yrene production p rocesses have a facility
- wide cancer MIR greater than or equal to 1 in a million. The maximum facility
- wide cancer MIR for the source category is 1 0 in a million at one facility . At this facility , the source category contributes less than one**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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56 percent to the facility
- wide MIR, which is driven by emissions of acrylonitrile from an acryl onitrile
- butadiene
- sy trene (ABS) resins production process . The other facilit y has a cancer risk of 2 in a million. The poly st yr ene production source category contributes o ver 95 percent to the facility
- wide MIR, which is driven by emissions of tetrachloroethyl ene from storage vessels. The maximum facility
- wide TOSHIfor the source category is less than 1. **Table 6.2 -**  **2 Source Category Contribution to Facility**  **- Wide Cancer**  **Risks**
**– Polystyrene Production**  **Polystyrene Production**  **Number of Facilities Binned by Facility -**  **Wide MIR (in 1 million)**  **Source Category MIR Contribution to Facility**  **- Wide MIR**  < 1 1 ≤ MIR<10 10 ≤ MIR<100 > 100 **Total**

> 90% 3 1 0 0 4 50 - 90% 1 0 0 0 1 10 - 50% 0 0 0 0 0 < 10% 5 0 1 0 6 **Total** 9 1 1 0 11 

### 7. **Risk Results for the P&R IV Poly ethy**  **lene Terephthalate Source Categor** **y 7.1**  **Source Category**

**Description and Results** Three different ty

pes of resins are made by sources covered b y the poly ethylene ter ephthalate ( PET ) source category : solid
- state resins (PET bottle grade resins) , poly ester film , and engineering resins. They are all thermoplastic linear condensation poly mers based on dimethyl terephthalate (DMT) or terephthalic acid (TPA). PET productio n can occur via either a batch or continuous process. PET solid
- state resin is produced in a two
- step process. The most common use of PET solid
- state resins is in soft drink bottles, some industrial fiber
graded pol yester (e.g., for tire cord) is also pro duced from PET solid
- state resins. Poly ester film is a high performance film made from PET resin. The most common uses of PET film are photogr aphic film and magnetic media. PET is used extensively in the manufacture of sy nthetic fibers (i.e., pol yester fibers), which compose the largest segment of the synthetic fiber industry . The most common uses of polyester fibers are apparel, home furnishings, carpets, fiberfill, and other industrial processes. Emissions sources present at PET production processes include raw material storage tanks, mix tanks, prepol ym erization and poly merization reaction vents and process tanks, equipment leaks and ancillary s ys tems, and wastewater operations. A complete description of the polyeth yl ene terephthalate production source category

can be found in the text of the NPRM.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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57 We curr entl y estimate that there are 12 PET production facilities operating in the U.S. 45 The data set contains 15 facilities identified with a PET production MACT code in the 2005 NEI. The 2005 NEI was updated for this category with more recent data from industry and enhanced quality

assurance of facility

and emission locations. All 15 of these facilities are identified as major sources in the NEI
. The emissions for the PET production source category data set (of 15 facilities) are summarized in Table 7.1
- 1 . The total HAP emissions for the source category are approximately

1,200 tons per year. Based on these data, the HAP emitted in the larg est quantities across these 1 5 facilities are eth yl ene glycol, acetaldehyde, methanol, and biphen yl
. These four HAP account for over 90 percent of the total emissions by mass. PB - HA P 46 in the data set for the PET production source category include cadmium compounds, polycyclic organic matter (POM), and lead compounds
. **Table 7.1 -**  **1 Summary of**  **Em issions from the**  **Polyethylene Terephthalate Production Source Category**  **and Availability of Dose -**  **Response Values**

**HAP a**  **Emissions (tpy)**  **Number of**

**Facilities Reporting**  **HAP (**  **1 5**  **facilities in data set)**  **45 Prioritized Inhalation Dose**  **- Response Value**  **Identified by OAQPS b**  **PB -**  **HAP? Unit Risk**  **Estimate for Cancer?**  **Reference**

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

**Benchm ark**  **Values for Acute Noncancer?**  Ethylene Glycol 500 15  Acetaldehyde 278 15    Methanol 270 11   Biphenyl 59 7  1,4 - dioxane 18 14    Methyl bromide 12 1   o - Xylene 9 2   m - Xylene 8 1   p - Xylene 7 2   Hydrochloric acid 5 1   Toluene 4 2   Benzene 4 3    Formaldehyde 3 4    Glycol Ethers 3 1   Antimony & compounds 0.5 2  Trichloroethylene 0. 5 1   

45 After the risk assessment was completed, we learned that three facilities included in the data set for po lyethylene terephthalate production have been shut down or closed the PET production process. These facilities, Dupont in Florence, SC (NEI41302), Dupont in Old Hickory, TN (NEI45591), and Wellman in Darlington, SC (NEI43310), are still included in the em issions summary but risk results have been removed from the risk summary. We will update the data set with this information, and any additional information received during the comment period, before the final rule. 46 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Volume 1, EPA
- 453K - 04 - 001A, as referenced in the NPRM and provided on the EPA’s Technology Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html
.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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58 **Table 7.1 -**  **1 Summary of**  **Em issions from the**  **Polyethylene Terephthalate Production Source Category**  **and Availability of Dose -**  **Response Values**

**HAP a**  **Emissions (tpy)**  **Number of**

**Facilities Reporting**  **HAP (**  **1 5**  **facilities in data set)**  **45 Prioritized Inhalation Dose**  **- Response Value**  **Identified by OAQPS b**  **PB -**  **HAP? Unit Risk**  **Estimate for Cancer?**  **Reference**

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

**Benchm ark**  **Values for Acute Noncancer?**  Xylenes (Mixture of o, m, and p Isomers) 0.4 3   Ethylene oxide 0.4 2    Selenium & compounds 0.1 1  Manganese & compounds 0.09 2  Hexane 0.03 2   Chlorine 0.01 1   Acrolein 0.0 1 1   Nickel compounds Nickel 0.0003 1    Nickel & compounds 0.0 0002 1    Cadmium compounds Cadmium 0.0002 1    Cadmium & compounds 0.00001 1    Propylene Oxide 0.0001 1    1,4 - Dichlorobenzene 0.00001 1   Lead compounds (Inorganic) 0.000005 1 c  Naphthalene 0.000004 1   Arsenic & Compounds (Inorganic Including Ar sine) 0.000002 1    Polycyclic Organic Matter 2 - Methylnaphthalene 0.0000002 1   Phenanthrene 0.0000002 1   Py rene 0.00000004 1   Fluoranthene 0.00000001 1   Fluorene 0.00000001 1  

a Notes for how HAP were speciated for risk assessment:  For most metals, emissions reported as the elemental metal are combined with metal compound emissions (e.g., “cadmium” emissions modeled as “cadmium & compounds”). In the absence of speciation information, we assume the reported mass is 100 percent metal.  For emissions reported generically as “Glycol Ethers” or specific glycol ethers not found on EPA’s Technology Transfer network for air toxics (see fo otnote b), emissions will be treated as ethylene glycol methyl ether.  For emissions of any chemicals or chemical groups classified as POM, emissions were grouped into POM subgroups as found on EPA’s Technology Transfer Network website for the 2005 National
- Scale Air Toxics Assessment at http://www.epa.gov/ttn/atw/nata2005/methods.html#pom ( Approach to Modeling POM) . These POM subgroups (e.g., POM 7 2 002, not shown above) all have unit ri sk estimates for cancer, and are considered PB - HAP. b Specific dose
- response values for each chemical are identified on EPA’s Technology Transfer Network website for air toxics at http://www. epa.gov/ttn/atw/toxsource/summary.html
. c There is no reference concentration for lead. In considering noncancer hazards for lead in this assessment, we compared maximum annual ambient exposure estimates to the National Ambient Air Quality Standards (NAA QS) for lead**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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59 (0.15 μg/m3 ). These NAAQS for lead were reviewed with revisions adopted in October 2008 ( http://www.epa.gov/air/lead/actions.html ). The primary (health
- based) standard is a maximum or not
- to - be
- exceeded, rolling three
- month average, measured as total suspended particles (TSP). The secondary (welfare
- based) standard is identical to the primary standard
. 

### 7.2 **Risk Characterization** This section presents the results of the risk assessment for the pol yeth yl ene terephthalate (PET) production source category . The basic chronic inhalation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients, as well as the results of our preliminary screen for potenti al non
- inhalation risks from PB
- HAP. Also presented are the HAP “drivers,” which are the HAP that colle ctively contribute 90 percent of the maximum cancer risk or maximum hazard index at the highest exposure location , as well as a summary of the results of our facility
- wide assessments and our anal ys is of risks associated with the maximum allowed emissions under the current MACT standards. A detailed summary of the facility
- specific risk assessment results is available in Appendix 4 . Table s 7.2 - 1 and 7.2
- 2 summarize the chronic and acute inhalation risk results for this source category . The results indicate that maximum lifetime individual cancer risks could be as high as 9 in a million, with acetaldeh yde and 1,4
- dioxane as major contributors to the risk. The total estimated cancer incidence from the source category is 0.002, or one case in every 50 0 ye ars. Approximately

4,200 people are estimated to have cancer risks at or above 1 in a million as a result of the emissions from 6 facilities. The population exposed to cancer risk would be less than presented in the table below due to the adjusted em issions. The maximum chronic noncancer TOSHI value for the source category could be up to 0.5, indicating no significant potential for chronic noncancer impacts. Worst - case a cute HQs were calculated f or every HAP that has an acute benchmark
. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries. An additional adjustment to the multiplier of 10 was made for 2 facilities. The multiplier was adju sted from 10 to a value of 2 based on o ur approach as described in the memorandum “Emission Data and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active Ingredients, Poly ether Pol yols, Polymers and Resins IV” available in the docket for th is action . Other facility multiplier s were adjusted from 10 to 2 since the emissions are from equipment leaks and we believe there is less variability associated with emissions from equipment leaks ( see Appendix 7 of this document and the memorandum “Emis sion Data and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active Ingredients, Polyether Polyols, Pol ym ers and Resins IV” in the docket for this action). Using these adjustments to the multiplier of 10 resulted in the highest acute refined screening HQ value of 8 (based on the acetaldehyde REL) as shown in Table 7.2
- 1. Analy sis of potential off
- site acute impacts for this source category identified six facilities with the potential to exceed the acute REL for acetaldehyde. Table 7.2 - 2 pro vides more information on the acute risk estimates for HAP that had an acute HQ greater than 1 for an y benchmark. The maximum HQ for acetaldeh yde based on the 1 - hour AEGL
- 1 value is 0.2 , and the maximum HQ for acetaldeh yd e based on the 1
- hour ERPG
- 1**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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60 value is 1 . The ERPG
- 1 value is a no effect level which is expect ed to be protective for sensitive populations from ey e and upper respiratory irritation. The AEGL
- 1 value is a level at which we expect to see mild eye or upper respiratory irritation in the general population. All other HAP emissions at all other facilities indicated no potential to cause acute impacts of concern. While these estimated worst
- case exceedances indicate that there is some potential for such acute exposures to occur, we note th at exceeding the modeled REL or ERPG
- 1 values does not necessarily indicate that adverse effects will occur, onl y that they cannot be ruled out. Further, in characterizing the potential for acute noncancer impacts of concern, it is important to remember the upward bias of these worst
- case exposure estimates and to consider the results along with the rather large uncertainties related to the emissions estimates and screening methodology
. Upon further evaluation, we identified that, for 2 facilities with the highest HQ values (based on both the RELand the ERPG
- 1) equipment leaks were primarily responsible for the high acute HQ values, and that they were modeled assuming that they all emanate from a single emission location, rather than from numerous ph ysi cal locations throughout the processing area. We note that this assumption further biases the HQ values high, but to an unknown extent, given that we do not know the actual size of the processing areas at each of these facilities
. W e also identified that one of the high HQ values was associated with acetaldeh yd e emissions from wastewater treatment operations which w ere modeled from a single emission location versus being modeled as emissions emanating across a large area , again biasing the HQ estimate high . Taking all of this into consideration, these acute impact screening results indicate only

the potential for acute impacts of concern, while the uncertainties and bias associated with them suggest that there may be no real acute issues. We conducted a screening
- level evaluation of the potential human health risks associated with emissions of PB
- HAP. Reported emissions of PB
- HAP were compared to emission thresholds established by EPA for the purposes of the RTR risk assessments. 47 The PB
- HAP emitted b y facilities from this category are cadmium compounds (2 facilities), polycyclic organic matter (POM) as benzo(a)p yrene toxicity equivalence (TEQ) (1 facility), and lead compounds (1 facility)
. All cadmium and POM as benzo(a)p yrene TEQ emissions were belo w the screening threshold levels, and therefore we do not expect an y significant multipathway

exposure and risk due to these emissions. Le ad is a PB
- HAP, but the National Ambient Air Quality

Standards (NAAQS) value (which was used for the chronic noncancer risk assessment) takes into account multipathway exposures, so a separate multipathway screening value was not developed. Since we did not estimate any exceedances of the NAAQS in our chronic noncancer risk assessment, we do not expect an y significant mu ltipathway

exposure and risk due to lead emissions from these facilities.

47 ICF International. TRIM
-Based Multipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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61 **Table 7.2 -**  **1 Summary of Source Category Level Risks for Polyethylene Terephthalate**  **Production Result**  **HAP “Drivers” Facilities in Source Category**  **48** Number of Facilities Estimated to be i n Source Category 1 2 n/a Number of Facilities Identified in NEI and Modeled in Preliminary Risk Assessment 15 n/a **Cancer Risks** Maximum Individual Lifetime Cancer Risk (in 1 million) 9 acetaldehyde, 1,4
- dioxane 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 0 n/a Greater than or equal to 1 in 1 million 6 acetaldehyde, 1,4
- dioxane, ethylene oxide **Chronic Noncancer Risks** Maximum Respiratory Hazard Index 0.5 acetaldehyde, acrolein, ethylene glycol Number of Facilities with Maximum Respiratory Hazard Index: Greater than 1 0 n/a **Acute Noncancer Refined Screening**  **Results** Maximum Acute Hazard Quotient 8 1 0. 2 acetaldehyde (REL)

acetaldehyde (ERPG
- 1) acetaldehyde (AEGL
- 1 ) Number of Facilities With Potential for Acute Effects 9 acetaldehyde **Population Exposure** Number of People Living Within 50 Kilometers of Facilities Modeled 4 8 7,700,000 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 0 n/a Greater than or equal to 1 in 1 million 4,200 n/a
48 After the risk asses sment was completed, we learned that three facilities included in the data set for polyethylene terephthalate production have been shut down or closed the PET production process. These facilities, Dupont in Florence, SC (NEI41302), Dupont in Old Hickory, TN (NEI45591), and Wellman in Darlington, SC (NEI43310), are still included in the emissions summary but risk results have been removed from the risk summary. All three facilities have acute HQs greater than 1 based on the acetaldehyde REL, and one of the m has the maximum value. The risks presented in the summary table represent the results based on the updated information. The population exposed to cancer risk would be less than presented in the table due to the adjusted emissions. We will update the d ata set with this information, and any additional information received during the comment period, before completing the final rule.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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62 **Table 7.2 -**  **1 Summary of Source Category Level Risks for Polyethylene Terephthalate**  **Production Result**  **HAP “Drivers”** Number of People Exposed to Noncancer Respiratory Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.002 n/a Contribution of HAP to Cancer Incidence acetaldehyde 74% n/a 1,4 - dioxane 16% n/a
**Table 7.2 -**  **2 Summary of Acute Refined**  **Screening Results for Polyethylene Terephthalate**  **Production**

**Results MAXIMUM ACUTE HAZARD QUOTIENTS**  **ACUTE DOSE -**  **RESPONSE VALUES**

**Based on REL Based on** 

**AEGL -**  **1/ ERPG**  **- 1**  **Based on**

**AEGL -**  **2/ ERPG**  **- 2**  **REL**

**(m g/m** **3 )**  **AEGL -**  **1**

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

**(m g/m** **3 )**  **AEGL -**  **2**

**(1 -**  **hr) (m**  **g/m 3**  **) ERPG**  **- 2** 

**(m g/m** **3 )**  **HAP Max. 1**  **- hr.** 

**Air Conc. (m**  **g/m 3**  **)** Acetaldehyde 19.3 8 0.2/ 1 0.04/ 0.05 0.47 81 18 490 360 Notes on Refined Process: 1) The screening was performed for all emitted HAP with available acute dose
- response values. Only those pollutants whose screening HQs were greater than 1 for at least one 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 health risks, based on an analysis o f currently available emissions 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. AE GL

– Acute exposure guideline levels represent emergenc y exposure (1
- hour) limits for the general public. AE GL
- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience effects that are notable discomfort, but which are transient and reversible upon cessation of exposure. AE GL
- 2 is 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 impaired ability to escape. EPRG

– Emergency Removal Program guidelines represent emergency exposure (1
- hour) limits for the general public. ERPG
- 1 is the maximum level 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. ERPG
- 2 is the maximum exposure 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 health effects or symptoms which could impair an individual’s ability to take protective action. The facility
- wide M IR

and TOSHI , available in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilitie s. The results of the facility
- wide assessment are summarized in Table 7 .2 - 3 . The results indicate that eight facilities with PET production processes have a facility
- wide cancer MIR greater than or equal to 1 in a million. The maximum facility
- wide can cer MIR for the source category is 9 in a million , and it occurs at two facilit ies . At one of these facilit ies , the source category contributes less than ten percent to the facility
- wide MIR, which is driven by emissions of arsenic and chromium from hazardous waste incineration. At the other facility , the PET production source category contributes almost 100 percent to the facility
- wide MIR, which is**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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63 driven by emissions of acetaldeh yde and 1,4
- dioxane from wastewater treatme nt operations
. The maximum facility
- wide TOSHI for the source category is 1, driven mainly by

emissions of chlorine from hazardous waste incineration. T he source category contributes approximately

five percent to the facility
- wide TOSHI
. **Table 7.2 -**  **3 Source Category Contribution to Facility**  **- Wide Cancer Risks** 
**–**

**Polyethylene Terephthalate Production Polyethylene Terephthalate**  **Production Number of Facilities Binned by Facility**  **- Wide**  **MIR (in 1 million) 48**  **Source Category MIR Contribution to**  **Fa cility**  **- Wide MIR**  < 1 1 ≤ MIR<10 10 ≤ MIR<100 > 100 **Total** > 90% 5 4 0 0 9 50 - 90% 1 0 0 0 1 10 - 50% 0 1 0 0 1 < 10% 0 1 0 0 1 **Total** 6 6 0 0 12 

### 8. **Risk Results for the P&R IV Methy l Methacry**  **late -**  **Butadiene**   ** St** **yr ene Source Category**  **8.1 Source Category**  **Description and Results**  Methyl methacrylate
- butadiene st yrene resins ( MBS ) are prepared by grafting meth yl methacrylate and st yrene onto a styrene - butadiene rubber in an emulsion process. In emulsion poly

merization, monomers are dispersed in water using a soap solut ion or an emulsifier. The product is a two
- phase pol ym er used as an impact modifier for rigid poly vinyl chloride products. These products are used for applications in packaging, building, and construction. Emission points for MBS resin production includ e process vents, equipment leaks, storage vessels, and wastewater operations. A complete description of the methyl methacrylate
- butadiene
- st yr ene production source category can be found in the text of the NPRM. We currentl y estimate that there are two M BS production facilities operating in the U.S. The data set contains two facilities identified with a MBS production MACT code in the 2005 NEI. The 2005 NEI was updated for this category with more recent data from industry and enhanced quality

assurance of facility

and emission locations. Both of these facilities are identified as major sources in the NEI. The emissions for the MBS production source category data set (of two facilities) are summarized in Table 8.1 - 1 . The total HAP emissions for the source category are approximately five tons per y ear. Based on these data, the HAP emitted in the largest quantities for these two facilities are: methyl methacrylate, 1,3
- butadiene, ethyl acrylate,**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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64 methanol, and sty

rene. T hese five HAP account for over 99 percent of the total emissions by mass. No PB - HA P 49 are reported in the data set for the MBS production source category
. **Table 8.1 -**  **1 Summary of**  **Em issions from the**  **Methyl Methacrylate -**  **Butadiene -**  **Styrene Production**

**Source Category and Availability of Dose**  **- Response Values** 

**HAP Emissions**  **(tpy) Number of** 

**Facilities Reporting**  **HAP (2**  **facilities in data set)**  **Prioritized Inhalation Dose -**  **Response Value Identified by OAQPS**  **a PB**  **- HAP?**  **Unit Risk Estimate for**  **Cancer? Reference** 

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

**Benchm ark**  **Values for Acute Noncancer?**  Methyl Methacrylate 2 1   1,3 - Butadiene 2 1    Ethyl Acrylate 0.9 1  Methanol 0.2 1   Styrene 0.2 1   Hydrochloric Acid 0.008 1  

a Specific dose
- response values for each chemical are identified on EPA’s Technology Transfer Network website for air toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html
. 

### 8.2 **Risk Characterization**  This section presents the results of the risk assessment for the meth yl methacrylate
- butadiene
sty rene production source category . The basic chronic inhalation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients. Also presented are the HAP “drivers,” which are the HAP that collectivel y contribute 90 percent of the maximum cancer risk or maximum hazard index at the highest exposure location , as well as a summary of the results of our facility
- wide assessments and our anal ys is of risks associated with the maximum allowed emissions under the current M A CT standards. A detailed summary of the facility
- specific risk assessment results is available in Appendix 4 . Table 8.2
- 1 summarizes the chronic and acute inhalation risk results for this source category
. The results indicate that maximum lifetime individual cancer risks could be as high as 0.4 in a million, with 1,3
- butadiene as the major contributor to the risk. The total estimated cancer incidence from the source category is 0.00003 excess cancer cases per ye ar or one case in every 33,000 y ears. There are no people with an estimated cancer risk greater than 1 in a million. The maximum chronic noncancer TOSHI value for the source category could be up to 0.007 from emissions of 1,3
- butadiene, indicating no significant potential for chronic noncan cer impacts.

49 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Volume 1, EPA
- 453K - 04 - 001A , as referenced in the EPA’s Technology Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html
.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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

65 Worst - case acute HQs were calculated f or every HAP that has an acute benchmark
. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries. Analy sis of potential off
- site acute impacts for this source category identified one facility

with the potential to exceed the acute ERPG
- 1 value for ethyl acrylate. Table 8.2
- 2 provides more information on the acute risk estimates for HAP that had an acute HQ greater than 1 for any benchmark. After these refinements, the highest worst
- case acute HQ value is 9 (based on the ethyl acryl ate ERPG
- 1). Th is worst
- case exposure estimate corresponds to an HQ of 0.01 based on the 1
- hour AEGL
- 1 value . For eth ylacrylate, the ERPG
- 1 value is indicative of the odor recognition threshold, while the AEGL
- 1 value is indicative of a level which could result in eye irritation. This suggests that, at this worst
- case exposure level, a person might smell the pollut ant, but not experience an y eye irritation. All other HAP emissions at all other facilities indicated no potential to cause acute impacts of concern. While these estimated worst
- case exceedances indicate that there is some potential for such acute exposures to occur, we note that exceeding the modeled ERPG
- 1 or AEGL
- 1 values does not necessarily indicate that adverse effects will occur, onl y that they cannot be ruled out. Further, in characterizing the potential for acute noncancer impacts of concern, it is important to remember the upward bias of these worst
- case exposure estimates and to consider the results along with the rather large uncertainties related to the emissions estimates and screening methodology
. Upon further evaluation, we identified that at the facility with the highest HQ values (based on the ERPG
- 1) equipment leaks were primarily responsible for the high acute HQ values, and that they

were modeled assuming that they all emanate from a single e mission location, rather than from numerous phy sical locations throughout the processing area. We note that this assumption further biases the HQ values high, but to an unknown extent, given that we do not know the actual size of the processing areas at e ach of these facilities. Taking all of this into consideration, these acute impact screening results indicate only the potential for acute impacts of concern, while the uncertainties and bias associated with them suggest that there may be no real acute is sues at all. A screening
- level evaluation of the potential human health risks associated with emissions of PB - HAP was not necessary for this source category

since no PB
- HAP are emitted
.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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66 **Table 8.2 -**  **1 Summary of Source Category Level Risks for Meth**  **yl Methacrylate**   ** Butadiene** **- Styrene Production**  **Result HAP “Drivers”**  **Facilities in Source Category** Number of Facilities Estimated to be i n Source Category 2 n/a Number of Facilities Identified in NEI and Modeled in Preliminary Risk Assessment 2 n/a **Cancer Risks** Maximum Individual Lifetime Cancer Risk (in 1 million) 0.4 1,3 -butadiene 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 0 n/a Greater than or equal to 1 in 1 million 0 n/a **Chronic Noncancer Risks** Maximum Reproductive Hazard Index 0.007 1,3 -butadiene Number of Facilities with Maximum Reproductive Hazard Index: Greater than 1 0 n/a **Acute Noncancer Refined Screening**  **Results** Maximum Acute Hazard Quotient 9 0.0 1 ethyl acrylate (ERPG
- 1)

ethyl acrylate (AEGL
- 1 ) Number of Facilities With Potential for Acute Effects 1 ethyl acrylate **Population Exposure** Number of People Living Within 50 Kilometers of Facilities Modeled 1,600,000 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 0 n/a Greater than or equal to 1 in 1 million 0 n/a Number of People Exposed to Noncancer Reproductive Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.00003 n/a Contribution of HAP to Cancer Incidence 1,3 -butadiene 100% n/a**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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67 **Table 8 .2**  **- 2**  **Summary of Acute Refined Screening**  **Results for Methyl Methacrylate**  **- Butadiene**  **** **Styrene Production**  **Facilities**

**Results MAXIMUM ACUTE HAZARD QUOTIENTS**  **ACUTE DOSE -**  **RESPONSE VALUES**

**Based on REL Based on** 

**AEGL -**  **1/ ERPG**  **- 1**  **Based on**

**AEGL -**  **2/ ERPG**  **- 2**  **REL**

**(m g/m** **3 )**  **AEGL -**  **1**

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

**(m g/m** **3 )**  **AEGL -**  **2**

**(1 -**  **hr) (m**  **g/m 3**  **) ERPG**  **- 2** 

**(m g/m** **3 )**  **HAP Max. 1**  **- hr.** 

**Air Conc. (m**  **g/m 3**  **)** Ethyl acrylate 0.37 0.01/ 9 0. 002/ 0.0 03 34 0.041 150 120 Notes on Refined Process: 1) The screening was performed for all emitted HAP with available acute dose
- response values. Only those pollutants whose screening HQs were greater than 1 for at least one 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 health risks, based on an analysis of cur rently available emissions 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. AE GL

– Acute exposure guideline levels represent emergency exp osure (1
- hour) limits for the general public. AE GL
- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience effects that are notable discomfort, but which are transient and reversible upon cessation of exposure. AE GL
- 2 is 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 impaired ability to escape. EPRG

– Emergency Removal Program guidelines represent emergency exposure (1
- hour) limits for the general public. ERPG
- 1 is the maximum level below which it is believed that nearly all individuals could be exposed for up to 1 hour wit hout experiencing other than mild, transient adverse health effects. ERPG
- 2 is the maximum exposure 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 facility
- wide M IR

and TOSHI , available in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facili ties. The results of the facility
- wide assessment are summarized in Table 8.2
- 3 . The results indicate that one facility with MBS production processes has a facility
- wide cancer MIR greater than or equal to 1 in a million. The maximum facility
- wide cance r M IR for the source category is 2 in a million , driven by emissions of acrylonitrile from a source without a MACT code assigned to it in the NEI. T he source category does not contribute to the facilit y - wide risk because the source category does not emit any

pollutants with cancer dose
- response values
. At the other facility , with a facility
- wide cancer MIR of 0.4 in a million, the facility
- wide cancer risk is driven almost exclusively

by emissions of 1,3
- butadiene from equipme nt leaks from the MBS process . The maximum facility
- wide TOSHI for the source category is less than 1. **Table 8.2 -**  **3 Source Category Contribution to Facility**  **- Wide Cancer Risks** 
**– Methyl** 

**Methacrylate -**  **Butadiene -**  **Styrene Production Methyl Methacrylate**  **- Butadiene**  **** **Styrene Production**  **Number of Facilities Binned by Facility -**  **Wide MIR (in 1 million)**  **Source Category MIR Contribution to Facility**  **- Wide MIR**  < 1 1 ≤ MIR<10 10 ≤

MIR<100 > 100 **Total** > 90% 1 0 0 0 1**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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68

50 - 90% 0 0 0 0 0 10 - 50% 0 0 0 0 0 < 10% 0 1 0 0 1 **Total** 1 1 0 0 2 

### 9. **Risk Results for the P&R IV A cr** **yl onitrile**  **- Butadiene**  **- St**  **yr ene**  **Source Category 9.1**  

### Source Category **Description and Results** Acrylonitrile
- butadiene
- sty rene ( ABS ) resins consist of a terpoly mer of acrylonitrile, butadiene, and st yr ene and can be s ynthesized b y e mulsion, suspension, and continuous mass poly merization. The majority of ABS resin production is by batch emulsion. In emulsion poly merization, monomers are dispersed in water using a soap solution or an emulsifier. The emulsion process involves three dis tinct poly merizations: poly

merization of butadiene to form poly butadiene, grafting of sty rene and acrylonitrile monomers to the poly butadiene substrate, and co
- pol ym erization of sty rene - acrylonitrile. Specialized ABS resins are produced b y suspension poly

m erization, where the monomer is suspended in a water phase. In mass poly merization, monomers are reacted without the use of emulsifiers, suspending agents, salts or waters. The primary

HAP emissions during the ABS production process occur via equipment leaks and process vents. Ty pical products made from ABS resins are piping, refrigerator door liners and food compartments, automotive components, telephones, luggage and cases, to y s, mobile homes, and margarine tubs
. A complete description of the acryl onitrile
- butadiene
- sty rene production source category can be found in the text of the NPRM. We currentl y estimate that there are five acrylonitrile
- butadiene
- sty rene production facilities operating in the U.S. The data set contains five facilities id entified with a acrylonitrile
butadiene
- st yrene production MACT code in the 2005 NEI
. The 2005 NEI was updated for this category

with more recent data from industry and enhanced qualit y assurance of facility and emission locations. All 5 of these faciliti es are identified as major sources in the NEI. The emissions for the acrylonitrile
- butadiene
- st yrene production source category data set (of five facilities) are summarized in Table 9.1
- 1 . The total HAP emissions for the source category are approximat ely

200 tons per ye ar. Based on these data, the HAP emitted in the largest quantities across these five facilities are: sty rene, acrylonitrile, 1,3
- butadiene, cumene, methyl methacrylate, and xylenes (mixed). These six HAP account for over 90 percent of the total emissions by

mass. No PB - HA P 50 are reported in the data set for the acrylonitrile
butadiene
- st yrene production source category .

50 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Volume 1, EPA
- 453K - 04 - 001A, as referenced in the NPRM and provided on the EPA’s Technology Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html
.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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69 **Table 9.1 -**  **1 Summary of Emissions from the Acrylonitrile**  **- Butadiene**  **- Styrene Production Source**  **Category and Avai la**  **bility of Dose -**  **Response Values**

**HAP a**  **Emissions (tpy)**  **Number of**

**Facilities Reporting HAP**  **(5 facilities in data set)**  **Prioritized Inhalation Dose -**  **Response Value Identified by OAQPS**  **b PB**  **- HAP?**  **Unit Risk Estimate for**  **Cancer? Reference** 

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

**Benchm ark**  **Values for Acute Noncancer?**  Styrene 92 4   Acrylonitrile 32 5    1,3 - Butadiene 32 5    Cumene 14 4   Methyl Methacrylate 11 3   Xylenes (Mixture of o, m, and p Isom ers) 10 2   Ethyl Benzene 7 4    Aniline 2 1    Ethylene Glycol 2 1  Triethylamine 0.9 1   Propylene Oxide 0.8 1    Acrylic Acid 0.7 2   Chloromethyl Methyl Ether 0.5 1  Acetaldehyde 0.5 1    o - Xylene 0.3 1   Vinyl Acetate 0.2 1   2,4 - Dichlorophenoxy Acetic Acid 0.03 1 Chloroacetic Acid 0.02 1  Glycol Ethers 0.02 1   Ethyl Acrylate 0.01 1  2,4,6 - Trichlorophenol 0.007 1  N,N - Dimethylformamide 0.004 1   Phosgene 0.003 1   Hydroquinone 0.002 1 Naphthalene 0.002 1   Ethylene Oxide 0 1   

a Notes for how HAP were speciated for risk assessment:  For emissions reported generically as “Glycol Ethers” or specific glycol ethers not found on EPA’s Technology Transfer network for air toxics (see footnote b), emissions will be treated as ethylene glycol methyl ether. b Specific dose
- response values for each chemical are identified on EPA’s Technology Transfer Network website for air toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html .**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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70 **9.2** 

### Risk Characterization This section presents the results of the risk assessment for the acrylonitrile
- butadiene
- st yr ene production source category . The basic chronic inhalation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients. Also pr esented are the HAP “drivers,” which are the HAP that collectively

contribute 90 percent of the maximum cancer risk or maximum hazard index at the highest exposure location , as well as a summary of the results of our facility
- wide assessments and our analy sis or risks associated with the maximum allowed emissions under the current MACT standards. A detailed summary of the facility
- specific risk assessment results is available in Appendix 4 . Table s 9.2 - 1 and 9.2
- 2 summarize the chronic and acute inhal ation risk results for this source category . The results indicate that maximum individual lifetime cancer risks could be as high as 30 in a million, with acrylonitrile and 1,3
- butadiene as the major contributors to the risk. The total estimated cancer in cidence from the source category is 0.003 excess cancer cases per year, or one case in every 333 y ears. Approximately 530 people are estimated to have cancer risks at or above 10 in a million and approximately 32,000 people are estimated to have cancer ri sks at or above 1 in a million as a result of the emissions from 4 facilities. The maximum chronic noncancer TOSHI value for the source category could be up to 0.2 from emissions of 1,3
- butadiene, indicating no significant potential for chronic noncancer impacts. Worst - case a cute HQs were calculated f or every HAP that has an acute benchmark, and the highest acute HQ value of 2 (based on the acetaldehyde REL) is shown in Table 9.2
- 1. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries. Table 9.2
- 1 provides more information on the acute risk estimates for HAP that had an acute HQ greater than 1 for any benchmark. The highest refined worst
- case acute HQ value remains 2 based on the acetaldeh yde REL , with only one facility

showing the potential to exceed the REL . Th is estimated worst
- case acute impact correspond s to an acute HQ of 0. 0 4 based on the a cetaldeh yde ERPG
- 1. Refer to Table 9.2
- 2 for further information on the refined acute risk estimate. All other HAP emissions at all other facilities indicated no potential to cause acute impacts of concern. While these estimated worst
- case exceedances indicate that there is some potential for such acute exposures to occur, we note that exceeding the modeled REL or ERPG
- 1 values does not necessarily indicate that adverse effects will occur, onl y that they cannot be ruled out. Further, in characterizing the potential for acute noncancer impacts of co ncern, it is important to remember the upward bias of these worst
- case exposure estimates and to consider the results along with the rather large uncertainties related to the emissions estimates and screening methodology
. A screening
- level evaluation o f the potential human health risks associated with emissions of PB - HAP was not necessary for this source category

since no PB
- HAP are emitted.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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71 **Table 9.2 -**  **1 Summary of Source Category Level Risks for Acrylonitrile**  **- Butadiene**  **** **Styrene Production Result**  **HAP “Drivers” Facilities in Source Category**  Number of Facilities Estimated to be i n Source Category 5 n/a Number of Facilities Identified in NEI and Modeled in Preliminary Risk Assessment 5 n/a **Cancer Risks** Maximum Individual Lifetime Cancer Risk (in 1 million) 30 acrylonitrile, 1,3
-butadiene 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 3 acrylonitrile, 1,3
-butadiene Greater than or equal to 1 in 1 million 4 acrylonitrile, 1,3
-butadiene, ethyl benzene **Chronic Noncancer Risks** Maximum Reproductive Hazard Index 0.2 1,3 -butadiene Number of Facilities with Maximum Reproductive Hazard Index: Greater than 1 0 n/a **Acute Noncancer Screening**  **Results** Maximum Acute Hazard Quotient 2 0. 0 4 acetaldehyde (REL)

acetaldehyde (ERPG
- 1) Number of Facilities With Potential for Acute Effects 1 acetaldehyde **Population Exposure** Number of People Living Within 50 Kilometers of Facilities Modeled 3,900,000 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 530 n/a Greater than or equal to 1 in 1 million 32,000 n/a Number of People Exposed to Noncancer Reproductive Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.003 n/a Contribution of HAP to Cancer Incidence acrylonitrile 66% n/a 1,3 -butadiene 32% n/a**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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72 **Table 9.2**  **- 2**  **Summary of Acute Screening**  **Results for Acrylonitrile -**  **Butadiene -**  **Styrene Production** 

**Results MAXIMUM ACUTE HAZARD QUOTIENTS**  **ACUTE DOSE -**  **RESPONSE VALUES**

**Based on REL Based on** 

**AEGL -**  **1/ ERPG**  **- 1**  **Based on**

**AEGL -**  **2/ ERPG**  **- 2**  **REL**

**(m g/m** **3 )**  **AEGL -**  **1**

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

**(m g/m** **3 )**  **AEG**

**L -**  **2 (1**  **- hr)**  **(m g/**  **m 3**  **) ERP**  **G -**  **2 (m**  **g/ m** **3 )**  **HAP Max. 1**  **- hr.** 

**Air Conc. (m**  **g/m 3**  **)** Acetaldehyde 0.71 2 0.009/ 0.04 0.001/ 0.002 0.47 81 18 490 360 Notes on Screening Process: 1) The screening was performed for all emitted HAP with available acute dose
- response values. Only those pollutants whose screening HQs were greater than 1 for at least one 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 pos ing acute health risks, based on an analysis of currently available emissions 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. AE GL

– Acute exposure guideline levels represent emergency exposure (1
- hour) limits for the general public. AE GL
- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience effects that are notabl e discomfort, but which are transient and reversible upon cessation of exposure. AE GL
- 2 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long
- l asting adverse health effects or an impaired ability to escape. ERPG

– Emergency Removal Program guidelines represent emergency exposure (1
- hour) limits for the general public. ERPG
- 1 is the maximum level below which it is believed that nearly all individ uals could be exposed for up to 1 hour without experiencing other than mild, transient adverse health effects. ERPG
- 2 is the maximum exposure below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing or d eveloping irreversible or other serious health effects or symptoms which could impair an individual’s ability to take protective ac tion. The facility
- wide M IR

and TOSHI , available in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility
- wide assessment are summarized in Table 9.2
- 3. The results indicate that four facilities with ABS production processes have a facility
- wide cancer M IR greater than or equal to 1 in a million. The maximum facility
- wide cancer MIR for the source category is 30 in a million, with the source category contributing almost 100 percent of the facilit y - wide risk, driven b y emissions of acrylonitrile and 1,3
- butadiene from process vents. The maximum facility
- wide TOSHIfor the source category is less than 1.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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73 **Table 9.2 -**  **3 Source Category Contribution to Facility**  **- Wide Cancer Risks** 
**–**

**Acrylonitrile -**  **Butadiene -**  **Styrene Production Acrylonitrile**  **- Butadiene**  **- Styrene** 

**Production Number of**  **Facilities Binned by Facility -**  **Wide MIR (in 1 million)**  **Source Category MIR Contribution to Facility**  **- Wide MIR**  < 1 1 ≤ MIR<10 10 ≤ MIR<100 > 100 **Total** > 90% 0 0 3 0 3 50 - 90% 0 0 1 0 1 10 - 50% 1 0 0 0 1 < 10% 0 0 0 0 0 **Total** 1 0 4 0 5 

### 10. **General Discussion of Uncertainties and How** **They Have Been**  **Ad dressed**  **10.1** 

### Exposure Modeling Uncertainties 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 inventory likel y dominate the uncertainties in our exposure modeling estimates. The chronic exposure modeling uncertainties are considered relativel y small in comparison, since we are using EPA’s refined lo cal dispersion model with site
specific parameters and reasonabl y representative meteorology. If an ything, the population exposure estimates are biased high b y not accounting for short
- or long
- term population mobility and b y neglecting processes like dep osition, plume depletion, and atmospheric degradation. Additionally , estimates of the maximum individual risk (MIR) contain uncertaint y , 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 impact on the estimated MIR for a source category
. 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
- y ear chronic exposure period, leading to a potential downward bias in both the MIR and population risk estimates. A sensitivity

anal ys is performed for the 1999 NATA found that the selection of the meteorology

dataset location could result in a range of chr onic ambient concentrations which varied from as much as 17% below the estimated value to as much as 84% higher than the estimated value. This variability translates directly

to the estimated exposures and risks in our assessment, indicating that the actu al risks could vary from 17% lower to 84% higher than the estimated values.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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74 We have purposel y biased the acute screening results high, considering that they depend upon the joint occurrence of independent factors, such as hourly emissions rates, meteorolo gy and human activity

patterns. Furthermore, in cases where multiple acute threshold values are considered scientificall y acceptable we have chosen the most conservative of these assessments, erring on the side of overestimating potential health risks fro m acute exposures. In the cases where these results indicated the potential for exceeding short
- term health thresholds, we have refined our assessment b y developing a better understanding of the geograph y of the facility

relative to potential exposure loc ations and the true variability of short
- term emission rates. **10.2** 

### Uncertainties **in the Dose -**  **Response Relationships** Inthe sections that follow, separate discussions are provided on uncertainty associated with cancer potency

factors and noncancer reference values. Cancer potency values are derived for chronic (lifetime) exposures. Noncancer reference values are generall y derived for chronic exposures (up to a lifetime), but may also be derived for acute ( <24 hours), short
- term (>24 hours up to 30 day s), and subchronic (>30 day s up to 10% of lifetime) exposure durations, all of which are derived based on an assumption of continuous exposure throughout the duration specified. For the purposes of assessing all potential health risks associated with the emis sions included in an assessment, we rel y 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 sources 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. Additionally , chronic dose
- response values for certain compounds included in the assessment may be under EPA IRI S 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 significantl y mischaracterize human health risk **Cancer assessment** The discussion of dose
- response uncertainties in the estimation of cancer risk below focuses on the uncertainties associated with the specific approach currentl y used by the EPA to develop cancer potency

factors. In gen eral, these same uncertainties attend the development of cancer potency

factors by

CalEPA, the source of peer
- reviewed cancer potency factors used where EPA
- developed values are not yet available. To place this discussion in context, we provide a quote fr om the EPA’s Guidelines for Carcinogen Risk Assessment [ 30 ] (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 Ass essment for 7 Chemical Sector Source Categories** 

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75 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 estimation 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 populations 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 Guide lines 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). 51 In s ome circumstances, the true risk could be as low as zero; however, in other circumstances the risk could also be greater. 52 When developing an upper bound estimate of risk and to provide risk values that do not underestimate risk, EPA generall y relies on conservative default approaches. 53 EPA also uses the upper bound (rather than lower bound or central) estimates in its assessments, although it is noted that this approach can have limitations for some uses (e.g. priority setting, expected benefits anal ys i s). Such health risk assessments have associated uncertainties, some which may be considered quantitatively , and others which generally are expressed qualitativel y. 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 emplo yedmay differ in how well they

represent actual biological processes for the assessed substance. EPA’s Risk Cha racterization Handbook also recommends that risk characterizations present estimates demonstrating the impact on the assessment of alternative

51 IRIS glossary (www.epa.gov/NCEA/iris/help_gloss.htm). 52 The exception to this is the URE for benzene, which 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. 53 According to the NRC report Science and Judgment in Risk Assessment (NRC, 1994) “[Default] options are generic approaches, based on gener al 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 Federal Government: Managing the Proces s 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, th e 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 assumptions are used to ensure that risk to ch emicals 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.epa.gov/osa/pdfs/ratf
- final.pdf.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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76 choices, data, models and assumptions [ 31 ]. Some of the major sources of uncertaint y and variability

in deriving cancer risk values are described more full y below. (1) The qualitative similarities or differences between tumor responses observed in experimental animal bioassay s and those which would occur in humans are a source of uncertaint y in cancer risk assessm ent. 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. 54 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 species responses can lead to either under
- estimation or over
- estimation of human cancer risks. (2) Uncertai nties regarding the most appropriate dose metric for an assessment can also lead to differences in risk estimates . For example, the measure of dose is commonly expressed 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 metaboli zed in the body). Quantitative uncertainties result when the appropriate choice of a dose metric is uncertain or when dose metric estimates are themselves 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 differen ces in phy sical size of the species), which introduce another source of uncertaint y. 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 either greater than or less than that estimated by baseline scientific scaling predictions due to uncertaintie s associated with limitations in the test data and the correctness of scaled estimates. (4) EPA cancer risk estimates, whether based on epidemiological or experimental animal data, are generally

developed using a benchmark dose (BMD) anal ys is 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 generall y utilized the multistage model for estimation of the BMDL using cancer bioassay data (see further discussion below).

54 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 implicat ions of animal study results for humans.”**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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77 (5) Extrapolation from high to low doses is an important, and potentially large, source of uncertaint y 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 c auses cancer). EPA’s Cancer Guidelines express a preference for the use of reliable, compound
- specific, biologicall y - based risk models when feasible; however, such models are rarel y available. The mode of action for a pollutant (i.e., the manner in which a pollutant causes cancer) is a key consideration 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 respon se). 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
- specific 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 background 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 approach. 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 o f uncertainty and variability . EPA believes 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 generall y provide a health protective approach. Note that another source of uncertaint y is the characterization of low
- dose nonlinear, non
- threshold relationships. The National Academy of Sciences has encouraged the exploration of sigmoidal ty pe functions (e.g., log
- probit models) in representing dose response relationships due to the variability in response within human populations. Another National Research Council (NRC) report [ 32 ] suggests that models based on distributions of individual thresholds are likel y to lead to sigmoidal
- shaped dose
- response functi ons for a population. This report notes 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 suscept ibility

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 respon ses in bioassay s with geneticall y more uniform rodents). Note also that low dose linearit y 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 processes. 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 l ine extrapolation. The impact of the choice of the BMDL on bottom line**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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78 risk estimates can be quantified by comparing risk estimates using the BMDLvalue to central estimate BMD values, although these differences are generall y not a large contributor to un certaint y in risk assessment (Subramaniam et. al., 2006) [ 33 ]. It is important to note that earlier EPA assessments, including the majorit y of those for which risk values exist today , were generally

developed using the multistage model to extrapolate down to environmental dose levels and did not 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 confi dence limit of the multistage model. (6) Cancer risk estimates do not generall y 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 likely to be more sensitive to the action of a carcinogen than the t yp ical individual, although compound
- specific data to evaluate this variability are generally

not available. There may also be important life stage diffe rences in the quantitative potency of carcinogens 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 generall y quantitatively address life stage diff

erences. However, one approach used commonly 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 reliable data, thus 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. That is, EPA and other organizations which develop noncancer reference values (e.g., the Agency

for Toxic Substances and Disease Registry

– ATSDR) utilize an approach that is intended not to underestimate risk in the fa ce of uncertainty and variability
. When 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 commonly

default values 55 e.g., factors of 10 or 3, used in the absence of compound
- specific data; where data are available, uncertainty factors may also be developed using compound
- specific information. When data are limited, more
55 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 e lements 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 default option as “the option chosen on the basis of risk assess ment 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 s ubstance 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 (although defaults are not intended to overtl y 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 Ass essment for 7 Chemical Sector Source Categories** 

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79 assumptions are need ed and more default factors are used. Thus there may be a greater tendency to overestimate risk

—in the sense that further study might support development of reference values that are higher (i.e., less potent) because fewer default assumptions are needed. However, for some pollutants it is possible 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 a dail y 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 of deleterious effects during a lifetime. 56 To derive values that are intended to be “without appreciable risk,” EPA’s methodology relies upon an uncertainty factor (UF) approach [ 34 ],[ 35 ] which includes consideration of both uncertainty and variability
. EPA begins b y evaluating all of the available peer
- reviewed literature to determine non
cancer endpoints of concern, evaluating the quality, strengths and limitations of the available s tudies. EPA ty

picall y 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 deter mined 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 significantl y elevated (no observed adverse effect level

— NOAEL); or (3) use of the lowest observed adverse effect level (LOAEL). A series of downward adjustments using default UFs is then applied to the POD to estimate the reference value [ 36] . 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 study with less
- than
- lifetime exposure (i.e., extrapolating from subchronic to chronic exposure); (4) uncertaint y in extrapolating from a LOAE L 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, default adjustment values are selected for the individual UFs. For each t ype of uncertaint y (when relevant to the assessment) , EPA ty picall y applies an UF value of 10 or 3 with the cumulative UF value leading to a downward adjustment of 10
- 3000 fold from the selected 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 applying human toxicity data and an inters pecies extrapolation is not required) the associated UF is not used. The major adjustment steps are described more full y below. 1) Heterogeneit y among humans is a key source of variability

as well as uncertaint y. Uncertaint y related to human variation is considered in extrapolating doses from a subset or
56 See IRIS glossary**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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80 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
- specifi c data on human variation, a 10
- fold UF is 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 pot ential toxicity to humans , there are uncertainties in such extrapolations. Inthe absence of data to the contrary , the ty pical approach is to use the most relevant endpoint from the most sensitive species and the most sensitive sex in assessing risks to the average human. Ty picall y , compound specific data to evaluate relative sensitivity in humans versus rodents are lacking, thus leading to uncertaint y in this extrapolation. Size
- related differences (allometric relationships) indicate that ty picall y humans are more sensitive than rodents when compared on a mg/kg/day basis. 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 examine species differences in pharmacokinetic processing and associated uncertainties; however, such dosimetric adjustments are not alway s possible. Information may not be available to quantitatively assess toxicok inetic or toxicody namic differences between animals and humans, and in many cases a 10 - fold UF (with separate factors of 3 for toxicokinetic and toxicody namic components) is used to account for expected species differences and associated uncertainty in extrapolating from laboratory

animals to humans 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 may be used for the remaining component. 3) In the case of reference values for chronic exposures where onl y data 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 o r 10 - fold is ty picall y applied unless the available scientific information supports use of a different value. 4) Toxicity

data are t ypically 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 exposure 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 anal ys is, which is not alway s po ssible. Use of a NOAEL is the next preferred approach after BMD analy sis in determining a POD for deriving a health effect reference value. However, many studies lack a dose or exposure level at which an adverse effect is not observed (i.e., a NOAEL is n ot identified). When using data limited to a LOAEL, a UF of 10 or 3
- fold is often applied.**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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81 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 variabilit y and uncertaint y 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 ba sed on chemical
specific or health effect
- specific information (e.g., simple irritation effects do not vary appreciably

between human individuals, hence a value of 3 is ty picall y 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 extrapolating from animals to humans; 3) uncertainty in LOAEL 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 Ass essment for 7 Chemical Sector Source Categories** 

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82 

### 11 **References** 1 . US EPA. National Emission Standards for Hazardous Air Pollutants
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the EPA’s Science Advisory Board with C ase Studies

– MACT I Petroleum Refining Sources and Portland Cement Manufacturing
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– AERMOD. EPA
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Planning and Standards. htt p://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
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ntegrated Risk I

nformation System. http://www.epa.gov/iris/index.html
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for Toxic Substances and Disease Registry. 2006. Minimum Risk Levels (MRL s) for Hazardous Substances. http://www.atsdr.cdc.gov/mrls/index.html
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83 15
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mplementation Workgroup Communication II : Memo from W.H. Farland dated 14 June 20 06. http://www.epa.gov/osa/spc/pdfs/CGIWGCommunication_II.pdf 26 . US EPA, 2005. Supplemental guidance for assessing earl y - life exposure to carcinogens. EPA/630/R
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. US EPA, 2005. Science Policy Council Cancer Guidelines Implementation Workgroup Communication I : Memo from W.H. Farland dated 4 Octob er 2005 to Science Policy Council. http://www.epa.gov/osa/spc/pdfs/canguid1.pdf**Draft Risk Ass essment for 7 Chemical Sector Source Categories** 

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84 28 . US EPA, 1986. Guidelines for the Health Risk Assessment of Chemical Mixtures. EPA
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lene. National Academies Press, Washington DC
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– 830. 34
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nhalation Dosimetry
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