1



## Residual Risk Assessment for 7 Source Categories:

Pesticide Active Ingredient Production Polyether Polyols Production Polymers and Resins IV

-- Styrene Acrylonitrile Polymers and Resins IV

-- Polystyrene Polymers and Resins IV

– Polyethylene Terephthalate 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 January 20142



### 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 Screenin g and Refined Assessments

................................ ...................... 11

2.5. Multipathway human health and environmental risk screening

................................ 12

2.6. Dose

- Response Assessment

................................ ................................ ...................... 15

2.6.1. Sources of chronic dose

- response information

................................ .................. 15

2.6.2. Sources of acute dose

- response information

................................ ...................... 24

2.7. Risk Characterization

................................ ................................ ................................ 29

2.7.1. General

................................ ................................ ................................ ............... 29

2.7.2. Mixtures

................................ ................................ ................................ ............. 31

2.7.3. Facility

- wide Risks

................................ ................................ ............................ 31

2.7.4. MACT

- Allowable Risks

................................ ................................ .................... 32

3. Risk Results for Pesticide Active Ingredient Production

................................ ...................... 32

3.1 Source Category Description and Results

................................ ................................ . 32

3.2 Risk Characterization

................................ ................................ ................................ 35

4. Risk Results for the Polyether Polyols Production Sou rce Category

................................ ... 38

4.1 Source Category Description and Results

................................ ................................ . 38

4.2 Risk Characterization

................................ ................................ ................................ 42

5. Risk Results for the P&V IV Styrene Acrylonitrile Source Category

................................ .. 47

5.1 Source Category Description and Results

................................ ................................ . 47

5.2 Risk Characterization

................................ ................................ ................................ 48

6. Risk Results for the P&R IV Polystyrene Production Source Category

............................... 50

6.1 Source Category Description and Results

................................ ................................ . 50

6.2 Risk Characterization

................................ ................................ ................................ 51

7. Risk Results for the P&R IV Polyethylene Terephthalate Source Category

........................ 55

7.1 Source Category Description and Results

................................ ................................ . 55

7.2 Risk Characterization

................................ ................................ ................................ 57

8. Risk Results for the P&R IV Methyl Methacrylate

- Butadiene

- Styrene Source Category

... 62

8.1 Source Category Description and Results

................................ ................................ . 62

8.2 Risk Characterization

................................ ................................ ................................ 63

9. Risk Results for th e P&R IV Acrylonitrile

- Butadiene

- Styrene Source Category

................ 67

9.1 Source Category Description and Results

................................ ................................ . 67

9.2 Risk Characterization

................................ ................................ ................................ 69

10. General Discussion of Uncertainties and How They Have Been Addressed

........................ 73

10.1 Exposure Modeling Uncertainties

................................ ................................ ......... 73

10.2 Uncertainties in the Dose

- Response Relationships

................................ ............... 73

11 References

................................ ................................ ................................ ............................. 823

Index of Tables

Table 2.2

- 1 AERMOD version 11103 model options for RTR mod eling

................................ . 8

Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcinogens

...... 19

Table 2.6

- 1 (b) Dose

- Response Values for Chronic Inhalation Exposure to Noncarcinogens 21

Table 2.6

- 2 Dose

- Response Values for Acute Exposure

................................ ......................... 27

T able 3.1

- 1 Summary of Emissions from the Pesticide Active Ingredients Source Category and Availability of Dose

- Response Values

................................ .............................. 33

Table 3.2

- 1 Summary of Source Category Level Risks for Pesticide Active Ingredient

Production 36

Table 3.2

- 1 Summary of Environme ntal Risk Screen Results for the Pesticide Active Ingredient Production Source Category

................................ ................................ ................... 37

Table 3.2

- 2 Source Category Contributi on to Facility

- Wide Cancer Risks

– Pesticide Active Ingredient

................................ ................................ ................................ ...................... 38

Table 4.1

- 1 Summary of Emissions from the Polyether Polyols Production Source Category and Availability of Dose

- Response Values

................................ .............................. 39

Table 4.2

- 1 Summary of Source Category Level Inhalation Risks for Polyether Polyols

Production 44

Table 4.2

- 2 Summary of Acute Results for Polyether Polyols Production Facilities

........ 45

Table 4.2

- 3 Summary of Environmental Risk Screen Results for the Polyeth er Polyols Production Source Category

................................ ................................ ................................ .... 46

Table 4.2

- 4 Source Category Contribution to Facility

- Wide Cancer Risks

– Polyether Polyo ls Production

................................ ................................ ................................ ................... 46

Table 5.1

- 1 Summary of Emissions from the Styrene

- Acrylonitrile Production Source Category and Availability of D ose

- Response Values

................................ .............................. 48

Table 5.2

- 1 Summary of Source Category Level Risks for Styrene

- Acrylonitrile

Production 49

Table 5.2

- 2 Source Category Contribution to Facility

- Wide Cancer Risks

– Styrene

Acrylonitrile Production

................................ ................................ ................................ ........... 50

Table 6.1

- 1 Summary of Emissions from the Polystyrene Production Source Category and Availability of Dose

- Response Values

................................ ................................ .................... 51

Table 6.2

- 1 Summary of Source Category Level Risks for Polystyrene Production

........ 53

Table 6.2

- 2 Summary of Environmental Risk Screen Results for the Polystyrene Production Source Category

................................ ................................ ................................ .... 54

Table 6.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

– Polystyrene

Production 54

Table 7.1

- 1 Summary of Emissions from the Polyethylene Terephthalate Production Source Category and Availability of Dose

- Response Values

................................ .................. 56

Table 7.2

- 1 Summary of Source Category Level Risks for Polyethylene Terephthalate

Production 60

Table 7.2

- 2 Summary of Acute Results for Polyethylene Terephthalate Production

........ 61

Table 7.2

- 3 Summary of Environmental Risk Screen Results for Polyethylene Terephthalate Production

................................ ................................ ................................ ......... 61

Table 7.2

- 4 Source Category Contribution to Facility

- Wide Cancer Risks

– Polyethylene Terephthalate Production

................................ ................................ ................................ ......... 624

Table 8.1

- 1 Summary of Emissions from the Methyl Methacrylate

- Butadiene

- Styrene Production Source Category and Availability of Dose

- Response Values

............................... 63

Table 8.2

- 1 Summary of Source Category Level Risks for Methyl Methacrylate

Butadiene

- Styrene Production

................................ ................................ ................................ . 65

Table 8.2

- 2 Summary of Acute Results for Methyl Methacrylate

- Butadiene

- Styrene

Production Facilities

................................ ................................ ................................ ................ 66

Table 8.2

- 3 Summary of Environmental Risk Screen Results for Methyl Methacrylate

Butadiene

- Styrene Production Facilities

................................ ................................ .................. 66

Table 8.2

- 4 Source Category Contribution to Facility

- Wide Cancer Risks

– Methyl Methacrylate

- Butadiene

- Styrene Production

................................ ................................ ........... 67

Table 9.1

- 1 Summary of Emissions from the Acrylonitrile

- Butadiene

- Styrene Production Source Category and Availability of Dose

- Response Values

................................ .................. 68

Table 9.2

- 1 Summary of Source Category Level Risks for Acrylonitrile

- Butadiene

Styrene Production

................................ ................................ ................................ ................... 71

Table 9.2

- 2 Summary of Environmental Risk Screen Results for Acrylonitrile

- Butadiene

Styrene Production

................................ ................................ ................................ ................... 72

Table 9.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

– Acrylonitrile

Butadiene

- Styrene Production

................................ ................................ ................................ . 72

Appendices

Appendix 1 Technical Support Document for HEM3 Modeling Appendix 2 Meteorological Data for HEM3 Modeling Appendix 3 Analysis of data on short

- term emission rates relative to l ong

- term emission

rates Appendix 4 Technical Support Document for TRIM

- Based Multipathway Screening

Scenario for RTR: Summary of Approach and Evaluation Appendix 5 Detailed Risk Modeling Results Appendix 6 Acute Impacts Refined Analysis Appendix 7 Dispers ion Model Receptor Revisions and Additions5

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 Age ncy ERPG Emergency Response Planning Guideline

HAP Hazardous Air Pollutant

HEM Human Exposure Model

HI Hazard index HQ Hazard quotient

IRIS Integrated Risk Information System

MACT Maximum Achievable Control Technology

MIR Maximum Individual Risk

MOA Mode of action

NAC National Advisory Committee

NACAA National Association of Clean Air Agencies

NATA National Air Toxics Assessment

NEI National Emissions Inventory

PB

- HAP Persistent and Bioaccumulative

- HAP

POM Polycyclic organic matter

REL Reference exposure level

RfC Reference concentration

RfD Reference dose

RTR Risk and Technology

TOSHI Target

- organ

- specific hazard index

URE Unit risk estimate6



### 1. Introduction

Section 112 of the Clean Air Act (CAA) establishes a two

- stage regulatory pro cess for addressing emissions of hazardous air pollutants (HAPs) from stationary sources. In the first stage, section 112(d) requires the Environmental Protection Agency (EPA, or the Agency) to develop technology

- based standards for categories of sources ( e.g., petroleum refineries, pulp and paper mills, etc.) [ 1 ]. EPA has largely completed the initial Maximum Achievable Control Technology (MACT) standards as required under this provision. Under section 112(d)(6), EPA must review each of these technology

- ba sed standards at least every eight years and revise a standard, as necessary, “taking into account developments in practices, processes and control technologies.” In the second stage, EPA is required under section 112(f)(2) to assess the health and environ mental risks that remain after implementation of the MACT standards. If additional risk reductions are necessary to protect public health with an ample margin of safety or to prevent an adverse environmental effect, EPA must develop

standards to address th ese 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 residual 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 Plan” 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 Methodologies” [ 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 assessments and we will be continuing our efforts to improve our assessments by incorporating updates based on the SAB recommendations as they are developed and become available. Our responses to the key recommendations of the SAB are outlined in the memo entitled, “EPA’s Actions in Response to Key Recommendations from the SAB Review of RTR Risk Assessment Methodologies”
[ 4 ].

This document contains the metho ds 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 originally addressed under the Polymers

and Resins IV MACT. The seven source categories are:

Pesticide Active Ingredient Production, Polyether Polyols Production, Polymers and Resins IV

-- Styrene Acrylonitrile, Polymers and Resins IV

-- Polystyrene, Polymers and Resins IV

-- Polyethylene Terephthalate, Polymers and Resins IV

-- Methyl Methacrylate

- Butadiene Styrene, and Polymers and Resins IV

-- Acrylic Butadiene Styrene.

The methods discussion includes descriptions of the methods used to develop refined estimates of chronic inhalation exposures and human health risks for cancer and noncancer7

endpoints, as well as descriptions of the methods used to screen for acute health risks, chronic

non

- inhalation health risks, and adverse environmental effects. Since the screening assessments indicated low potential for chronic non

- inhalation health effects or environmental impacts, including effects to threatened and endangered species, no further refinement of these assessments was performed.



### 2. Methods

2.1. Emissions and source data

The 2005 National Emissions Inventory (NEI) that was used in the 2005 National

- scale Air Toxics Assessment (NATA) 1 served as the starting point for these assessments for the proposed rule. During the comment period after proposal the data were reviewed by industry

and also the National Associa tion of Clean Air Agencies (NACAA). The 2005 NATA NEI was updated based on the comments received and contains information on actual emissions during the entire 2005 base year. For the final rule this updated 2005 NATA NEI database was our primary source of data. Using the process MACT code, 2 we developed a subset of the 2005 NATA NEI that contains facility, process, and emissions data for each facility in these seven source categories. An engineering review of the information was performed using EPA enginee rs 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 readily

- 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. In dustry and NACAA provided revisions to emissions, stack parameters, and location coordinates. EPA engineers reviewed the suggested industry and NACAA revisions and performed a comprehensive review of the

location coordinates. These data underwent an extens ive QA/QC procedure, and revisions were made to the dataset as necessary. The emissions data and modifications made to the

2005 NATA NEI data are discussed in the memo entitled “Emissions Data Used in Residual Risk Modeling: Pesticide Active Ingredient Pro duction, Polyether Polyols Production, and Group IV Polymers and Resins ” 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 ris k from each facility in the source category of interest were estimated using the Human Exposure Model (HEM3) in combination with the American Meteorological Society/EPA Regulatory Model (AERMOD) dispersion modeling system. The approach used in applying thi s modeling system is outlined below, and further details are provided in Appendix 1. The HEM3 performs three main operations: atmospheric dispersion modeling, estimation of individual human exposures and health risks, and estimation of population risks. Th is section

1 http://www.epa.gov/ttn/atw/nata2005/

2 Assigning data with MACT codes allows 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.8

focuses on the dispersion modeling component. The exposure and risk characterization components are discussed in other subsections of Sections 2 and 3.

The dispersion model in the HEM3 system, AERMOD version 11103, is a state

- of

- the

science Gau ssian plume dispersion model that is preferred by EPA for modeling point, area, and volume sources of continuous air emissions from facility applications [ 5 ]. Further details on AERMOD can be found in the AERMOD Users Guide [ 6 ]. The model is used to develo p annual average ambient concentrations through the simulation of hour

- by

- hour dispersion from the emission sources into the surrounding atmosphere. Hourly emission rates used for this simulation are generated by evenly dividing the total annual emission r ate from the inventory into the 8,760 hours of the year.

The first step in the application of the HEM3 modeling system 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 model 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 800 stations)

In HEM3, meteorological data are ordinarily selected from a list of over 800 National Weather Service ( NWS) surface observation stations across the continental United States, Alaska, Hawaii, and Puerto Rico. In most cases the nearest station is selected as representative of the conditions at the subject facility. Ideally, when considering off

- site meteorolo gical data,

most site

- specific dispersion modeling efforts will employ up to five years of data to capture variability in weather patterns from year to year. However, because we had an insufficient number of appropriately formatted model input files derive d from available meteorological data, we modeled only a single year, typically 1991. While the selection of a single year 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 by its characteristic latitude and longitude coordinates, the closest meteorological station was used in the dispersion modeling. The average distance between a modeled facility and the applicable meteorological station9

was 10 mil es (19 km). Appendix 2 (Meteorological Data Processing Using AERMET for HEM3) provides a complete listing of stations and assumptions along with further details used in processing the data through AERMET. The sensitivity of model results to the selection o f the nearest weather station and the use of one year of meteorological data is discussed in “Risk and Technology Review (RTR) Risk Assessment Methodologies” [ 2 ].

The HEM3 system estimates ambient concentrations at the geographic centroids of census

block s (using the 2000 Census), and at other receptor locations that can be specified by the

user. The model accounts for the effects of multiple facilities when estimating concentration impacts at each block centroid. Typically we combined only the impacts of facilities within the same source category, and assessed chronic exposure and risk only 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 facilit y). 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 currently uninhabited areas was not

considered. Census blocks, the fin est 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 carefully evaluated for proximity to each facility’s property 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 generally no nearer than 100 meters from the center of the facility (note that for large facilities, this

100

- meter ring could still contain locations inside the facility property). Since short

- term emission rates were needed to screen for the potential for hazard via acute exposures, and since the NATA NEI contains only annual emission totals, we generally apply the assumption to all source categories that the maximum one

- hour emission rate from any source is ten times the average annual hourly 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 yea r. A factor of ten was initially applied to these estimates to account for potential for peak emissions rates to exceed average values; this factor was originally based on an 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 performed an analysis using a short

- term emissions dataset from a number of sources located in Texas (originally reported on by Allen et al. 2004)[ 7 ]. In

that report, the Texas Environmental Research Consortium Project compared hourly and annual emissions data for volatile organic compounds for all facilities in a heavily

industrialized 4

- county area (Harris, Galveston, Chambers, and Brazoria Counties, TX) over

an eleven

- month time period in 2001. We obtained the dataset and performed our own analysis, focusing that analysis on sources which reported emitting high quantities of HAP over short periods of time (see Appendix 3, “Analysis of data on short

- term emissi on rates

3 In situations where we have information on hourly emissions, we will take this into account when evaluating

acute risks.10

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
percentile ratio of peak hourly emission rate to the annual hourly emi ssion 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 ar e intended to cover all possible hourly peaks associated with routinely

- variable emissions. While there have been some documented emission excursions above this level, our analysis of the data from the Texas Environmental Research Consortium suggests that these factors should cover more than 99% of the short

term peak gaseous or volatile HAP emissions from typical industrial sources. We have no data relating specifically to peak short

- term emissions of particulate HAP. In the absence of source

category

- spec ific 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 Survey 1

- degree digital elevation model (DEM) data files, which have a spatial resolution of about 90 meters. Elevations of polar grid points used in estimating short

- and long

- term ambient concentrations were assumed to be equal to the highest elevation of any census block falling within the polar grid sector corresponding to the grid point. If a sector does not contain any blocks, the model defaults the elevation to that of the nearest block. If an elevation is not provided for the emission so urce, the model uses the average elevation of all sectors within the innermost model ring.

In addition to using receptor elevation to determine plume height, AERMOD adjusts the plume’s flow if nearby elevated hills are expected to influence the wind patte rns. For details on how hill heights were estimated and used in the AERMOD modeling, see Appendix 1.



### 2.3. Estimating chronic human inhalation exposure

We used the 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 people who reside in the census block. That is, the risk analysis 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 daily activity using EPA’s HAPEM model) suggests that, given our current understanding of microenviro nment concentrations and daily activities, modeling short

- term activity would, on average, reduce risk estimates about 25% for particulate HAPs; it would also reduce risk estimates for gaseous HAPs, but typically by much less. Second, basing exposure estim ates on average ambient concentrations at census block centroids may underestimate or overestimate actual exposure concentrations at some residences. Further reducing exposure estimates for the most highly exposed residents by modeling their short

- term beh avior could add a systematic low bias to these results.11

We did not address long

- term migration or population growth or decrease over 70 years, and instead based the assessment on the assumption that each person’s estimated exposure is

constant over the co urse of their lifetime which is assumed to be 70 years. In assessing cancer risk, we generally estimated three metrics; the maximum individual risk (MIR), which is defined as the risk associated with a lifetime of exposure at the highest concentration; the population risk distribution; and the cancer incidence. The decision not to consider 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 nu mber 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 low er risks, thereby increasing the estimated number of people at specific 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 any individual.



### 2.4. Acute Risk Screening and Refined Assessments

In establishing a scientifically defensible approach for the assessment of potential health risks due to acute exposures to HAP, we followe d the same general approach that has been used for developing chronic health risk assessments under the residual risk program. That is, we developed a tiered, iterative approach. This approach to risk assessment was endorsed by the National Academy of Scie nces in its 1993 publication “Science and Judgment in Risk Assessment” and subsequently was adopted in the EPA’s “Residual Risk Report to Congress”

in 1999.

The assessment methodology is designed to eliminate from further consideration those

facilities fo r which we have confidence that no acute adverse health effects of concern will occur. To do so, we use what is called a tiered, iterative approach to the assessment. This means that we begin with a screening assessment, which relies on readily available d ata and uses conservative assumptions that in combination approximate a potential 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 i t requires further, more refined assessment. A refined assessment could use industry

- or site

- specific data on the temporal pattern of emissions, the layout of emission points at the facility, the boundaries of the facility, and/or the local meteorology. I n some cases, all of these site

- specific data would be needed to refine the assessment; in others, lesser amounts of site

- specific data can be used to determine that acute exposures are not a concern, and significant additional data collection is

not neces sary.

Acute health risk screening was performed 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:12 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. For facilities with multiple emission points, 1

- hour concentrat ions at each receptor

were assumed to be the sum of the maximum concentrations due to each emission point, regardless of whether those maximum concentrations occurred during the same

hour.

Worst

- case meteorology (from one year of local meteorology) was as sumed 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 possible acute health risk might exist. These

benchmarks are describ ed in section 2.6 of this report.

As mentioned above, when we identify potential worst

- case exposures which exceed relevant health benchmarks, we refine our acute screening estimates to the extent possible. In some cases, this includes the use of a refine d emissions multiplier to estimate the peak hourly emission rates from the average rates (rather than the default factor of 10). For the source categories in this document, we conducted a review of the layout of emission points at the

facilities with the f

acility 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 sites.



### 2.5. Multipathway human health and environmental risk scree ning

The potential for significant human health risks due to exposures via routes other than inhalation (i.e., multipathway exposures) was screened by first determining whether any sources emitted any hazardous air pollutants known to be persistent and bio accumulative 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 Library [ 8 ]. Examples of PB

HAP are cadmium compounds, chlordane, chlorinated dibenzodioxins and furans, DDE, heptachlor, hexachlorobenzene, hexachlorocyclohexane, lead compounds, mercury compounds, methoxychlor, polychlorinated biphenyls, polycyclic organic matter (POM), toxaphene, and trifluralin. There were PB

- HAP emissions identified for three of the source categories addressed in this risk document. For the polyethylene terephthalate production source category, we identified emissions of cadmium compounds, polycyclic organic matter (POM), and lead compounds. For the pesticide active ingredient pr oduction source category, we identified emissions of lead compounds and polychlorinated biphenyls (PCBs). For the

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 persistent and bioaccumulative in the enviro nment. 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).13

polyether polyols production source category, we identified emissions of POM, lead compounds, and hexachlorobenzene.

These PB

- HAP emissions w ere evaluated for potential non

- inhalation risks and adverse environmental impacts using our recently

- developed screening scenario which was developed

for use with the TRIM.FaTE 5 model. This screening scenario uses environmental media outputs from the peer

- reviewed TRIM.FaTE to estimate the maximum potential ingestion risks for any specified emission scenario by using a generic farming/fishing exposure scenario that simulates a subsistence environment. The screening scenario retains many of the ingestion an d scenario inputs developed for EPA’s Human Health Risk Assessment Protocols (HHRAP) for hazardous waste combustion facilities. 6 In the development of the screening scenario, a sensitivity analysis was conducted to ensure that its key design parameters wer e established such that environmental media concentrations were not underestimated, and to also minimize the occurrence of false positives for human health endpoints. See Appendix 4 for a complete discussion of the development and testing of the screening scenario, as well as for the values of facility

- level 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 tha n developing a screening emission rate for them, we compared maximum estimated chronic atmospheric concentrations with the current National Ambient Air Quality Standard (NAAQS) for lead. Values below the NAAQS were considered to have a low potential for

mu lti

- pathway risks.

The EPA has developed a screening approach to examine the potential for adverse environmental effects as required under section 112(f)(2)(A) of the CAA. The environmental screen focuses on the following seven environmental HAP:

Five p ersistent bioaccumulative HAP (PB

- HAP)

– cadmium, dioxins/furans, polycyclic organic matter (POM), mercury (both inorganic mercury and methyl mercury) and lead. Two acid gases

- hydrogen chloride (HCl), and hydrogen fluoride (HF).

HAP that persist and bi oaccumulate are of particular environmental concern because they accumulate in the soil, sediment and water. The acid gases, HCl and HF, were included due to

their well

- documented potential to cause direct damage to terrestrial plants.

For the environment al risk screening analysis, EPA first determined whether any facilities in the source category emitted any of the seven environmental HAP. If one or more of the seven

5 EPA’s Total Risk Integrated Methodology (General 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#volume114

environmental HAP evaluated are emitted by at least one facility in the source category we proceed to the second step of the evaluation.

For cadmium, mercury, POM and dioxins/furans, the environmental screening analysis

consists of two tiers. In the first tier, TRIM.FaTE modeling was conducted under worst

- cast environmental conditionals to determine whether the facility

- specific off

- site emission rates of each of the emitted environmental HAP exceeded ecological benchmarks represented as

emissions threshol d values. If off

- site emissions from a facility do not exceed the Tier 1 thresholds the facility “passes” the screen, and therefore, is not evaluated further under the screening approach. If off

- site emissions from a facility exceed the Tier 1 thresholds, we evaluate the facility further in Tier 2.

In Tier 2 of the environmental screening analysis, the screening emission thresholds are adjusted to account for local meteorology and the actual location of lakes in the vicinity of facilities that did not pass the Tier 1 screen. If off

- site emissions from a facility do not exceed the Tier 2 thresholds, the facility passes the screen, and is typically not evaluated further. If

off

- site emissions from a facility exceed the Tier 2 thresholds, the facility does not pass the screen and, therefore, may have the potential to cause adverse environmental effects. Such facilities are evaluated further to investigate factors such as the magnitude and characteristics

of the area of exceedance.

For acid gases, the environmental screening analysis evaluates the p otential phytotoxicity and reduced productivity of plants due to chronic exposure to acid gases. The environmental risk screening methodology for acid gases is a single

- tier screen that compares the average o ff

- site ambient air concentration over the modeling domain to ecological benchmarks for each of the acid gases. For purposes of ecological risk screening, EPA identifies a potential for adverse environmental effects to plant communities from exposure to ac id gases when the average concentration of the HAP around a facility exceeds the LOAEL ecological benchmark. In such cases, we further investigate factors such as the magnitude and characteristics of the area of exceedance (e.g., land use of exceedance are a, size of exceedance area) to determine if

there is an adverse environmental effect.

For lead compounds, we currently do not have the ability to calculate media concentrations using the TRIM.FaTE model. However, air concentrations of lead are already cal culated as part of the human health exposure and risk analysis using the HEM

- 3 AERMOD air dispersion model. To evaluate the potential for adverse environmental effects from lead, we compare the average modeled air emission concentrations of lead from each facility in the source category emissions to the level of the secondary National Ambient Air Quality Standard (NAAQS) for lead. The secondary lead NAAQS is a reasonable means of evaluating environmental risk because it is set to provide substantial protect ion against adverse welfare

effects which can include “effects on soils, water, crops, vegetation, man

- made materials, animals, wildlife, weather, visibility and climate, damage to and deterioration of property, and hazards to transportation, as well as ef fects on economic values and on personal comfort and

well

- being.” 7

7 A secondary standard, as defined in Section 109(b)(2), must “specify a level of air quality the attainment and maintenance of which, in the judgment of the Administrator, based on criteria, is requisite to protect the public15



### 2.6. Dose

- Response Assessment

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 obtai ned from various sources and prioritized according to (1) conceptual consistency with EPA risk assessment guidelines and (2) level of peer review received. The prioritization process was aimed at incorporating into our assessments the best

available scienc e with respect to dose

- response information. The recommendations are based on the following sources, in order of priority:

1) US Environmental Protection Agency (EPA). EPA has developed dose

- response assessments for chronic exposure for many of the pollutan ts in this study. These assessments typically 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 uncertainty spanning perhaps an order of magnitude) of a continuous inh alation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime.” The RfD is “an estimate (with uncertainty spanning perhaps an order of magnitude) of a dail y oral exposure to the human population (including 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 continuou s lifetime exposure to an agent at a concentration of 1 μg/m 3 in air.” The SF is “an upper bound, approximating a 95% confidence limit, on the increased cancer risk from a lifetime exposure to an agent. This estimate, [is] usually expressed in units of

pro portion (of a population) affected per mg/kg

- day...” EPA disseminates dose

- response assessment information in several forms, based on the level of review. The Integrated Risk Information System (IRIS) [ 11 ] is an EPA database that contains scientific health

as sessment information, including dose

- response information. All IRIS assessments since 1996 have also undergone independent external peer review. The current IRIS process includes review by EPA scientists, interagency reviewers from other federal agencies, and the public, and peer review by independent scientists external to EPA. New IRIS values are developed and old IRIS values are updated as new health effects data become

available. Refer to the “IRIS Track” website for detailed information on status and

s cheduling of current individual IRIS assessments and updates ( http://cfpub.epa.gov/ncea/iristrac/index.cfm ). EPA’s science policy approach, under the

welfare from any known or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.” Welfare effects as defined in section 302(h) (42 U.S.C. 7602(h)) include, but are not limited to, “effects on soils, water, crops, vegetation, man

- made materials, animals, wildlife, weather, visibility and climate, damage to and deterioratio n of property, and hazards to transportation, as well as effects on economic values and on personal comfort and well

- being.”16

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 analyses (once they a re 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

.

2) US Agency for Toxic Substances and Disease Registry (ATSDR). ATSDR, wh ich is part of the US Department of Health and Human Services, develops and publishes Minimum Risk Levels (MRLs) [ 12 ] for inhalation and oral exposure to many toxic substances. As stated on the ATSDR web site: “Following discussions with scientists within t he Department of Health 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 endp oints.” The MRL is defined as “an estimate of daily 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 MRLs as substance

- specific est imates 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 sett ing cleanup levels.

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 c ancer. 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 assessmen ts 8 : “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 r eference exposure levels (RELs) [ 15 ]. CalEPA defines the REL as “the concentration 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 professio nal judgment, as follows:

1) In the case of HAP categories such as glycol ethers and cyanide compounds, the most

conservative dose

- response value of the chemical category is used as a surrogate for other compounds in the group for which dose

- response values are not available. This is done in order to examine, under conservative assumptions, whether these HAPs that lack dose

-

8 Air Toxics Hot Spots Program, Risk Assessment Guidelines, Part III

- Technical Support Document

for the Determination of Non

- can cer Chronic Reference Exposure Levels. Air Toxicology and Epidemiology Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. February 2000 (http://www.oehha.ca.gov/air/chronic_rels/pdf/relsP32k.pdf)17

response values may pose an unacceptable risk and require further examination, or screen

out from further assessment.

2) Where possible, for emissions of unspecified mixtures of HAP categories such as metal compounds and POM, we apply category

- specific chemical speciation profiles appropriate to the source category to develop a composite dose

- response value for the category.

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 us ing the IRIS value to the CIIT value in risk assessments supporting regulatory actions. Subsequent research published by EPA suggested that the CIIT model was not appropriate and in 2010 EPA returned to using 1991 IRIS value. EPA has been working

on revisi ng the formaldehyde IRIS assessment and the National Academy of Sciences (NAS) completed its review of the EPA’s draft assessment in April of 2011. 9 EPA will follow the NAS Report recommendations and will present results obtained by implementing the biolog ically

- based dose

- response (BBDR) model for formaldehyde. EPA will compare these estimates with those currently presented in the External Review draft of the assessment and will discuss their strengths and weaknesses. As recommended by the NAS committee, a ppropriate sensitivity and uncertainty analyses will be an integral component of implementing the BBDR model. In the interim, we will present findings using the 1991 IRIS value as a primary estimate, and EPA may also consider other

information as the scien ce evolves.

4) A substantial proportion of POM emissions reported to EPA’s National Emission Inventory (NEI) are not speciated into individual compounds. As a result, it is necessary to apply the same simplifying assumptions to assessments that are used in N ATA.[ 17 ] The NATA approach partitions POM into eight different non

- overlapping “groups” that are modeled as separate pollutants. Each POM group comprises POM species of similar carcinogenic potency, for which we can apply the same URE.

5) In the case of nicke l compounds, to provide a health

- protective estimate of potential cancer risks, we used the IRIS URE value for nickel subsulfide in this assessment. Based on past scientific and technical considerations, the determination of the percent of nickel

subsulfid e was considered a major factor for estimating the extent and magnitude of the

risks of cancer due to nickel

- containing emissions. 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 crystalline nickel) could be deriv ed to reflect the assumption that 65 percent of the total mass of nickel may be carcinogenic. Based on consistent views of major scientific bodies (i.e., National Toxicology Program

9 http:/ /www.nap.edu/catalog.php?record_id=1314218

(NTP) in their 12 th Report of the Carcinogens (ROC) 10 , International Agency for Research on Cancer (IARC) 11 , and other international agencies) 12 that consider all nickel 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 carcinogenic studies in rodents support the concept that nickel compounds generate nickel ions in target cells at sites critical for carcinogenesis, thus allowing consid eration and evaluation of these compounds as a single group.” Although the precise nickel compound (or compounds) responsible for the carcinogenic effects in humans is not always clear, studies

indicate that nickel sulfate and the combinations of nickel su lfides and oxides encountered in the nickel refining industries cause cancer in humans (these studies are summarized in a review by Grimsrud et al., 2010 13 ). The major scientific bodies mentioned above have also recognized that there are differences in toxi city and/or carcinogenic potential across the different nickel compounds. In this inhalation 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 14 derived for exposure to mixtures of nickel compounds, as a group, that are 2

- 3 fold lower than the IRIS URE for nickel subsulfide, 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 p lausible range of cancer potency values for different mixtures of nickel compounds.

The emissions inventory for the source categories in this risk document includes emissions of HAP with available chronic quantitative inhalation dose

- response values. These HAP, their

dose

- response values, and the source of the values are listed in Tables 2.6

- 1 (a) and (b).

10 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.n ih.gov/ntp/roc/twelfth/roc12.pdf

11 International Agency for Research on Cancer (IARC), 1990. IARC monographs on the evaluation of carcinogenic risks to humans. Chromium, nickel, and welding. Vol. 49. Lyons, France: International Agency for

Research on Canc er, World Health Organization Vol. 49:256.

12 World Health Organization (WHO, 1991) and the European Union’s Scientific Committee on Health and Environmental Risks (SCHER, 2006).

13 Grimsrud TK and Andersen A. Evidence of carcinogenicity in humans of water

- s oluble nickel salts. J Occup Med Toxicol 2010, 5:1

- 7. Available online at http://www.ossup

- med.com/content/5/1/7.

14 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 Quality (http://www.epa.gov/ttn/atw/nata1999/99pdfs/healtheffectsinfo.pdf).19

Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcinogens

URE (unit risk estimate for cancer) 15 = cancer risk per μg/m 3 of average lifetime exposure. Sources: IRIS = EPA Integrated Risk Information System, EPA OAQPS = interim value recommended by 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 16 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 17 71432 0.0000078 IRIS Benzyl chloride 100447 0.000049 CAL 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

Carbon tetrachloride 56235 0.000006 IRIS Chromium (VI) compounds 18540299 0.012 IRIS Dichloroethyl ether 111444 0.00033 IRIS Epichlorohydrin (1

- Chloro

- 2,3

- epoxypropane) 106898 0.0000012 IRIS Ethyl benzene 100414 0.0000025 CAL Ethylene dichloride 107062 0.000026 IRIS Ethylene oxide 75218 0.000088 CAL Formaldehyde 18 50000 0.000013 IRIS

Hexachlorobenzene 118741 0.00046 IRIS

Hexachloroethane 67721 0.000004 IRIS Hydrazine 302012 0.0049 IRIS Methyl tert

- butyl ether 1634044 0.00000026 CAL

15 The URE is the upper

- bound excess cancer ri sk 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.

16 Chemical Abstract Services identifica tion 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.

17 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

. 18 The EPA has used the CIIT URE value, 5.5X10 - 9 per mg/m 3 , to c haracterize formaldehyde cancer risk in some

instances.20

Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcinogens

URE (unit risk estimate for cancer) 15 = cancer risk per μg/m 3 of average lifetime exposure. Sources: IRIS = EPA Integrated Risk Information System, EPA OAQPS = interim value recommended by 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 16 URE 7

(1/μg/m 3 ) Source

Methylene chloride 75092 0.00000047 IRIS Naphthalene 91203 0.000034 CAL Nickel compounds 7440020 0.00048 EPA OAQPS

o

- Toluidine 95534 0.000051 CAL
Polychlorinated biphenyls 1336363 0.0001 IRIS
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
Propylene oxide 75569 0.0000037 IRIS
Tetrachloroethylene 127184 0.0000059 CAL Trichloroethylene 79016 0.000002 CAL Vinyl chloride 75014 0.0000088 IRIS

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#pom21 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: IRIS = EPA Integrated Ri sk Information System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables, EPA OAQPS = EPA Office of Air Quality Planning & Standards

Pollutant CAS Number 8 RfC (mg/m 3 ) Source 20

1,1,1

- Trichloroethane (methyl chloroform) 71556 5 IRIS

- M
1,2

- Epoxybutane 106887 0.02 IRIS

- M
1,3

- Butadiene 106990 0.002 IRIS

- M
1,3

- Dichloropropene 542756 0.02 IRIS

- H
1,4

- Dichlorobenzene 106467 0.8 IRIS

- M
1,4

- Dioxane 123911 3.6 ATSDR
2,4

- Toluene diisocyanate 584849 0.00007 IRIS

- M
4,4'

- Methylenedianiline 101779 0.02 CAL Acetaldehyde 75070 0.009 IRIS

- L

Acrolein 107028 0.00002 IRIS

- M Acrylic acid 79107 0.001 IRIS

- M Acrylonitrile 107131 0.002 IRIS

- M

Aniline 62533 0.001 IRIS

- L Antimony compounds 7440360 0.0002 IRIS

- L Arsenic compounds 7440382 0.000015 CAL

Benzene 71432 0.03 IRIS

- M Beryllium compounds 7440417 0.00002 IRIS

- M Bis(2

- ethylhexyl)phthalate 117817 0.01 CAL

Cadmium compounds 7440439 0.00001 ATSDR

Carbon tetrachloride 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 Cresols (mixed) 1319773 0.6 CAL

Cumene 98828 0.4 IRIS

- M
Cyanide & Cyanide Compounds Cyanide compounds 21 57125 0.003 IRIS

- L Hydrogen cyanide 74908 0.003 IRIS

- L

Diethanolamine 111422 0.003 CAL

20 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 IR IS.

21 The value for hydrogen cyanide was used as a surrogate for all cyanide compounds without an RfC.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: IRIS = EPA Integrated Ri sk Information System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables, EPA OAQPS = EPA Office of Air Quality Planning & Standards

Pollutant CAS Number 8 RfC (mg/m 3 ) Source 20

Epichlorohydrin (1

- Chloro

- 2,3

- epoxypropane) 106898 0.001 IRIS

- M Ethyl benzene 100414 1 IRIS

- L Ethyl chloride 75003 10 IRIS

- M Ethylene dichloride 107062 2.4 ATSDR Ethylene glycol 107211 0.4 CAL Ethylene oxide 75218 0.03 CAL Formaldehyde 50000 0.0098 ATSDR
Glycol Ethers 22

2

- (Hexyloxy)ethanol 112254 0.02 IRIS

- M

2

- Butoxyethyl acetate 112072 0.02 IRIS

- M Butyl Carbitol acetate 124174 0.02 IRIS

- M Diethylene glycol monobutyl

ether 112345 0.02 HEAST Diethylene glycol monoethyl

ether 111900 0.02 IRIS

- M Ethoxytriglycol 112505 0.02 IRIS

- M Ethylene glycol ethyl ether 110805 0.2 IRIS

- M Ethylene glycol methyl ether 109864 0.02 IRIS

- M Glycol ethers 171 0.02 IRIS

- M Methoxytriglycol 112356 0.02 IRIS

- M Propyl cellosolve 2807309 0.02 IRIS

- M Triglycol monobutyl ether 143226 0.02 IRIS

- M

Hexachlorobenzene 118741 0.003 CAL

Hexachloroethane 67721 0.08 CAL

Hexane 110543 0.7 IRIS

- M Hydrazine 302012 0.0002 CAL Hydrochloric acid (hydrogen chloride) 7647010 0.02 IRIS

- L Hydrofluoric acid (hydrogen fluoride) 7664393 0.014 CAL Isophorone 78591 2 CAL Lead compounds 7439921 0.00015 EPA OAQPS Maleic anhydride 108316 0.0007 CAL

22 The RfC value for ethylene glycol methyl ether was used as a surrogate for all glycol ethers without an RfC.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: IRIS = EPA Integrated Ri sk Information System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables, EPA OAQPS = EPA Office of Air Quality Planning & Standards

Pollutant CAS Number 8 RfC (mg/m 3 ) Source 20

Manganese compounds 7439965 0.00005 IRIS

- M

Methanol 67561 4 CAL Methyl bromide 74839 0.005 IRIS

- H Methyl chloride 74873 0.09 IRIS

- M Methyl isobutyl ketone 108101 3 IRIS

- L/M Methyl isocyanate 624839 0.001 CAL Methyl methacrylate 80626 0.7 IRIS

- M/H Methyl tert

- butyl ether 1634044 3 IRIS

- M Methylene chloride 75092 1 ATSDR Naphthalene 91203 0.003 IRIS

- M Nickel compounds 7440020 0.00009 ATSDR

Phenol 108952 0.2 CAL Phosgene 75445 0.0003 IRIS

- M Phthalic anhydride 85449 0.02 CAL Propionaldehyde 123386 0.008 IRIS

– L/M Propylene dichloride 78875 0.004 IRIS

- M Propylene oxide 75569 0.03 IRIS

- M Selenium compounds 7782492 0.02 CAL Styrene 100425 1 IRIS

- M Tetrachloroethylene 127184 0.27 ATSDR

Titanium tetrachloride 7550450 0.0001 ATSDR

Toluene 108883 5 IRIS

- H Trichloroethylene 79016 0.6 CAL Triethylamine 121448 0.007 IRIS

- L Vinyl acetate 108054 0.2 IRIS

- H Vinyl chloride 75014 0.1 IRIS

- M Xylenes (mixed) 1330207 0.1 IRIS

- M

m

- Xylene 18 108383 0.1 IRIS

- M

o

- Xylene 23 95476 0.1 IRIS

- M

p

- Xylene 18 106423 0.1 IRIS

- M

23 The RfC for mixed xylene was used as a surrogate.24 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 a ssessments are compared to both “no effects” reference levels for the general public, such as the California Reference Exposure Levels (RELs), as well as emergency response levels, such as Acute Exposure Guideline Levels (AEGLs) and Emergency Response Plan ning Guidelines (ERPGs), with the recognition that the ultimate interpretation of any potential risks associated with an estimated exceedance of a particular reference level depends on the definition of that level and any limitations expressed therein. Com parisons among different available inhalation health effect reference values (both acute and chronic) for selected HAPs can be found in an EPA document [ 19 ].

California Acute Reference Exposure Levels (RELs ). The California Environmental Protection Agency (CalEPA) has developed acute dose

- response reference values for many substances, expressing the results as acute inhalation Reference Exposure Levels (RELs).

The acute REL ( http://www.oehha.ca.gov/air/pdf/acuterel.pdf ) is defined by CalEPA as

“ the concentration level at or below which no adverse health effects are anticipated for a specified exposure duration [ 20 ]. RELs 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 safety. Since margins of safety are incorporated to address data gaps and uncertainti es, exceeding the REL does not automatically indicate an adverse health impact.” Acute RELs are developed for 1

- hour (and 8

- hour) exposures. The values incorporate uncertainty factors similar to those used in deriving EPA’s Inhalation Reference

Concentrati ons (RfCs) for chronic exposures (and, in fact, California also has developed chronic RELs).

Acute Exposure Guideline Levels (AEGLs ). AEGLs are developed by the National Advisory Committee (NAC) on Acute Exposure Guideline Levels (NAC/AEGL) for Hazardous Substances, and then reviewed and published by the National Research Council As described in the Committee’s “Standing Operating Procedures (SOP)” ( http://www.epa.gov/opptintr/aegl/pubs/sop.pdf ), AEGLs “represent threshold exposure limits for the general public and are applicable to emergency exposures ranging from 10 min to 8 h.” Their intended application is “for conducting risk assessments to aid in the development of emergency preparedness and prevention plans, as well as real time emergency response 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 acutely toxic, high

- priority chemicals.” In detailing the intended application of AEGL values, the document states, “It is 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, planning, and prevention programs. More specifically, the AEGL values will be used for conducting various risk assessments to aid in the development of emergency preparedness and25

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 asymptomatic nonsensory effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure.”

“AEGL

- 2 is the airborne concentration (expressed as ppm or mg/m 3 ) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long

- lasting adverse health effects or an impaired ability to escape.”

“Airborne concentrations below AEGL

- 1 represent exposure levels that c an produce mild and progressively increasing but transient and nondisabling odor, taste, and sensory irritation or certain asymptomatic, nonsensory effects. With increasing airborne concentrations above each AEGL, there is a progressive increase in the lik elihood 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 idiosyncratic responses, could experience the effects described at concentrations 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 populatio n (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/insideaiha/GuidelineDevelopment/ERPG/Pages/default.aspx ) 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 guidelines (i.e., the ERPG Documents and ERPG values) are intended for use as planning tools for assessing the adequacy of accident preve ntion and emergency response plans, including transportation emergency planning and for developing community emergency response plans. The emphasis is on ERPGs as planning values: When an actual chemical emergency occurs there is seldom

time to measure air

borne concentrations and then to take action.”

ERPG

- 1 and ERPG

- 2 values are defined by AIHA as follows:26

“ERPG

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

odor.”

“ERPG

- 2 is the maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hour wi thout experiencing or developing irreversible or other serious health effects or symptoms which could impair 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

- 2.27 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
1,1,1

- Trichloroethane (methyl chloroform) 71556 1300 3300 1900 3800 68

1,2

- Epoxybutane 106887 210 410

1,3

- Butadiene 106990 1500 12000 22 440
1,4

- Dioxane 123911 61 1200 3

2,4

- Toluene diisocyanate 584849 0.14 0.59 0.071 1.1 Acetaldehyde 75070 81 490 18 360 0.47

Acetonitrile 75058 22 540

Acrolein 107028 0.069 0.23 0.11 0.34 0.0025 Acrylic acid 79107 4.4 140 3 150 6 Acrylonitrile 107131 10 130 22 77

Aniline 62533 30 46
Arsenic compounds 7440382 0.0002

Benzene 71432 170 2600 160 480 1.3
Benzyl chloride 100447 5.2 52 0.24
Beryllium compounds 7440417 0.025
Biphenyl 92524 61

Carbon tetrachloride 56235 280 1200 130 630 1.9

Chlorine 7782505 1.5 5.8 2.9 8.7 0.21

Chloroacetic acid 79118 26

Chlorobenzene 108907 46 690

Chloroform 67663 310 240 0.15
Chloromethyl methyl ether 107302 1.6 3.3

Cumene 98828 250 1500 Hydrogen cyanide 74908 2.2 7.8 11 0.34
Dimethyl formamide 68122 270 6 300
Dimethyl sulfate 77781 0.12 0.62 Epichlorohydrin (1

- Chloro

- 2,3

- epoxypropane) 106898 22 91 19 76 1.3
Ethyl acrylate 140885 34 150 0.041 120
Ethyl benzene 100414 140 4800
Ethylene dichloride 107062 200 810
Ethylene oxide 75218 81 90 Formaldehyde 50000 1.1 17 1.2 12 0.055
Glycol Ethers 24

2

- (Hexyloxy)ethanol 112254 0.093

2

- Butoxyethyl acetate 112072 0.093

24 The acute REL for ethylene glycol methyl ether was used as a surrogate for glycol ether compounds without

an acute REL.28 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 acetate 124174 0.093
Ethoxytriglycol 112505 0.093
Ethylene glycol ethyl ether 110805 0.37
Ethylene glycol methyl ether 109864 0.093
Glycol ethers 171 0.093
Methoxytriglycol 112356 0.093
Propyl cellosolve 2807309 0.093
Triglycol monobutyl ether 143226 0.093

Hexane 110543 12000
Hydrazine 302012 0.13 17 0.65 6.5 Hydrochloric acid 7647010 2.7 33 4.5 30 2.1 Hydrogen fluoride 7664393 0.82 20 1.6 16 0.24
Maleic anhydride 108316 0.8 8

Methanol 67561 690 2700 260 1300 28
Methyl bromide 74839 820 190 3.9
Methyl chloride 74873 1900 830
Methyl hydrazine 60344 3.2
Methyl isocyanate 624839 0.16 0.058 0.6
Methyl methacrylate 80626 70 490
Methyl tert

- butyl ether 1634044 180 2100 Methylene chloride 75092 690 1900 1000 2600 14
Nickel compounds 7440020 0.006

Phenol 108952 58 89 38 190 5.8
Phosgene 75445 1.2 2 0.004
Propionaldehyde 123386 110 620 Propylene oxide 75569 170 690 120 1100 3.1 Styrene 100425 85 550 210 1100 21 Tetrachloroethylene 127184 240 1600 680 1400 20

Titanium tetrachloride 7550450 0.54 7.8 5 20

Toluene 108883 750 4500 190 1100 37
Trichloroethylene 79016 700 2400 540 2700
Triethylamine 121448 2.8
Vinyl acetate 108054 24 630 18 260 Vinyl chloride 75014 640 3100 1300 13000 180 Xylenes (mixed) 1330207 560 4000 22

m

- Xylene 25 108383 22

o

- Xylene 20 95476 22

p

- Xylene 20 106423 22

25 The REL for mixed xylenes was used as a surrogate.29



### 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 synthesized that is complete, informative, and useful for decision makers. In gene ral, 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 identified 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 sim ilar 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/OSTP Se ptember 2007 Memorandum on Updated Principles for Risk Analysis 26 , and are incorporated in these assessments.

Estimates of health risk are presented in the context of uncertainties and limitations in the data and methodology. Through our tiered, iterative analytical approach, we have attempted to reduce both uncertainty 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 individual canc er 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, individual and population cancer risks were calculated by multiplying the corresponding lifetime average exposure estimate by the appropriate URE. This calculated cancer risk is defined as the upper

- bound probability of developing cancer over a 70

- yr 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 estimate d, and could be

zero.

For EPA’s list of carcinogenic HAPs that act by 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 adjustin g the URE by factors of 10 (for children aged 0

- 1), 3 (for children aged 2

- 15), or 1.6 (for 70 years of exposure beginning at birth), as needed in risk assessments. In this case, this has the effect of increasing the estimated life time risks for these pol lutants by a factor of 1.6. In addition, although only 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]pyrene

26 Memorandum for the Heads of E xecutive Departments and Agencies

- Updated Principles for Risk Analysis (September 19, 2007), From Susan E. Dudley, Administrator, Office of Information and Regulatory Affairs, Office of Management and Budget; and Sharon L. Hays, Associate Director and De puty Director for Science, Office of Science and Technology Policy (http://www.whitehouse.gov/omb/memoranda/fy2007/m07

- 24.pdf)30

equivalence, based on evid ence that carcinogenic POM have the same mutagenic mechanism of action as does benzo[a]pyrene. For this reason, EPA implementation policy [ 27 ] recommends applying the Supplemental Guidance to all carcinogenic PAHs for which risk

estimates are based on relat ive potency. Accordingly, we applied the Supplemental Guidance to all unspeciated POM mixtures.

Increased cancer incidence for the entire receptor population within the area of analysis was estimated by multiplying the estimated lifetime cancer risk for e ach 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 was divided by 70 years to obtain an estimate of the number of cancer cases per year.

In t he 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 estimates that are approximately 3.5 times higher tha n use of the equally plausible low end value. If the estimated benzene

– associated risks exceed 1 in a million, we also evaluated the impact of using the low end of the URE range on our risk

results.

Unlike linear dose

- response assessments for cancer, nonc ancer 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 di vided by a reference level (e.g., the RfC). For a given HAP, exposures at or below the reference level (HQ≤1) are not likely to cause adverse health effects. As exposures increase above the reference level (HQs increasingly greater than 1), the potential f

or 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., high, medium, or low confidence) and discusses the impac t of this on possible health interpretations.

The risk characterization for chronic effects other than cancer is expressed in terms of the HQ for inhalation, calculated for each HAP at each census block centroid. As discussed above, RfCs incorporate gene rally 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
th reshold 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, a dditional information is used to determine if there is a potential for significant acute risks.31 2.7.2. Mixtures

Since most or all receptors in these assessments receive exposures to multiple pollutants rather than a single pollutant, we estimated the aggregate h ealth 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 assumption of additivity of effects, and combine risks by su mming them using the independence formula in the mixtures guidelines.

In assessing noncancer hazard from chronic exposures, in cases where different pollutants cause adverse health effects via completely different modes of action, it may be inappropriate to aggregate HQs. In consideration of these mode

- of

- action differences, the mixtures guidelines support aggregating effects of different substances in specific and limited ways. To conform to these guidelines, we aggregated non

- cancer HQs of HAP that act b y 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 t hat affect the same organ or organ system. All 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 h ave been aggregated into more than one TOSHI, this has been done only in cases where the critical dose affects more than one target organ. Because impacts on organs or systems that occur above the critical dose have not been included in the

TOSHI calculati ons, 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 advers e 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 exp osures, acute impacts were screened on an individual pollutant basis, not using the TOSHI approach.

2.7.3. Facility

- wide Risks
To help place the source category risks in context, we examined “facility

- wide” risks using 2005 NATA 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 noncancer risks associated with all HAP emissions sources at the facility, including emissions sources that are not part of t he source categories but are located within a contiguous area and are under common control. We analyzed risks due to the inhalation of HAP for the populations residing within 50 kilometers of each facility. The results of these facility

- wide assessments ar e summarized below in the Risk Characterization sections of this document. The complete results of the facility

- wide assessments are provided in Appendix 5.32 2.7.4. MACT

- Allowable Risks

The emissions data in the data sets for these seven source categories are est imates of actual emissions on an annual basis. The risk results presented in the following sections are based on these actual emissions. 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

memorandum titled “ MACT Allowable Emissions and Risks for the Pesticide Active Ingredient (PAI), Polyether Polyols, and Polymers and Resins IV Production Source Categories” available in the docket for this actio n. Therefore, except for certain sources, the

risks based on MACT

- allowable emissions would be equivalent to the actual risks presented below. See the source category risk characterization sections and the memorandum MACT

Allowable Emissions and Risks for the Pesticide Active Ingredient, Polyether Polyols, and Polymers and Resins IV Production Source Categories (available in the docket for this action)

for details on the MACT

- allowable risk.



### 3. Risk Results for Pesticide Active Ingredient Production

3.1 Source Ca tegory Description and Results

The pesticide active ingredient (PAI) production source category consists of major source facilities that manufacture active ingredients in insecticides, herbicides, fungicides, and related products. The HAP emission sources at PAI production facilities include storage vessels, process vents, equipment leaks, wastewater systems, heat exchange systems, and bag dumps and product dryers. The primary HAP emitted by these facilities include toluene, methanol, methylene chloride, an d hydrochloric acid, but numerous other organic HAP, chlorine, cyanide compounds, metal compounds, and hydrogen fluoride are also emitted. A complete description of the pesticide active ingredient production source category can be

found in the text of the final rule preamble.

We currently estimate that there are 18 pesticide active ingredient production facilities operating in the U.S. The final rule data set contains all 18 facilities identified with a pesticide active ingredient production MACT code in t he 2005 NATA NEI. The 2005 NATA NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and emission locations. All 18 of these facilities are identified as major sources in

the 2005 NATA NEI.

The e missions for the PAI production source category data set (of 18 facilities) are

summarized in Table 3.1

- 1. The total HAP emissions for the source category are approximately 300 tons per year. Based on these data, the HAP emitted in the largest quantities a cross these 18 facilities are: toluene, methanol, methylene chloride, hydrochloric acid, chlorine, xylenes (mixed), formaldehyde, N

- hexane, tetrachloroethene, trichloroethylene, triethylamine, phenol, ethylene dichloride, ethylene glycol, chlorobenzene,

m

- xylene, carbon tetrachloride, o

- xylene, ethyl benzene, benzene, ethyl chloride, methyl isobutyl ketone, chloroform, methyl bromide, 1,4

- dioxane, N,n

- dimethylaniline, 1,3

- butadiene, hydrogen cyanide, and acetonitrile. These 29 HAP account for 99 percent of the33

total emissions by mass. Persistent and bioaccumulative HAP (PB HAP) 27 in the final rule data set for the pesticide active ingredient production source category include polychlorinated biphenyls (PCBs). The following environmental HAP are emitted from t he source category and are included in the environmental risk screen: hydrogen chloride and hydrogen fluoride.

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 (17

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

Benchmark

Values for Acute

Noncancer?

Toluene 78 7

Methanol 59 13
Methylene chloride 42 5
Hydrochloric Acid 34 11

Chlorine 10 8
Xylenes (Mixed) 10 7
Formaldehyde 10 3

N

- Hexane 7 5

Tetrachloroethene 6 4
Trichloroethylene 5 2
Triethylamine 5 5

Phenol 5 3
Ethylene dichloride 3 3
Ethylene Glycol 3 5

Chlorobenzene 3 5

m

- Xylene 2 1

Carbon tetrachloride 2 4

o

- Xylene 2 1
Ethyl Benzene 2 4

Benzene 1 6
Ethyl chloride 1 4
Methyl Isobutyl Ketone 1 3

Chloroform 0.9 5
Methyl bromide 0.8 1

1,4

- dioxane 0.8 1

N,n

- dimethylaniline 0.8 1

1,3

- butadiene 0.7 1
Cyanide Compounds
Hydrogen Cyanide 0.6 2
Cyanide & Compounds 0.02 2

Acetonitrile 0.5 5

27 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 final rule 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

.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 (17

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

Benchmark

Values for Acute

Noncancer?
Glycol Ethers Ethylene glycol methyl

ether 0.5 1
Glycol Ethers 0.01 1
Methyl Chloride 0.5 3
Captan 0.5 1
Naphthalene 0.3 3
Acrylonitrile 0.2 2
Phthalic Anhydride 0.2 1

 Dimethyl formamide 0.1 3
Phosgene 0.09 3

1,1,1

- Trichloroethane 0.08 1

Cumene 0.04 2
Maleic anhydride 0.04 2

Hexachlorobenzene 0.03 3
Vinyl Chloride 0.02 1
Ethyl acrylate 0.02 1
Methyl isocyanate 0.01 1
Acetaldehyde 0.01 1
Cresols (mixed) 0.01 1
Hydrazine 0.009 1
Propoxur 0.009 1

1,3

- Dichloropropene 0.006 1
Benzyl chloride 0.004 1
Allyl chloride 0.003 1

Hexachloroethane 0.003 2
Hydrofluoric acid 0.002 1
Biphenyl 0.0005 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 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

.35



### 3.2 Risk Characterization

This section presents th e 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 cancer risk, the maximum chronic hazard index, and the cancer

in cidence. 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

inhalation risks from PB

- HAP. Also presented are the HAP “drivers,” whic h 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 analysis of risks associated with the ma ximum allowed emissions under

the current MACT standards. A detailed summary of the facility

- specific risk assessment results is available in Appendix 5.

Tables 3.2

- 1 and 3.2

- 2 summarize the chronic and acute inhalation risk results for this source

catego ry. The results for the pesticide active ingredient production source category indicate that maximum lifetime individual cancer risks could be as high as 6 in a million. The major contributor to this risk is hydrazine. Approximately 370 people were estimat ed to have cancer

risks above 1 in a million as a result of the emissions from 2 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, i ndicating no significant potential for chronic noncancer impacts.

Worst

- case acute HQs were calculated for 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 dete rmining the highest HQ value that might occur outside facility boundaries. We adjusted the multiplier of 10 to 2 for emissions associated with equipment leaks. Analysis of potential off

- site impacts for the PAI source category identified no facilities with acute values greater than one.

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 th e RTR risk assessments. 28 The PB

- HAP emitted from this category are hexachlorobenzene and polychlorinated biphenyls (PCBs). There is currently not a screening value for PCBs or hexachlorobenzene and they were not evaluated for potential non

- inhalation risks . As shown in Table 3.1

- 1, these HAP are not emitted in appreciable quantities.

We conducted a screening

- level evaluation of the potential adverse environmental risks associated with emissions of the following environmental HAP from the source category:

h ydrogen chloride and hydrogen fluoride. The results of the environmental screening analysis

are summarized in Table 3.2

- 2. For hydrogen fluoride and hydrogen chloride, the average modeled concentration around each facility (i.e., the average concentration of all off

- site data points in the modeling domain) did not exceed the ecological benchmarks. In addition, each

28 ICF Inte rnational. TRIM

- Based Multipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.36

individual modeled concentration of hydrogen chloride and hydrogen fluoride (i.e., each off

site data point in the modeling domain) was below th e ecological benchmarks for all facilities.

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 in Source Category 18 n/a

Number of Facilities Identified in NATA NEI

and Modeled in Risk Assessment 18 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 6 hydrazine, acrylonitrile, trichloroethylene 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 2 hydrazine, acrylonitrile, trichloroethylene, ethylene dichloride, formaldehyde

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 Results Maximum Acute Hazard Quotient 1 formaldehyde (REL)

Number of Facilities With Potential for Acute

Effects 0 n/a

Population Exposure Number of People Living Within 50 Kilometers

of Facilities Modeled 16,000,000 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 370 n/a Number of People Exposed to Noncancer Respiratory Hazard Index:

Greater than 1 0 n/a Estimated Cancer Incidence (excess cases per year) 0.0006 n/a

Contribution of HAP to Cancer Incidence formaldehyde 34% n/a hydrazine 13% n/a
1,3

- butadiene 9% n/a ethylene dichloride 9% n/a

carbon tetrachloride 8% n/a methylene chloride1 7% n/a trichloroethylene 5% n/a acrylonitrile 4% n/a37

Table 3.2

- 1 Summary of Source Category Level Risks for Pesticide Active Ingredient Production

Result HAP “Drivers”

hexachlorobenzene 3% n/a

Table 3.2

- 1 Summary of Environmental Risk Screen Results for the

Pesticide Active Ingredient Production Source Category

Environmental

HAP Number of Facilities In Category Exceeding Percent of Modeled Area in Category Exceeding 2

Tier 1 Screen Tier 2 Screen 1 NOAEL LOAEL NOAEL LOAEL NOAEL LOAEL

Acid

Gases HF 3 NA None

- - NA 0%

HCl 4 NA None

- - NA 0%

NA

– Not Applicable.

1

- Tier 2 screen is performed for PB

- HAP when there are exceedances of the Tier 1 screen. The acid gas screen

is a one tier screen.

2

- A value of 0% indicates that none of the modeled data points exceeded the benchmark. For PB

- HAP the percent area is based on the Tier 2 results, if a Tier 2 analysis is performed. Otherwise, the percent area is based

on the Tier 1 results.

3

– For HF, we evaluated two benchmarks, one from Canada and the other from the State of Washington. Although, they are both considered to be LOELs

- the level between a NOAEL and a LOAEL, we have listed the

results under the LOAEL column.

4

– For HCl, we evaluated o ne benchmark at the LOAEL level.

The facility

- wide MIR and TOSHI, available in Appendix 5, are based on emissions, as identified in the 2005 NATA 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 8 facilities with pesticide 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 40 in a million, and it occurs at 1 facility. At this facility, the risk is mainly driven by ethylene dichloride from a mercury cell chlor

- alkali process and other processes not covered by MACT, and the PAI source category contributes

le ss than one percent to the facility

- wide risk. At the other 2 facilities with facility

- wide MIR greater than 10, the source category contribution to risk is less than 1 percent. The maximum facility

- wide TOSHI for the source category is 4, driven primarily by emissions of chlorine from industrial inorganic chemical manufacturing (44%), synthetic organic chemical manufacturing (28%), and mercury cell chlor

- alkali processes (5%). The source category contributes less than 3 percent to the facility

- wide TOSHI.38

Table 3.2

- 2 Source Category Contribution to Facility

- Wide Cancer Risks

– Pesticide Active Ingredient

Pesticide Active Ingredient

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% 2 2 0 0 4

50

- 90% 3 0 0 0 3

10

- 50% 2 2 0 0 4

< 10% 3 1 3 0 7

Total 10 5 3 0 18



### 4. Risk Results for the Polyether Polyols Production Source Category

4.1 Source Category Description and Results

The polyether polyols 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 ethylene oxide, propylene oxide, or other cyclic ethers with compounds having

one or more reactive hydrogens. Polyether polyols do not have significant uses of their own, but rather are used to make a variety of other products. Polyether polyols can be produced by either polymerization of epoxides (i.e., a three

- membered cyclic ether, such as e thylene oxide or propylene oxide) or tetrahydrofuran (THF). In the production of polyether polyols, HAP are used primarily as reactants or extraction solvents and include ethylene oxide, propylene oxide, hexane, toluene, and other HAP. Potential sources of emissions for this category, regardless of the specific process employed, include process vents, storage vessels, equipment leaks, wastewater operations, and heat exchangers/cooling towers. A complete description of the polyether polyols production source category can be found in the text of the final rule preamble.

We currently estimate that there are 23 polyether polyols production facilities operating in the U.S. The data set contains all 23 facilities identified with a polyether polyols production

MAC T code in the 2005 NATA NEI. The 2005 NATA NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and emission locations. All 23 of these facilities are identified as major sources in the NATA NEI.

The emissions for the polyether polyols production source category data set (of 23 facilities)

are summarized in Table 4.1

- 1. The total HAP emissions for the source category are approximately 397 tons per year. Based on these data, the HAP emitted in the largest quantities across these 23 facilities are: ethylene glycol, ethylene oxide, propylene oxide, acetaldehyde, methanol, ethyl benzene, benzene, chlorobenzene, glycol ethers, hexane, propionaldehyde, 1,3

- butadiene, and p

- dioxane. These 13 HAP account f or more than 9039

percent of the total emissions by mass. PB

- HAP 29 reported as emissions from these facilities include POM (fluoranthene) and lead compounds. The following environmental HAP are emitted from the source category and are included in the environm ental risk screen: hydrogen

chloride and PAH.

Table 4.1

- 1 Summary 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) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer?

Ethylene Glycol 161 7
Ethylene Oxide 43 22
Propylene Oxide 31 18
Acetaldehyde 26 10

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

N

- hexane 6 6
Propionaldehyde 5 4

1,3

- Butadiene 5 3

1,4

- Dioxane (p

- Dioxane) 5 6
Styrene 4 5

29 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.h tml

.40

Table 4.1

- 1 Summary 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) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer?

Acrylic Acid 4 2

Toluene 3 7
Formaldehyde 3 8
Vinyl Acetate 1 3

Diethanolamine 1 5
Xylenes (mixed) 1 7
Ethyl Acrylate 1 2
Methyl Tert

- Butyl Ether 1 2
Propylene Dichloride 1 1
Ethyl Chloride 1 5
Ethylene Dichloride 0.9 4
Hydrochloric Acid 0.8 3

Phenol 0.8 7

1,2

- Epoxybutane 0.8 2
Naphthalene 0.7 4
Acetophenone 0.6 3

Acrolein 0.4 2
Acrylonitrile 0.2 2
Trichloroethylene 0.2 1

Cumene 0.2 5
Phosgene 0.2 2
Vinyl Chloride 0.2 3
Dimethyl Formamide 0.1 1

2,4

- d, Salts and Esters 0.1 1
Dimethyl 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
Methylene Chloride 0.04 3

Chloroacetic Acid 0.03 2
Polycyclic Organic Matter

Fluoranthene 0.03 1

Chloroform 0.03 4
Triethylamine 0.02 3
Methyl Isobutyl Ketone 0.02 341

Table 4.1

- 1 Summary 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) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer?

Chlorine 0.02 2

m

- Xylene 0.01 1

Acetonitrile 0.01 2
Diethyl Sulfate 0.01 1
Methyl Methacrylate 0.008 1
Hydroquinone 0.006 1

Tetrachloroethene 0.006 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 0.001 1

p

- Xylene 0.0009 1

2,4

- Toluene Diisocyanate 0.0005 1
Bis(2

- Ethylhexyl)Phthalate 0.0005 1
Dibutylphthalate 0.0005 1
Lead compounds 0.0005 1 c

o

- Toluidine 0.0005 1
Quinoline 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 N etwork 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 72002, not shown above) all have unit risk estimates for cancer, and are considered

PB

- HAP. 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), emis sions 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://ww w.epa.gov/ttn/atw/toxsource/summary.html

.

c There is no reference concentration for lead. In considering noncancer hazards for lead in this preliminary assessment, we compared the maximum annual ambient exposure estimates to the National Ambient Air Quali ty Standards (NAAQS) for lead (0.15 μg/m 3 ). 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. These NAAQS for lead were reviewed with revisions adopted in October 2008 ( http://www.epa.gov/air/lead/actions.html ).42



### 4.2 Risk Characterization

This section presents the results of the risk ass essment for the polyether polyols 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 fr om our acute inhalation impact screening in the form of maximum hazard quotients, as well as the results of our preliminary screen for potential non

- inhalation

risks from PB

- HAP. Also presented are the HAP “drivers,” which are the HAP that collectively con tribute 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 analysis of risks associated with the maximum allowed emissions under

the c urrent MACT standards. A detailed summary of the facility

- specific risk assessment results is available in Appendix 5.

Tables 4.2

- 1 and 4.2

- 2 summarize the chronic and acute inhalation risk results for this source category. The results indicate that maxim um lifetime individual cancer risks could be as high as 30 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 835 people are estimated to have cancer risks at or above 10 in a million, and approximately 140,000 people are estimated to have cancer risks at or above 1

in a million as a result of the emissions from 19 facilities. The maximum chron ic noncancer TOSHI value for the source category could be up to 0.7 from emissions of acrolein.

Worst

- case acute HQs were calculated for every HAP that has an acute benchmark. For cases where the screening acute HQ was greater than 1, we further refined t he 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 App endix 7 of this document and the memorandum “Emission Data and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active Ingredients, Polyether Polyols, and Group IV Polymers and Resins” in the docket for this action). The highest acute HQ value o f 6 (based on the glycol ether REL) is

shown in Table 4.2

- 1. Analysis of potential off

- site acute impacts for this source category identified five facilities with the potential to exceed the acute REL for five pollutants (acrolein (1 facility), 2

- butxyethy l acetate (1 facility), glycol ethers (1 facility), acetaldehyde(1 facility), and formaldehyde (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 any

benchmark.

The highest refined worst

- case acute HQ value is 4 (based on the REL for acrolein). 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 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 consid er the results along with the rather large uncertainties related to the emissions estimates and screening methodology.43

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. 30 The PB

- HAP emitted by facilities in this category include POM fluoranthene as benzo(a)pyrene TEQ (1 facility) and lead compounds (1 facility). Th e emissions of the POM fluoranthene were below the de

minimis threshold level. 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 any exceedances of the NAAQS in our chronic noncancer risk assessment, we do not expect any significant multipathway exposure and risk due to lead emissions from these facilities.

We conducted a screening

- level evaluation of the potential adverse environmental risks associated with emissions of the following environmental HAP from the source category: hydrogen chloride and PAH. The results of the environmental screening analysis are

summarized in Table 4.2

- 3. For hydrogen chloride and PAH, the average modeled concentration around each facility (i.e., the average concentration of all off

- site data points in the modeling domain) did not exceed the ecological benchmarks. In addition, each individual

modeled co ncentration of hydrogen chloride and PAH (i.e., each off

- site data point in the modeling domain) was below the ecological benchmarks for all facilities.

30 ICF International. TRIM

- Based Multipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.44

Table 4.2

- 1 Summary of Source Category Level Inhalation Risks for Polyether Polyols

Production

Res ult HAP “Drivers”
Facilities in Source Category

Number of Facilities Estimated to be in Source Category 23 n/a

Number of Facilities Identified in NATA NEI

and Modeled in Risk Assessment 23 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 30 ethylene oxide, 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 7 ethylene oxide, 1,4

- dioxane, , acrylonitrile, 1,3

- butadiene, benzene, ethylene dichloride, napthalene, propylene oxide, ethyl benzene, acetaldehyde

Greater than or equal to 1 in 1 million 19 ethylene oxide, 1,4

- dioxane,acrylonitrile, 1,3

- butadiene, benzene, ethylene dichloride, naphthalene, propylen e oxide, ethyl benzene, acetaldehyde, benzyl chloride

Chronic Noncancer Risks Maximum Respiratory Hazard Index 0.7 acrolein, acrylic acid Number of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Acute NoncancerResults

Maximum Acute Hazard Quotient 4/0.14 acrolein (REL/AEGL

- 1)

Number of Facilities With Potential for Acute

Effects 5 acrolein, glycol ethers, formaldehyde, 2

- butoxyethyl acetate, acetaldehyde Population Exposure 41
Number of People Living Within 50 Kilometers

of Facilities Modeled 19,500,000 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 835 n/a Greater than or equal to 1 in 1 million 140,000 n/a Number of People Exposed to Noncancer Respiratory Hazard Index:

Greater than 1 0 n/a Estimated Cancer Incidence (excess cases per year) 0.02 n/a

Contribution of HAP to Cancer Incidence ethylene oxide 79% n/a propylene oxide 5% n/a45

Table 4.2

- 1 Summary of Source Category Level Inhalation Risks for Polyether Polyols

Production

benzene 5% n/a
1,3

- butadiene 4% n/a

Table 4.2

- 2 Summary of Acute 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

(mg/m 3 ) AEGL

- 1

(1

- hr) (mg/m 3 ) ERPG

- 1

(mg/m 3 ) AEG

L

- 2 (1

- hr) (mg/

m 3 ) ERP

G

- 2 (mg/

m 3 ) HAP Max. 1

- hr.

Air Conc. (mg/m 3 )

Acrolein 0.01 4 0.14/0.09 0.04/0.03 0.0025 0.069 0.11 0.23 0.34

Glycol Ethers 0.28 3 0.093

2

- Butoxyethyl

Acetate 0.28 3 0.093

Acetaldehyde 0.71 2 0.009/0.04 0.001/0.002 0.47 81 18 490 360

Formaldehyde 0.1 2 0.1/0.08 0.006/0.008 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.

AEGL

– Acute exposure guideline levels represen t emergency exposure (1

- hour) limits for the general public.

AEGL

- 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 transi ent and reversible upon cessation of exposure.

AEGL

- 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 a n 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 se rious health effects or symptoms which could impair an individual’s ability to take protective action.46 Table 4.2

- 3 Summary of Environmental Risk Screen Results for the

Polyether Polyols Production Source Category

Environmental

HAP Number of Facilities In Category Exceeding Percent of Modeled Area in Category Exceeding 2

Tier 1 Screen Tier 2 Screen 1 NOAEL LOAEL LOAEL LOAEL NOAEL LOAEL

PB

HAP PAH None None

- - 0% 0%

Acid

Gases 3 HCl NA None

- - NA 0%

NA

– Not Applicable.

1

- Tier 2 screen is performed for PB

- HAP when there are exceedances of the Tier 1 screen. The acid gas screen

is a one tier screen.

2

- A value of 0% indicates that none of the modeled data points exceeded the benchmark. For PB

- HAP the percent area is based on the Tier 2 resu lts, if a Tier 2 analysis is performed. Otherwise, the percent area is based

on the Tier 1 results.

3

– For HCl, we evaluated one benchmark at the LOAEL level.

The facility

- wide MIR and TOSHI, available in Appendix 5, are based on emissions, as

identifie d in the 2005 NATA NEI, from all emissions sources at the identified facilities. The results of the facility

- wide assessment are summarized in Table 4.2

- 3. The results indicate that 22 facilities with polyether polyols production processes have a facility

- wide cancer MIR greater than or equal to 1 in a million. The maximum facility

- wide MIR is 40 in a million, with the polyether polyols production source category contributing 100 percent of the risk, driven by emissions of 4,4

- methylenendianiline, 2,4

- tolue ne diamine, and hydrazine all from “not a MACT process”. The maximum facility

- wide TOSHI for the source category is 4, driven by emissions of chlorine from industrial inorganic chemical manufacturing and HON process units. The source category contributes a pproximately 6 percent to the facility

- wide

TOSHI.

Table 4.2

- 4 Source Category Contribution to Facility

- Wide Cancer Risks

– Polyether Polyols Production

Polyether Polyols

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 4 5 0 9

50

- 90% 0 3 2 0 5

10

- 50% 1 2 2 0 5

< 10% 0 0 4 0 4

Total 1 9 13 0 2347



### 5. Risk Results for the P&V IV Styrene Acrylonitrile Source Category

5.1 Source Category Description and Results

This section summary presents the risk assessment for the styrene

- acrylonitrile (SA) resin production source category. Styrene

- acrylonitrile resins are copolymers of styrene and acrylonitrile. Styrene

- acrylonitrile r esins may be synthesized by emulsion, suspension, and continuous mass polymerization; however, the majority of production is by batch emulsion. In emulsion polymerization, monomers are dispersed in water using a soap solution or an emulsifier. In suspensio n polymerization, the monomer is suspended in a water phase. In mass polymerization, monomers are reacted without the use of emulsifiers, suspending agents, salts or waters. Emission points along the SA resin production process include equipment leaks,

pro cess vents, storage vessels, and wastewater operations. Many facilities that produce Acrylonitrile

- Butadiene

- Styrene (ABS) resins also produce SA, because much of the SA resins that are produced are used as feedstock in the production of ABS. Typical uses include automobile instrument panels and interior trim and housewares. A complete description of the

styrene

- acrylonitrile production source category can be found in the text of the final rule preamble.

We currently estimate that there are three styrene

- a crylonitrile production facilities operating in the U.S. For the proposal two facilities were known to us and modeled. During the comment period an additional facility was identified and has been included in the results for

the final rule. The data set now contains three facilities identified with a styrene

- acrylonitrile production MACT code in the 2005 NATA NEI. The 2005 NATA NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and

emission locati ons. All three of these facilities are identified as major sources in the NATA

NEI.

The emissions for the styrene

- acrylonitrile production source category data set (of three facilities) are summarized in Table 5.1

- 1. The total HAP emissions for the source category are approximately 4 tons per year. Based on these data, the HAP emitted in the largest quantities for these facilities are: styrene, ethyl benzene, acrylonitrile and methylene chloride. These four HAP account for 100 percent of the total emission s by mass. No PB

- HAP 31 are reported in the data set for the styrene

- acrylonitrile production source category. A screening

- level evaluation of the potential adverse environmental risks was not necessary since no

environmental HAP are emitted from this source category.

31 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Lib rary , 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

.48

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

Benchmark

Values for Acute

Noncancer?
Styrene 2 3
Ethyl Benzene 0.7 1
Acrylonitrile 0.7 2
Methylene chloride 0.4 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 and are also available in Appendix 3 of Methodology for Developing Preliminary Risk Estimates for Source Categories Previously Subjected to Technology

- based Standards (U.S. EPA Office of Air Quality Plannin g and Standards. EPA

- HQ

- OAR

- 2006

- 0859

- 0102. April 2007).



### 5.2 Risk Characterization

This section presents the results of the risk assessment for the styrene

- 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 prelimina ry screen for potential non

- inhalation

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 summ ary of the results of our facility

- wide assessments and our analysis 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 5.

T able 5.2

- 1 summarizes the chronic and acute inhalation risk results for this source category. The results indicate that maximum lifetime individual cancer risks is below 1 in a million,

with acrylonitrile as the major contributor to risk. The total estimat ed cancer incidence from the source category is 0.0003 excess cancer cases per year, or one case in every 3,300 years. 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 0.003, based primarily on emissions of acrylonitrile, indicating no significant potential for chronic noncancer impacts.

Worst

- case acute HQs were calculated for every HAP that has an acute benchmark, and the highest acute HQ v alue of 0.05 (based on the methylene chloride REL) is shown in Table 5.2

- 1. There were no screening acute HQs greater than 1. A screening

- level evaluation of the potential human health risks associated with emissions of PB

- HAP was not necessary for this

so urce category since no PB

- HAP are emitted.49

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 in Source Category 3 n/a

Number of Facilities Identified in NATA NEI

and Modeled in Risk Assessment 3 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 0.4 acrylonitrile

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 0.003 acrylonitrile Number of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Results Maximum Acute Hazard Quotient 0.05 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 1,900,000 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 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) 0.0003 n/a

Contribution of HAP to Cancer Incidence acrylonitrile 97% n/a ethyl benzene 3% n/a

The facility

- wide MIR and TOSHI, available in Appendix 5, are based on emissions, as identified in the 2005 NATA NEI, from all emissions sources at the identified facilities. The results of the facility

- wide assessment are summarized in Table 5.2

- 2. The re sults indicate that all three facilities with styrene

- acrylonitrile production processes have a facility

- wide cancer MIR greater than or equal to 1 in a million. The maximum facility

- wide cancer MIR is 40 in a million for 1 facility. At this facility, the source category contributes less than one percent to50

the facility

- wide MIR, which is driven by emissions of ethylene dichloride from a mercury

cell chlor

- alkali process. The other two facilities have cancer risk at 30 in a million and 2 in a million. Again , the styrene

- acrylonitrile source category contributes less than one percent to the facility

- wide MIR, which is driven by emissions of acrylonitrile from the acrylonitrile

butadiene

- styrene resins production source category. The maximum facility

- wide TOSH I for the source category is 4, driven by emissions of chlorine from inorganic chemical manufacturing, synthetic 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 1 0 0 1

< 10% 0 0 2 0 2

Total 0 1 2 0 3



### 6. Risk Results for the P&R IV Polystyrene Production Source Category

6.1 

### Source Category Description and Results

Polystyrene resins (PS) are those produced by the polymerization of styrene monomer. This type of resin can be produced by three methods: (1) suspension polymerization (operated in batch mode); (2) mass (operated in a continuous mode); and (3) emulsion pro cess (operated in a continuous mode). The mass and suspension methods are the most commercially 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 crystal, impact, or expandable polystyrene beads. In this process, polymerization is carried out in an aqueous medium that permits the removal of heat resulting from the reaction. The polystyrene is formed in small beads which are separated from th e aqueous phase. The mass process uses no water or organic solvents and is the simplest process for producing polystyrene. There are four major stages in the process: prepolymerization, polymerization, devolatilization, and extrusion. The uses for polystyr ene resin include packaging and one

- time use, expandable polystyrene 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 polystyrene resins, including disposable dinnerware, 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 th e polystyrene production source category can be found in the text of the final rule preamble.51

We currently believe that there are 10 polystyrene production facilities operating in the U.S. The final rule data set contains 10 facilities identified with a p olystyrene production MACT code in the 2005 NATA NEI. The 2005 NATA NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and emission locations. All 10 of these facilities are identified as major sources in the NATA NEI.

The emissions for the polystyrene production source category data set (of 10 facilities) are

summarized in Table 6.1

- 1. The total HAP emissions for the source category are approximately 80 tons per year. Based on these data, the H AP emitted in the largest quantities for these 10 facilities is styrene, toluene, ethyl benzene, tetrachloroethene, and xylenes (mixed). These five HAP account for 99 percent of the total emissions by mass. No PB

- HAP 32
are reported in the data set for the p olystyrene production source category. The following environmental HAP is emitted from the source category and is included in the environmental risk screen: hydrogen chloride.

Table 6.1

- 1 Summary of Emissions from the Polystyrene Production Source Catego ry 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

Benchmark

Values for Acute

Noncancer?
Styrene 76 9

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 polystyrene 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 c ancer 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 collectively

32 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

.52

contribute 90 percent of the maximum cancer risk or maxim um hazard index at the highest exposure location, as well as a summary of the results of our facility

- wide assessments and our analysis of risks associated with the maximum allowed emissions under the current MACT standards. A detailed summary of the facil ity

- specific risk assessment results is available in Appendix 5.

Table 6.2

- 1 summarizes the chronic and acute inhalation risk results for this source category. The results indicate that maximum lifetime individual cancer risks is below 1 in a million,

wit h ethyl benzene as the major contributor to risk. The total estimated cancer incidence from the source category is 0.00001 excess cancer cases per year, or one case in every 100,000 years. There are no people estimated to have cancer risks at or above 1 in a million as a result of the emissions from this source category. The maximum chronic noncancer TOSHI value for the source category could be up to 0.006 from emissions of tetrachloroethene, 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 styrene REL) is shown in Table 6.2

- 1. There were no acute HQs greater than 1, indicating no potential concerns about acute im pacts. 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.

We conducted a screening

- level evaluation of the potential adverse environm ental risks associated with emissions of the following environmental HAP from the source category: hydrogen chloride. The results of the environmental screening analysis are summarized in

Table 6.2

- 2. For hydrogen chloride, the average modeled concentratio n around each facility (i.e., the average concentration of all off

- site data points in the modeling domain) did not exceed the ecological benchmarks. In addition, each individual modeled concentration of hydrogen chloride (i.e., each off

- site data point in the modeling domain) was below the ecological benchmarks for all facilities.53

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 in Source Category 10 n/a

Number of Facilities Identified in NATA NEI

and Modeled in Risk Assessment 10 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 0.08 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 Neurological Hazard Index 0.006 tetrachloroethylene

Number of Facilities with Maximum Neurological Hazard Index:

Greater than 1 0 n/a

Acute Noncancer 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 0 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) 0.00001 n/a

Contribution of HAP to Cancer Incidence ethyl benzene 78% n/a tetrachloroethylene 21% n/a54 Table 6.2

- 2 Summary of Environmental Risk Screen Results for the

Polystyrene Production Source Category

Environmental

HAP Number of Facilities In Category Exceeding Percent of Modeled Area in Category Exceeding 2

Tier 1 Screen Tier 2 Screen 1 NOAEL LOAEL NOAEL LOAEL NOAEL LOAEL

Acid

Gases HCl 3 NA None

- - NA 0%

NA

– Not Applicable.

1

- Tier 2 screen is performed for PB

- HAP when there are exceedances of the Tier 1 screen. The acid gas screen

is a one tier screen.

2

- A value of 0% indicates that none of the modeled data points exceeded the benchmark. For PB

- HAP the percent area is based on the Tier 2 results, if a Tier 2 analysis is performed. Otherwise, the percent area is based

on the Tier 1 results.

3

– For HCl , we evaluated one benchmark at the LOAEL level.

The facility

- wide MIR and TOSHI, available in Appendix 5, are based on emissions, as identified in the 2005 NATA NEI, from all emissions sources at the identified facilities. The results of the facility

- wid e assessment are summarized in Table 6.2

- 2. The results indicate that two facilities with polystyrene 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 30 in a million at one facility. At this facility, the source category contributes less than one percent to the facility

- wide MIR, which is driven by emissions of acrylonitrile from an acrylonitrile

- butadiene

- sytrene (ABS) resins production process. Th e other facility has a

cancer risk of 3 in a million. The maximum facility

- wide TOSHI for the source category is 1, driven by chlorine.

Table 6.2

- 3 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 0 0 0 3

50

- 90% 2 0 0 0 2

10

- 50% 0 0 0 0 0

< 10% 2 2 1 0 5

Total 7 2 1 0 1055



### 7. Risk Results for the P&R IV Polyethylene Terephthalate Source Category

7.1 Source Category Description and Results

Three different types of resins are made by sources covered by the PET source category:

solid

- state resins (PET bottle grade resins); polyester film; and engineering resins. They are all thermoplastic linear condensation polymers based on dimethyl terephthalate (DMT) or terephthalic acid (TPA). PET melt

- phase polymer is used in the production of all three of these resins. This polymer is produced by polycondensation of ethylene glycol with either DMT or TPA. PET polymer is prepared commercially via the intermediate bis

- (2

- hydroxyethyl)

- terephthalate (BHET), which is obtained either by transesterification of DMT

or direct esterification of TPA. The transesterification consists of the catalyzed exchange of ethylene glycol for methyl alcohol to yield the intermediate BHE. The liberated methyl alcohol is removed from the system to drive the exchange to completion and is either recycled

to the DMT producer for credit or sold. PET production can occur via either a batch or continuous process.

PET solid

- state resin is produced in a two

- step process. In the first step, PET polymer is produced by conventional PET melt polymerization. This low

- molec ular weight PET is then transferred in pellet form to a solid

- state polymerization unit in which the polymerization

continues at lower

- than

- melt temperature, until the desired molecular weight PET is achieved. By

- product ethylene glycol and acetaldehyde ar e swept out of the system either by circulating hot nitrogen gas over the moving bed of chip or by carrying out solid

- state polymerization

under vacuum. The most common use of PET solid

- state resins is in soft drink bottles, some

industrial fiber

- graded po lyester (e.g., for tire cord) is also produced from PET solid

- state
resins.

Polyester film is a high performance film made from PET resin. The PET resin used to produce this film has a similar intrinsic viscosity to fiber grade, but has a higher purity. P ET film is made by quenching molten PET resin to form an amorphous film. This film is then oriented by stretching it at elevated temperatures. The most common uses of PET film are photographic film and magnetic media.

PET is used extensively in the manufa cture of synthetic fibers (i.e., polyester fibers), which compose the largest segment of the synthetic fiber industry. Melt spinning accounts for virtually all commercial production of polyester fibers worldwide. The polymer is made from ethylene glycol an d either DMT or purified TPA. The manufacturing process for the PET polymer used in PET fibers is similar to PET melt

- phase polymer production. 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, prepolymerization and polymerization reaction vents and process tanks, equipment leaks and ancillary systems, and wastewater operations. A co mplete description of the PET production source category can be found in the text of the final rule preamble.56

We currently estimate that there are 13 polyethylene terephthalate production facilities operating in the U.S. The final rule data set contains 1 3 facilities identified with a polyethylene terephthalate production MACT code in the 2005 NATA NEI. The 2005 NATA NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and emission locations. All 13 of these facilities are identified as major

sources in the NATA NEI.

The emissions for the PET production source category final rule data set (of 13 facilities) are

summarized in Table 7.1

- 1. The total HAP emissions for the source category are approxim ately 800 tons per year. Based on these data, the HAP emitted in the largest quantities across these 13 facilities are: ethylene glycol, methanol, acetaldehyde, 1,4

- dioxane, biphenyl, m

- xylene and o

- xylene. These 7 HAP account for 99 percent of the total e missions by mass. Persistent and bioaccumulative HAP (PB HAP) 33 in the final rule data set for the polyethylene terephthalate production source category include cadmium compounds, polycyclic organic matter (POM), and lead compounds. The following environmen tal HAP are emitted from the source category and are included in the environmental risk screen:

cadmium and PAH.

Table 7.1

- 1 Summary of Emissions from the Polyethylene Terephthalate Production Source Category and Availability of Dose

- Response Values

HAP a Emissions (tpy) Number of

Facilities Reporting HAP (15

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

Benchmark

Values for Acute

Noncancer?
Ethylene Glycol 349 13

Methanol 209 9
Acetaldehyde 152 13

1,4

- dioxane 53 11
Biphenyl 44 4

m

- Xylene 8 1

o

- Xylene 7 1
Formaldehyde 3 3

p

- Xylene 0.9 1
Xylenes (mixed) 0.4 2
Ethylene oxide 0.4 2

Antimony compounds 0.3 1

Manganese compounds 0.09 2
Glycol Ethers 0.05 1

n

- Hexane 0.03 3

Benzene 0.003 3

Toluene 0.00004 2
Nickel compounds 0.00002 1

33 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Volume 1,

EPA

- 453K

- 04

- 0 01A, as referenced in the final rule 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

.57

Table 7.1

- 1 Summary of Emissions from the Polyethylene Terephthalate Production Source Category and Availability of Dose

- Response Values

HAP a Emissions (tpy) Number of

Facilities Reporting HAP (15

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

Benchmark

Values for Acute

Noncancer?

p

- Dichlorobenzene 0.00001 1
Cadmium compounds 0.00001 1

Lead compounds 0.000005 1 c Arsenic compounds 0.000002 1

Polycyclic Organic Matter

2

- Methylnaphthalene 0.0000002 1

Phenanthrene 0.0000002 1

Pyrene 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 footnote b), emissions will be treated as ethylene glycol methyl ether. For emissions of any chemicals or che mical 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 72002, not shown above) all have unit risk estimates for cancer, and are considered

PB

- HAP.

b Specific dose

- response values for each chemical a re 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 (NAAQS) for lead (0.15 μg/m 3 ). 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 polyethylene 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 o f our preliminary screen for potential non

- inhalation 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

- wide assessments and our analysis of risks associated with the maximum allowed58

emissions under the current MACT standards. A detailed summary of the facility

- specific risk

assessment results is available in Appendix 5.

Tables 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 10 in a million, with 1,4

- dioxane as major contrib utor to the risk. The total estimated cancer incidence from the source category is 0.002 or one case in every 500 years. Approximately 2,300 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 emissions. The maximum chronic noncancer TOSHI value for the source category could be up to 0.4, indicating no significant potential for chronic non cancer impacts.

Worst

- case acute HQs were calculated for 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 adjusted from 10 to a value of 2 based on our approach as described in the memorandum “Emission Data and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active Ingredients, Polyether Polyols, and Group IV Polym ers and Resins” available in the docket for this action. The facility multipliers 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 “Emission Data and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active Ingredients, Polyether Polyols, Polymers and Resins IV” in the docket for this action). Using these adjustments to the multiplier of 10 resulted in the highest acute HQ value of 4 (based on the acetaldehyde REL) as shown in

Table 7.2

- 1. Analysis of potential off

- site acute impacts for this source category identified six facilities with the potential to exceed the acute REL for acetalde hyde. Table 7.2

- 2 provides more information on the acute risk estimates for HAP that had an acute HQ greater than 1 for any benchmark. The maximum HQ for acetaldehyde based on the 1

- hour AEGL

- 1 and the maximum HQ for acetaldehyde based on the 1

- hour ERPG

- 1 value is less than 1. The ERPG

1 value is a no effect level which is expected to be protective for sensitive populations from eye and upper respiratory irritation. The AEGL

- 1 value is a level at which we expect to see mild eye or upper respiratory irritat ion in the general population.

All other HAP emissions at all other facilities indicated no potential to cause acute impacts of concern. 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 valu es ( based

on both the REL and 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 physical locations throu ghout the processing area. We note that this assumption further biases the HQ values high, but to an unknown59

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 v alues was associated with acetaldehyde

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 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 th e 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. 34 The PB

- HAP emitted by facilities from this category are cadmium compounds (1 facilities), polycyclic organic matter (POM) as benzo(a)pyrene toxicity equivalence (TEQ) (1 facility), and lead compounds (1 facility). All cadmium and POM as benzo(a)pyrene TEQ emissions were below the screening threshold levels, and therefore we do not expect any significant multipathway exposure and

risk due to these emissions. 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 any exceedances of the NAAQS in our chronic noncancer risk assessment, we do not expect any significant multipathway exposure and risk

due to le ad emissions from these facilities.

We conducted a screening

- level evaluation of the potential adverse environmental risks associated with emissions of the following environmental HAP from the source category:

cadmium and PAH. The results of the environ mental screening analysis are summarized in

Table 7.2

- 3. For cadmium and PAH, the average modeled concentration around each facility (i.e., the average concentration of all off

- site data points in the modeling domain) did not exceed the ecological benchmar ks. In addition, each individual modeled concentration of cadmium and PAH (i.e., each off

- site data point in the modeling domain) was below the ecological benchmarks for all facilities.

34 ICF International. TRIM

- Based Multipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.60

Table 7.2

- 1 Summary of Source Category Level Risks for Polyethyle ne Terephthalate

Production

Result HAP “Drivers”
Facilities in Source Category

Number of Facilities Estimated to be in Source Category 13 n/a

Number of Facilities Identified in NATA NEI

and Modeled in Risk Assessment 13 n/a

Cancer Risks

Maximum Individual Lifetime Cancer Risk (in 1 million) 10 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 1 1,4

- dioxane

Greater than or equal to 1 in 1 million 6 1,4

- dioxane, acetaldehyde,, ethylene

oxide

Chronic Noncancer Risks Maximum Respiratory Hazard Index 0.4 acetaldehyde Number of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Results

Maximum Acute Hazard Quotient 4

0.5

0.1 acetaldehyde (REL)

acetaldehyde (ERPG

- 1) acetaldehyde (AEGL

- 1)

Number of Facilities With Potential for Acute

Effects 6 acetaldehyde

Population Exposure Number of People Living Within 50

Kilometers of Facilities Modeled 48 8,500,000 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 40 n/a

Greater than or equal to 1 in 1 million 2,300 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) 0.002 n/a

Contribution of HAP to Cancer Incidence acetaldehyde 53% n/a
1,4

- dioxane 35% n/a ethylene oxide 9% n/a61

Table 7.2

- 2 Summary of Acute 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

(mg/m 3 ) AEGL

- 1

(1

- hr) (mg/m 3 ) ERPG

- 1

(mg/m 3 ) AEGL

- 2

(1

- hr) (mg/m 3 ) ERPG

- 2

(mg/m 3 )

HAP Max. 1

- hr.

Air Conc. (mg/m 3 )

Acetaldehyde 8.5 4 0.1/0.5 0.02/0.02 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 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.

AEGL

– Acute exposure guideline levels represent emergency exposure (1

- hour) limits for the general public.

AEGL

- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could

e xperience effects that are notable discomfort, but which are transient and reversible upon cessation of exposure.

AEGL

- 2 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience irre versible 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 abilit y to take protective action.

Table 7.2

- 3 Summary of Environmental Risk Screen Results for Polyethylene Terephthala te Production

Environmental

HAP Number of Facilities In Category Exceeding Percent of Modeled Area in Category Exceeding 2

Tier 1 Screen Tier 2 Screen 1 NOAEL LOAEL LOAEL LOAEL NOAEL LOAEL

PB

HAP PAH None None

- - 0% 0%

Cd None None

- - 0% 0%

NA

– Not applicable.

1

- Tier 2 screen is only performed for PB

- HAP when there are exceedances of the Tier 1 screen. The acid gas

screen is a one tier screen.

2

- A value of 0% indicates that none of the modeled data points exceeded the benchmark. For PB

- HAP the percent area is based on the Tier 2 results, if a Tier 2 analysis is performed. Otherwise, the percent area is based

on the Tier 1 results.

The facility

- wide MIR and TOSHI, available in Appendix 5, are based on emissions, as

identified in the 20 05 NATA NEI, from all emissions sources at the identified facilities. 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 greate r than or equal to 1 in a million. The maximum facility

- wide cancer MIR for the source category is 2062

in a million at one facility. The source category contributes 80% to the facility

- wide MIR, which is driven by emissions of 1,4

- dioxane from process vents and control devices. At the other facility (facility

- wide MIR = 10), the PET production source category contributes about 10 percent to the facility

- wide MIR, which is driven by emissions of acetaldehyde from wastewater treatment operations. The maximum f acility

- wide TOSHI for the source category is 1, driven by emissions of several HAP primarily from hazardous waste incineration. The source category contributes approximately five percent to the facility

- wide TOSHI.

Table 7.2

- 4 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 Facility

- Wide MIR <1 1≤ MIR< 10 10≤ MIR<100 > 100 Total

> 90% 5 3 0 0 8

50

- 90% 0 1 1 0 2

10

- 50% 1 0 0 0 1

< 10% 0 1 1 0 2

Total 6 6 2 0 13



### 8. Risk Results for the P&R IV Methyl Methacrylate

- Butadiene

Styrene Source Category

8.1 Source Category Description and Results

Methyl methacrylate

- butadiene styrene resins (MBS) are prepared by grafting methyl methacrylate and styrene onto a styrene

- butadiene rubber in an emulsion process. In emulsion polymerization, monomers are dispersed in water using a soap solution or an emulsifier. The product is a two

- phase polymer used as an impact modifier for rigid polyvinyl chloride products. These products are used for applications in packaging, building, and construction. Emission points for MBS resin production include process vents, equipme nt leaks, storage vessels, and wastewater operations. A complete description of the methyl methacrylate

butadiene

- styrene production source category can be found in the text of the final rule preamble.

We currently estimate that there are two MBS producti on facilities operating in the U.S. The data set contains two facilities identified with a MBS production MACT code in the 2005 NATA NEI. The 2005 NATA 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 NATA 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 sou rce category are approximately five tons per year. Based on these data, the HAP emitted in the largest quantities for these two facilities are: methyl methacrylate, 1,3

- butadiene, ethyl acrylate,63

methanol, and styrene. These five HAP account for over 99 pe rcent of the total emissions by

mass. No PB

- HAP 35 are reported in the data set for the MBS production source category. The following environmental HAP is emitted from the source category and is included in the environmental risk screen: hydrogen chloride.

Table 8.1

- 1 Summary of Emissions 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

Benchmark

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 methyl methacrylate

- butadiene

styrene 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 t he form of maximum 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 analysis 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 5.

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 1 in a million, with 1,3

- butadiene as the major contributor to the risk. The total estimated can cer incidence from the source category is 0.00009 excess cancer cases per year or one case in every 11,000 years. There are approximately 200 people with an estimated cancer risk greater

than 1 in a million. The maximum chronic noncancer TOSHI value for th e source category could be up to 0.02 from emissions of 1,3

- butadiene, indicating no significant potential for chronic noncancer impacts.

35 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Vo lume 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

.64

Worst

- case acute HQs were calculated for every HAP that has an acute benchmark. For cases where the screening acute H Q was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries. Analysis of potential off

site acute impacts for this source category identified one facility with the potential to exceed

the a cute 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 10 (based on the ethyl acrylate

ERPG

- 1). This worst

- case exposure estimate corresponds to an HQ of 0.01 based on the 1

- hour AEGL

- 1 value. For ethyl acrylate, the ERPG

- 1 value is indicative of the odor recognition threshold, while the AEGL

- 1 value is indicative of a level which c ould result in eye irritation. This suggests that, at this worst

- case exposure level, a person might smell the pollutant, but not experience any 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, 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 results along with the rather large unce rtainties 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,

a nd that they were modeled assuming that they all emanate from a single emission location, rather than from numerous physical 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. Taking all of this into consideration, these acute impact screening results indicate only the potential for acute impacts of concern, while the uncertainties an d bias associated with them suggest that there may be no real acute issues 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.

We conducted a screening

- level evaluation of the potential adverse environmental risks associated with emissions of the following environmental HAP from the source category: hydrogen chloride. The results of the environmental screening analysis are summa rized in

Table 8.2

- 3. For hydrogen chloride, the average modeled concentration around each facility (i.e., the average concentration of all off

- site data points in the modeling domain) did not exceed the ecological benchmarks. In addition, each individual modeled concentration of hydrogen chloride (i.e., each off

- site data point in the modeling domain) was below the ecological benchmarks for all facilities.65

Table 8.2

- 1 Summary of Source Category Level Risks for Methyl Methacrylate

Butadiene

- Styrene Produc tion

Result HAP “Drivers”
Facilities in Source Category

Number of Facilities Estimated to be in Source Category 2 n/a

Number of Facilities Identified in NATA NEI

and Modeled in Risk Assessment 2 n/a

Cancer Risks

Maximum Individual Lifetime Cancer Risk (in 1 million) 1 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 1 n/a

Chronic Noncancer Risks Maximum Reproductive Hazard Index 0.02 1,3

- butadiene Number of Facilities with Maximum Reproductive Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Results

Maximum Acute Hazard Quotient 10

0.01 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 1,700,000 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 200 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) 0.00009 n/a

Contribution of HAP to Cancer Incidence
1,3

- butadiene 100% n/a66

Table 8.2

- 2 Summary of Acute 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

(mg/m 3 ) AEGL

- 1

(1

- hr) (mg/m 3 ) ERPG

- 1

(mg/m 3 ) AEGL

- 2

(1

- hr) (mg/m 3 ) ERPG

- 2

(mg/m 3 )

HAP Max. 1

- hr.

Air Conc. (mg/m 3 )

Ethyl acrylate 0.37 0.01/10 0.002/0.003 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 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.

AEGL

– Acute exposure guideline levels represent emergency exposure (1

- hour) limits for the general public.

AEGL

- 1 is the exposure level abov e 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.

AEGL

- 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 max imum 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 abilit y to take protective action.

Table 8.2

- 3 Summary of Environmental Risk Screen Results for Methyl

Methacrylate

- Butadiene

- Styrene Production Facilities

Environmental

HAP Number of Facilities In Category Exceeding Percent of Modeled Area in Category Exceeding 2

Tier 1 Screen Tier 2 Screen 1 NOAEL LOAEL NOAEL LOAEL NOAEL LOAEL

Acid

Gases HCl 3 NA None

- - NA 0%

NA

– Not Applicable.

1

- Tier 2 screen is performed for PB

- HAP when there are exceedances of the Tier 1 screen. The acid gas screen

is a one tier screen.

2

- A value of 0% indicates that none of the modeled data points exceeded the benchmark. For PB

- HAP the percent area is based on the Tier 2 results, if a Tier 2 analysis is performed. Otherwise, the percent area is based

on the Tier 1 results.

3

– For HCl , we evaluated one benchmark at the LOAEL level.

The facility

- wide MIR and TOSHI, available in Appendix 5, are based on emissions, as identified in the 2005 NATA NEI, from all emissions sources at the identified facilities. The results of the facility

- wid e assessment are summarized in Table 8.2

- 3. The results indicate that two facilities with MBS production processes have a facility

- wide cancer MIR greater than or67

equal to 1 in a million. The maximum facility

- wide cancer MIR for the source category is 3 in a million, driven by emissions of acrylonitrile from a source without a MACT code assigned

to it in the NATA NEI. The source category does not contribute to the facility

- wide risk because the source category does not emit any pollutants with cancer dose

- r esponse values. At the other facility, with a facility

- wide cancer MIR of 1 in a million, the facility

- wide cancer risk is driven almost exclusively by emissions of 1,3

- butadiene from equipment leaks from the MBS process. The maximum facility

- wide TOSHI fo r the source category is less than 1.

Table 8.2

- 4 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% 0 1 0 0 1

50

- 90% 0 0 0 0 0

10

- 50% 0 0 0 0 0

< 10% 0 1 0 0 1

Total 0 2 0 0 2



### 9. Risk Results for the P&R IV Acrylonitrile

- Butadiene

- Styrene Source Category

9.1 Source Category Description and Results

Acrylonitrile

- butadiene

- styrene (ABS) resins consist of a terpolymer of acrylonitrile, butadiene, and styrene and can be synthesized by emulsion, suspension, and contin uous mass polymerization. The majority of ABS resin production is by batch emulsion. In emulsion polymerization, monomers are dispersed in water using a soap solution or an emulsifier. The emulsion process involves three distinct polymerizations: polymeriz ation of butadiene to form polybutadiene, grafting of styrene and acrylonitrile monomers to the polybutadiene substrate,

and co

- polymerization of styrene

- acrylonitrile. Specialized ABS resins are produced by suspension polymerization, where the monomer is suspended in a water phase. In mass polymerization, 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. Typical pr oducts made from ABS resins are piping, refrigerator door liners and food compartments, automotive components, telephones, luggage and cases, toys, mobile homes, and margarine tubs . A complete description of the acrylonitrile

- butadiene

- styrene production s ource category can be found in the text of the final rule preamble.

We currently estimate that there are six acrylonitrile

- butadiene

- styrene production facilities operating in the U.S. The data set contains six facilities identified with a acrylonitrile

b utadiene

- styrene production MACT code in the 2005 NATA NEI. The 2005 NATA NEI was updated for this category with more recent data from industry and enhanced quality assurance68

of facility and emission locations. All six of these facilities are identified as major sources in

the NATA NEI.

The emissions for the ABS production source category data set (of six facilities) are

summarized in Table 9.1

- 1. The total HAP emissions for the source category are approximately 271 tons per year. Based on these data, the HAP emitted in the largest quantities across these facilities are: styrene, acrylonitrile, hydrochloric acid, 1,3

- butadiene, cumene, methyl methacrylate, xylenes (mixed), ethyl benzene, aniline, and ethylene glycol. These ten HAP account for over 98 percen t of the total emissions by mass. No PB

- HAP 36 are reported in the data set for the ABS production source category. The following environmental HAP is emitted from the source category and is included in the environmental risk screen: hydrogen chloride.

Table 9.1

- 1 Summary of Emissions from the Acrylonitrile

- Butadiene

- Styrene Production Source Category and Availability of Dose

- Response Values

HAP a Emissions (tpy) Number of

Facilities Reporting HAP (6 facilities in data set) Prioritized Inhalation Dose

- R esponse Value Identified by OAQPS b

PB

- HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer? Styrene 114 5 Acrylonitrile 38 6 Hydrochloric Acid 35 1
1,3

- butadiene 34 4

Cumene 14 4 Methyl Methacrylate 11 3
Xylenes (mixed) 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 1
Chloromethyl Methyl Ether 0.5 1 Acetaldehyde 0.5 1

o

- xylene 0.3 1 Vinyl Acetate 0.2 1
2,4

- d, Salts And Esters 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

36 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

.69

Table 9.1

- 1 Summary of Emissions from the Acrylonitrile

- Butadiene

- Styrene Production Source Category and Availability of Dose

- Response Values

HAP a Emissions (tpy) Number of

Facilities Reporting HAP (6 facilities in data set) Prioritized Inhalation Dose

- R esponse Value Identified by OAQPS b

PB

- HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer? Dimethyl Formamide 0.004 1 Maleic Anhydride 0.003 1
Phosgene 0.003 1
Hydroquinone 0.002 1 Naphthalene 0.002 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

.



### 9.2 Risk Charac terization

This section presents the results of the risk assessment for the acrylonitrile

- butadiene

- styrene 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 collectively contribute 90 percent of t he 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 analysis 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 5.

Tables 9.2

- 1 summarizes the chronic and acute inhalation risk results for this source category.

The results indicate that maximum individual lifetime cancer ri sks could be as high as 20 in a million, with acrylonitrile and 1,3

- butadiene as the major contributors to the risk. The total estimated cancer incidence from the source category is 0.009 excess cancer cases per year, or one case in every 111 years. Approx imately 950 people are estimated to have cancer risks at or above 10 in a million and approximately 95,000 people are estimated to have cancer risks

at or above 1 in a million as a result of the emissions from 5 facilities. The maximum chronic

noncancer TO SHI value for the source category could be up to 0.3 (spleen) from emissions of aniline, indicating no significant potential for chronic noncancer impacts.

Worst

- case acute HQs were calculated for every HAP that has an acute benchmark, and the highest acu te HQ value of 0.9 (based on the acetaldehyde REL) is shown in Table 9.2

- 1. There were no screening acute HQs greater than 1, indicating no potential concerns about acute impacts, and further refinement was not performed.70

A screening

- level evaluation of th e potential human health risks associated with emissions of

PB

- HAP was not necessary for this source category since no PB

- HAP are emitted.

We conducted a screening

- level evaluation of the potential adverse environmental risks

associated with emissions o f the following environmental HAP from the source category: hydrogen chloride. The results of the environmental screening analysis are summarized in

Table 9.2

- 2. For hydrogen chloride, the average modeled concentration around each facility (i.e., the avera ge concentration of all off

- site data points in the modeling domain) did not exceed the ecological benchmarks. In addition, each individual modeled concentration of hydrogen chloride (i.e., each off

- site data point in the modeling domain) was below the

eco logical benchmarks for all facilities.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 in Source Category 6 n/a

Number of Facilities Identified in NATA NEI

and Modeled in Risk Assessment 6 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 20 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 5 acrylonitrile, 1,3

- butadiene, ethyl

benzene

Greater than or equal to 1 in 1 million 5 acrylonitrile, 1,3

- butadiene, ethyl

benzene

Chronic Noncancer Risks Maximum Spleen Hazard Index 0.3 aniline Number of Facilities with Maximum Reproductive Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Results

Maximum Acute Hazard Quotient 0.9

0.3 acetaldehyde (REL)

ethyl acrylate (ERPG

- 1)

Number of Facilities With Potential for Acute

Effects 0 n/a

Population Exposure Number of People Living Within 50

Kilometers of Facilities Modeled 5,900,000 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 950 n/a

Greater than or equal to 1 in 1 million 95,000 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) 0.009 n/a

Contribution of HAP to Cancer Incidence acrylonitrile 70% n/a
1,3

- butadiene 28% n/a72 Table 9.2

- 2 Summary of Environmental Risk Screen Results for

Acrylonitrile

- Butadiene

- Styrene Production

Environmental

HAP Number of Facilities In Category Exceeding Percent of Modeled Area in Category Exceeding 2

Tier 1 Screen Tier 2 Screen 1 NOAEL LOAEL NOAEL LOAEL NOAEL LOAEL

Acid

Gases HCl 3 NA None

- - NA 0%

NA

– Not Applicable.

1

- Tier 2 screen is performed for PB

- HAP when there are exceedances of the Tier 1 screen. The acid gas screen

is a one tier screen.

2

- A value of 0% indicates that none of the modeled data points exceeded the benchmark. For PB

- HAP the percent area is based on the Tier 2 results, if a Tier 2 analysis is perform ed. Otherwise, the percent area is based

on the Tier 1 results.

3

– For HCl, we evaluated one benchmark at the LOAEL level.

The facility

- wide MIR and TOSHI, available in Appendix 5, are based on emissions, as identified in the 2005 NATA NEI, from all emi ssions sources at the identified facilities. The results of the facility

- wide assessment are summarized in Table 9.2

- 3. The results indicate that six facilities with ABS production processes have a facility

- wide cancer MIR greater than or equal to 1 in a m illion. The maximum facility

- wide cancer MIR for the source category is 30 in a million, with the source category contributing about 60 percent of the facility

- wide risk, driven by emissions of acrylonitrile from equipment leaks and ancillary systems. The maximum facility

- wide TOSHI for the source category is 1, driven by chlorine from “not a MACT process”.

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 4 0 4

50

- 90% 0 0 1 0 1

10

- 50% 0 1 0 0 1

< 10% 0 0 0 0 0

Total 0 1 5 0 673



### 10. General Discussion of Uncertainties and How They Have Been

Addressed

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 likely dominate the unc ertainties in our exposure modeling estimates. The chronic exposure modeling uncertainties are considered relatively small in comparison, since we are using EPA’s refined local dispersion model with site

specific parameters and reasonably representative me teorology. If anything, the population exposure estimates are biased high by not accounting for short

- or long

- term population mobility and by neglecting processes like deposition, plume depletion, and atmospheric degradation. Additionally, estimates of th e maximum individual risk (MIR) contain uncertainty, because they are derived 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 indi vidual 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

- year 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

- year chronic exposure period, leading to a potential downward bias in both the MIR and population risk estimates.

A sensitivity analysis performed for the 1999 NATA found that the selection of the meteorology dataset location could result in a range of chronic ambient concentrations which varied from as much as 17% below the estimated value to as much as 84% higher t han the

estimated value. This variability translates directly to the estimated exposures and risks in our assessment, indicating that the actual risks could vary from 17% lower to 84% higher than the

estimated values.

We have purposely biased the acute sc reening results high, considering that they depend upon the joint occurrence of independent factors, such as hourly emissions rates, meteorology and human activity patterns. Furthermore, in cases where multiple acute threshold values are

considered scienti fically acceptable we have chosen the most conservative of these assessments, erring on the side of overestimating potential health risks from acute exposures. In the cases where these results indicated the potential for exceeding short

- term health

thresho lds, we have refined our assessment by developing a better understanding of the geography of the facility relative to potential exposure locations and the true variability of

short

- term emission rates.



### 10.2 Uncertainties in the Dose

- Response Relationships

In the 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 generally derived for chronic

- term (>24 hours up to 30 days), and subchronic (>30 days up to 10% of lifetime) exposure durations, all74

of which are derived based on an assumption of c ontinuous exposure throughout the duration specified. For the purposes of assessing all potential health risks associated with the emissions included in an assessment, we rely on both chronic (cancer and noncancer) and acute (noncancer) benchmarks, which a re described in more detail below.

Although every effort is made to identify peer

- reviewed 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 chr onic 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 IRIS review, and revised assessments may determine that these pollutants are more or less potent than currently thought. We will re

- evaluate risks if, as a resul t of these reviews, a dose

- response metric changes enough to indicate that the risk assessment may significantly mischaracterize human health risk

Cancer assessment

The discussion of dose

- response uncertainties in the estimation of cancer risk below focu ses on the uncertainties associated with the specific approach currently used by the EPA to develop cancer potency factors. In general, these same uncertainties attend the development of cancer potency factors by CalEPA, the source of peer

- reviewed cancer potency factors

used where EPA

- developed values are not yet available. To place this discussion in context, we provide a quote from 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; accordingly, 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 protective.” The approach adopted in this docum ent 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 Canc er Guidelines

, EPA uses animal cancer bioassays 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

estim ates developed following the procedures described in the Cancer Guidelines and outlined below generally provide an upper bound estimate of risk. That is, EPA’s upper bound75

estimates represent a “plausible upper limit to the true value of a quantity” (altho ugh this is usually not a true statistical confidence limit). 37 In some circumstances, the true risk could be as low as zero; however, in other circumstances the risk could also be greater. 38 When developing an upper bound estimate of risk and to provide ris k values that do not underestimate risk, EPA generally relies on conservative default approaches. 39 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 analysis).

Such health risk assessments have associated uncertainties, some which may be considered quantitatively, and others which generally are expressed qualitatively. Uncertainties may vary substantially among cancer risk assessments associated with exposures to different pollutants,

since the assessments employ different databases with different strengths and limitations and the procedures employed may differ in how well they represent actual biological processes for

the assessed substance. EPA’s Risk Characterization Handbook also recommen ds that risk characterizations present estimates demonstrating the impact on the assessment of alternative choices, data, models and assumptions [ 31 ]. Some of the major sources of uncertainty and variability in deriving cancer risk values are described more fully below.

(1) The qualitative similarities or differences between tumor responses observed in experimental animal bioassays and those which would occur in humans are a source of uncertainty in cancer risk assessment. In general, EPA does not assume that tumor sites observed in an experimental animal bioassay are necessarily predictive of the sites at which

tumors would occur in humans. 40 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) Uncertainties regarding the most appropriate dose m etric 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

37 IRIS glossary (www.epa.gov/NCEA/iris/help_gloss.htm).

38 The exception to this is the URE for benzene, which is considered to cover a range of values, eac h end of which is considered to be equally plausible, and which is based on maximum likelihood estimates.

39 According to the NRC report Science and Judgment in Risk Assessment (NRC, 1994) “[Default] options are generic approaches, based on general scientif ic 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 Process defined de fault option as “the option chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to the contrary” (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the

agency may depart from them in evaluating the risks posed by a specific substance when it believes this to be appropriate. In keeping with EPA’s goal of protecting public health and the environment, default assumptions

are used to ensure that risk to chemicals is not underestimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An Examination of EPA Risk Assessment Principles and Practices,

EPA/100/B

- 04/001 available at: http://www.epa.gov/osa/pdfs/ratf

- final.pdf.

40 Per the EPA Cancer Guidelines: “The default option is that positive effects in animal cancer studies indicate that the agent under study can have carcinogenic potential in humans.” and “Target organ concordance is not a prerequisite for evaluating the implications of animal study results for humans.”76

support development of a pharmacoki netic model for the absorption, distribution, metabolism and excretion of an agent, which may result in improved dose metrics (e.g., average blood concentration of the pollutant or the quantity of agent metabolized in the body). Quantitative

uncertainties result when the appropriate choice of a dose metric is uncertain or when dose metric estimates are themselves uncertain (e.g., as can occur when alternative pharmacokinetic models are available for a compound). Uncertainty in dose estimates may

lead to eit her over or underestimation of risk.

(3) For the quantitative extrapolation of cancer risk estimates from experimental animals to humans, EPA uses scaling methodologies (relating expected response to differences in physical size of the species), which int roduce another source of uncertainty. These methodologies are based on both biological data on differences in rates of process according to species size and empirical comparisons of toxicity between experimental animals and humans. For a particular polluta nt, 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 uncertainties associated with limitations in the

test data an d 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) analysis to estimate a dose at which there is a specified excess risk of cancer, which is used as the point of departure (or POD) for the remainder of the calculation. Statistical uncertainty in developing a POD using a benchmark dose (BMD) approach is generally addressed though use of the 95% lower

confidence limit on the d ose at which the specified excess risk occurs (the BMDL), decreasing the likelihood of understating risk. EPA has generally utilized the multistage model for estimation of the BMDL using cancer bioassay data (see further discussion below).

(5) Extrapolati on from high to low doses is an important, and potentially large, source of uncertainty in cancer risk assessment. EPA uses different approaches to low dose risk assessment (i.e., developing estimates of risk for exposures to environmental doses of an

agen t from observations in experimental or epidemiological studies at higher dose) depending on the available data and understanding of a pollutant’s mode of action (i.e., the manner in which a pollutant causes cancer). EPA’s Cancer Guidelines express a prefer ence for the use of reliable, compound

- specific, biologically

- based risk models when feasible; however, such models are rarely available. The mode of action for a pollutant (i.e., the manner in which a pollutant causes cancer) is a key consideration in det ermining how risks should be estimated

for low

- dose exposure. A reference value is calculated when the available mode of action data show the response to be nonlinear (e.g., as in a threshold response). A linear low

- dose (straight line from POD) approach i s 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. Linear extrapolation can be supported by both pollutant

- specific

data and broader s cientific 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 the77

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 a pproach as a baseline science

policy choice (a “default”) when available data do not allow a compound

- specific determination. This approach is designed to not underestimate risk in the face of uncertainty and variability. EPA believes that linear dose

- resp onse models, when appropriately applied as part of EPA’s cancer risk assessment process, provide an upper bound estimate of risk and generally provide a health protective approach. Note that another source of uncertainty is the

characterization of low

- dose nonlinear, non

- threshold relationships. The National Academy of Sciences has encouraged the exploration of sigmoidal type functions (e.g., log

- probit models) in representing dose response relationships due to the variability in response within human popul ations. Another National Research Council (NRC) report [ 32 ] suggests that models based on distributions of individual thresholds are likely to lead to sigmoidal

- shaped dose

response functions 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 susceptibility factors...” Thus, if a distribution of thresholds approach is c onsidered for a carcinogen risk assessment, application would depend on ability of modeling to reflect the degree of variability in response in human populations (as opposed to responses in bioassays with genetically more uniform rodents). Note also that l ow dose linearity in risk can arise for reasons separate from population variability: due to the nature of a mode of action and additivity of a chemical’s effect on top of background chemical exposures and biological

processes.

As noted above, EPA’s curre nt approach to cancer risk assessment typically utilizes a straight line approach from the BMDL. This is equivalent to using an upper confidence limit on the slope of the straight line extrapolation. The impact of the choice of the BMDL on bottom line

risk estimates can be quantified by comparing risk estimates using the BMDL value to central estimate BMD values, although these differences are generally not a large contributor to uncertainty in risk assessment (Subramaniam et. al., 2006) [ 33 ]. It is importan t to note that earlier EPA assessments, including the majority of those for which risk values exist today, were generally developed using the multistage model to extrapolate down to environmental

dose levels and did not involve the use of a POD. Subramania m et. al. (2006) also provide comparisons indicating that slopes based on straight line extrapolation from a POD do not show large differences from those based on the upper confidence limit of the multistage

model.

(6) Cancer risk estimates do not general ly 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 typical individual, although compound

- specific data to evaluate this variability are generally not available. There may also be important life stage differences in the quantitative potency of 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 generally quantitatively address life stage differences.78

However, one approach used commonly in EPA assessments that may help ad dress variability in response is to extrapolate human response from results observed in the most sensitive species and sex tested, resulting typically in the highest URE which can be supported by reliable data, thus supporting estimates that are designed n ot 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 d evelop 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 face of uncertainty and variability. When there are gaps in the available informati on, 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 41 e.g., factors of 10 or 3, used in the absence of compo und

- specific data; where data are available, uncertainty factors may also be developed using compound

- specific information. When data are limited, more assumptions are needed and more default factors are used. Thus there may be a greater tendency to overes timate 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 n on

- 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 m agnitude) of a daily oral exposure (RfD) or a continuous inhalation exposure (RfC) to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. 42 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 by evaluating all of the available peer

- reviewed literature to determine non

cancer endpoints of concern, evaluating the quality, strengths and limitations of the available studies. EPA typically chooses the relevant endpoint that occurs at the lowest dose, often

41 According to the NRC report Science and Judgment in Risk Assessment (NRC, 1994) “[Default] options are generic approaches, based on general scientific knowledge and policy judgment, that are applied to various

elements of the risk

- assessment process when the correct scientific model is unknown or uncertain.” The 1983

NRC report Risk Assessment in the Federal Government: Managing the Process defined default option as “the option chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to the contrary” (NRC, 1983a, p. 63). There fore, default options are not rules that bind the agency; rather, the agency may depart from them in evaluating the risks posed by a specific substance when it believes this to be appropriate. In keeping with EPA’s goal of protecting public health and the environment, default assumptions are used to ensure that risk to chemicals is not underestimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An examination of EPA Risk Assessment Principles and Practices,

EPA/100/B

- 04/00 1 available at: http://www.epa.gov/osa/pdfs/ratf

- final.pdf.

42 See IRIS glossary79

using statistical modeling of the available data, an d then determines the appropriate point of departure (POD) for derivation of the reference value. A POD is determined by (in order of preference): (1) a statistical estimation using the benchmark dose (BMD) approach; (2) use of

the dose or concentration at which the toxic response was not significantly elevated (no

observed adverse effect level

— NOAEL); or (3) use of the lowest observed adverse effect level (LOAEL).

A series of downward adjustments using default UFs is then applied to the POD to estimate

t he 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 accoun t 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 extrapolati ng from data obtained in a study with less

- than

lifetime exposure (i.e., extrapolating from subchronic to chronic exposure); (4) uncertainty in extrapolating from a LOAEL in the absence of a NOAEL; and (5) uncertainty when the database is incomplete or the re 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 type of uncertainty (when

relevant to the assessment) , EPA typically applies an UF value of 10 or 3 with the cumulative UF value leading to a downward adjustment of 10

- 3000 fold from the 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 interspecies extrapolation is not required) the associated UF is not used. The major adjustment steps are described more fully below.

1) Heterogeneity among humans is a key source of variability as well as uncertainty. Uncertainty related to human variation is considered in extrapolating doses from a subset or

smaller

- sized population, often of one sex or of a narrow range of life stages (typical of occupatio nal epidemiologic studies), to a larger, more diverse population. In the absence of pollutant

- specific 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; howev er, 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) i s extrapolated to estimate the human response. While there is long

- standing scientific support for the use of animal studies as indicators of potential toxicity to humans, there are uncertainties in such extrapolations. In the absence of data to the contra ry, the typical 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. Typically, compound specific data to evaluate relative sensitivity in humans versus rodents ar e lacking, thus leading to uncertainty in this extrapolation. Size

- related differences (allometric relationships) indicate that typically80

humans are more sensitive than rodents when compared on a mg/kg/day basis. The default choice of 10 for the interspeci es UF is consistent with these differences. For a specific 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 unc ertainties; however, such dosimetric adjustments are not always possible. Information may not be available to quantitatively assess toxicokinetic or toxicodynamic differences between animals and humans, and in many cases a 10

- fold UF (with separate factors of 3 for toxicokinetic and toxicodynamic components) is used to account for expected species differences and associated uncertainty in extrapolating from laboratory animals to humans in the derivation of a reference value. If information on one or

the oth er 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 only 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 or 10

- fold is typically applied unless the available scientific information supports use of a different value.

4) Toxi city data are typically 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 PO D is to use BMD analysis; however, this approach requires adequate quantitative results for a meaningful analysis, which is not always possible. Use of a NOAEL is the next preferred approach after BMD analysis in determining a POD for deriving a health eff ect reference value. However, many studies lack a dose or exposure level at which an adverse effect is not observed (i.e., a NOAEL is not identified). When using data limited to a LOAEL, a UF of 10 or 3

- fold is often applied.

5) The database UF is intend ed 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 typic ally applied.

Acute noncancer assessment

Many of the UFs used to account for variability and uncertainty in the development of acute reference values are quite similar to those developed for chronic durations, but more often using individual UF values th at may be less than 10. UFs are applied based 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 typically 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) unce rtainty in accounting for an incomplete database on toxic effects of potential concern. Additional adjustments are often applied to account for uncertainty in extrapolation from81

observations at one exposure duration (e.g., 4 hours) to arrive at a POD for d erivation 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 relat ive 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.82



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