Draft Risk Assessment for 7 Chemica l Sector Source Categories

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## Draft Residual Risk Assessment for 7 Source Categories:

Pesticide Active Ingredient Manufacturing Polyether Polyols Production Polymers and Resins IV

-- Styrene Acrylonitrile Polymers and Resins IV

-- Polystyrene Polymers and Resins IV

– Polyethylene Ter e phthalate Polymers and Resins IV

-- Methyl Methacrylate

- Butadiene Styrene Polymers and Resins IV

-- Acrylic Butadiene Styrene

by EPA’s Office of Air Quality Planning and Standards

Office of Air and Radiation

November 2011Draft Risk Assessment for 7 Chemica l Sector Source Categories

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### Table of Contents

1. Introduction

................................ ................................ ................................ ............................. 6

2. Methods

................................ ................................ ................................ ................................ ... 7

2.1. Emissions and source data

................................ ................................ ........................... 7

2.2. Dispersion modeling for inhalation exposure assessment

................................ ........... 7

2.3. Estimating chronic human inhalation exposure

................................ ........................ 10

2.4. Acute Risk Screening and Refined Assessments

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

2.5. Multipathway human health and environmental risk screening

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

2.6. Dose

- Response Assessment

................................ ................................ ...................... 14

2.6.1. Sources of chronic dose

- response information

................................ .................. 14

2 .6.2. Sources of acute dose

- response information

................................ ...................... 23

2.7. Risk Characterization

................................ ................................ ................................ 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 Manufacturing

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

3.1 Source Category Description and Results

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

3.2 Risk Characterization

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

4. Risk Results for the Polyether Polyols Production Source Category

................................ ... 40

4.1 Source Category Description and Results

................................ ................................ . 40

4.2 Risk Characterization

................................ ................................ ................................ 45

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

................................ .. 49

5.1 Source Category Description and Results

................................ ................................ . 49

5.2 Risk Characterization

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

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

............................... 53

6.1 Source Category Description and Results

................................ ................................ . 53

6.2 Risk Characterization

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

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

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

7.1 Source Category Description and Results

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

7.2 Risk Characterization

................................ ................................ ................................ 60

8. Risk Results for the P&R IV Methyl Met hacrylate

- Butadiene

- Styrene Source Category

... 64

8.1 Source Category Description and Results

................................ ................................ . 64

8.2 Risk Characterization

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

9. Risk Results for the P&R IV Acrylonitrile

- Butadiene

- Styrene Source Category

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

9.1 Source Category Description and Results

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

9.2 Risk Characterization

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

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

........................ 74

10.1 Exposure Modeling Uncertainties

................................ ................................ ......... 74

10.2 Uncertainties in the Dose

- Response Relationships

................................ ............... 75

11 References

................................ ................................ ................................ ............................. 83

Index of Tables

Table 2.2

- 1 AERMOD version 11103 model options for RTR modeling

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3 Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcinogens

.... 18

Table 2.6

- 1 (b) Dose

- Response Values for Chronic Inhalation Exposure to N oncarcinogens

................................ ................................ ................................ ................................ .................. 20

Table 2.6

- 2 Dose

- Response Values for Acute Exposure

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

Table 3.1

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

- Response Values

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

Table 3.2

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

Production 38

Table 3.2

- 2 Summary of Refined Acute Results for Pesticide Active Ingredient

Production Facilities

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

Table 3.2

- 3 Source Category Contribution to Facility

- Wide Ca ncer Risks

– Pesticide Active Ingredient

................................ ................................ ................................ ...................... 40

Table 4.1

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

- Response Values

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

Table 4.2

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

Production 47

Table 4.2

- 2 Summary of Acute Refined Results for Polyeth er Polyols Production

Facilities 48

Table 4.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

– Polyether Polyols Production

................................ ................................ ................................ ................... 49

Table 5.1

- 1 Summary of Emissions from the Styrene

- Acrylonitrile Production Source Category and Availability of Dose

- Response Values

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

Table 5.2

- 1 Summary of Source Category Level Risks f or Styrene

- Acrylonitrile

Production 52

Table 5.2

- 2 Source Category Contribution to Facility

- Wide Cancer Risks

– Styrene

Acrylonitrile Production

................................ ................................ ................................ ........... 53

Table 6.1

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

- Response Values

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

Table 6.2

- 1 Summary of Source Category Level Risks for Polystyrene Production

........ 56

Table 6.2

- 2 Source Category Contribution to Facility

- Wide Cancer Risks

– Polystyrene

Production 57

Table 7. 1

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

- Response Values

................................ .................. 58

Table 7.2

- 1 Summary of Source Category Level Risks for Polyethy lene Terephthalate

Production 62

Table 7.2

- 2 Summary of Acute Refined Results for Polyethylene Terephthalate

Production 63

Table 7.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

– Polyethylene Terephthalate Production

................................ ................................ ................................ ......... 64

Table 8.1

- 1 Summary of Emissions from the Methyl Methacrylate

- Butadiene

- Styrene

Production Source Category and Availability of Dose

- Response Values

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

Table 8.2

- 1 Summary of Source Category Level Risks for Methyl Methacrylate

Butadiene

- Styrene Production

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

Table 8.2

- 2 Summary of Acute Refined Results for Methyl Methacrylate

- Butadiene

Styrene Production Facilities

................................ ................................ ................................ ... 68Draft Risk Assessment for 7 Chemica l Sector Source Categories

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4 Table 8.2

- 3 Source Category Contribution to Facil ity

- Wide Cancer Risks

– Methyl Methacrylate

- Butadiene

- Styrene Production

................................ ................................ ........... 6 8

Table 9.1

- 1 Summary of Emissions from the Acrylonitrile

- Butadiene

- Styrene Production Source Category and Availability of Dose

- Response Values

................................ .................. 70

Table 9.2

- 1 Summary of Source Category Level Risks for Acrylonitrile

- Butadiene

Styrene Production

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

Table 9.2

- 2 Summary of Acute Refined Results for Acrylonitrile

- Butadiene

- Styrene

Production 73

Table 9.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

– Acrylonitrile

Butadiene

- Styrene Production

................................ ................................ ................................ . 74

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 long

- term emission

ra tes Appendix 4 Detailed Risk Modeling Results Appendix 5 Technical Support Document for TRIM

- Based Multipathway Screening

Scenario for RTR: Summary of Approach and Evaluation Appendix 6 Acute Impacts Refined Analysis Appendix 7 Dispersion Model Receptor R evisions and Additions

Index of Acronyms

AERMOD American Meteorological Society/EPA Regulatory Model

AEGL Acute exposure guideline level

ASTDR US Agency for Toxic Substances and Disease Registry

CalEPA California Environmental Agency

ERPG Emergency Re sponse 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

NATA National Air Toxics Assessment

NEI National Emissions Inventory

NPRM Notice of Proposed Rulemaking

PB

- HAP Persistent and Bioaccumulative

- HAP

POM Polycyclic organic matterDraft Risk Assessment for 7 Chemica l Sector Source Categories

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5 REL Reference exposure level

RfC Reference concentration

RfD Reference dose

RTR Risk and Technology

TOSHI Target

- organ

- specific hazard index

URE Unit risk estimateDraft Risk Assessment for 7 Chemica l Sector Source Categories

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### 1. Introduction

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

- stage regulatory process for addressing emissions of hazardo us 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 pa per mills, etc.) [ 1 ]. EPA has largely completed the initial Maximum Achievable Control Technology ( MACT ) standards as required under this provision. Under section 112(d)(6), EPA must review each of these technology

- based standards at least every eight

ye ars and revise a standard, as necessary, ―taking into account developments in practices,

processe s and control technologies.‖ In the second stage, EPA is required under section 112(f)(2) to assess the health and environmental risks that remain after imple mentation of the MACT standards. If additional risk reductions are necessary to protect public health with an ample margin of safety or to prevent an adverse environmental effect, EPA must develop standards to address these remaining risks. This second s tage 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 De cember 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 responde d to the key messages from this review in developing our current risk assessment s and we will be continuing our efforts to improve our assessments by incorporating updates based on the SAB recommendations as they are developed and become available . Our re sponses to the key

recommendations of the SAB are outlined in the me mo entitled, ―EPA’s Actions in Response to Key Recommendations from the SAB Review of RTR R isk Assessment Methodologies‖
[ 4 ].

This document contains the methods and the results of baseli ne 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 Manufacturing

, Polyether Polyols Production

, Polymers and Resins IV

-- Styrene Acrylonitri le, Polymers and Resins IV

-- Polystyrene

, Polymers and Resins IV

-- Polyethylene Ter e phthalate

, Polymers and Resins IV

-- M ethyl 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 a nd noncancerDraft Risk Assessment for 7 Chemica l Sector Source Categories

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

non

- inhalation health risks, and adverse e nvironmental effects. Since the screening

assessments indicated low potential for chronic non

- inhalatio n 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 200 5 Nat ional Emissions Inventory (NEI) that was used in th e 2005 National

- scale Air Toxics Assessment (NATA) 1 served as the starting point for th ese assessments

. The 2005 NEI contains information on actual emissions during the entire 2005 base year. Using the process MACT code, 2 we developed a subset of the NEI that contain s facility, process, and emissions data for each facility in the se seven source categories. Next, we performed an engineering review of the information using EPA engineers who were directly involved in the development of the MACT standards fo r 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. Industry trade groups then reviewed the data set to provide input on faci lity names, source classification codes, and MACT codes. Industry also provided revisions to emissions, stack parameters, and location coordinates. Finally, EPA engineers reviewed the suggested industry revisions and performed a comprehensive review of t he location

coordinates. These data underwent an extensive QA/QC procedure, and revisions were made

to the dataset as necessary. The emissions data and modifications made to the NEI data are

discussed in the memo entitled ― Emissions Data Used in Residual Risk Modeling: Pesticide Active Ingredient Manufacturing, Polyether Polyols Production, and Polymers and Resins IV ‖

available in the docket for this action

.



### 2.2. Dispersion modeling for inhalation exposure assessment

Both long

- and short

- term inhalation ex posure concentrations and associated health risk 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 mod eling system. The approach used in applying this modeling system is outlined below, and further details are provided in Appendix 1

. The

HEM 3 performs three main operations: atmospheric dispersion modeling, estimation of individual human exposures and hea lth risks, and estimation of population risks. This section focuses on the dispersion modeling component. The exposure and risk characterization components are discussed in other subsections of Sections 2 and 3.

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

2 Assigning data with MACT codes allows EPA to determine reductions attributabl e to the MACT program. The NEI associates MACT codes corresponding to MACT source categories with stationary major and area source

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

- of

- the

science Gaussian plume dispersion model that is preferred by EPA for modeling point, area, and volume sources of continuous air emissions from facility applications [ 5 ]. Further details

on AERMOD can be found in the AERMOD Users Guide [ 6 ]. The model is used to develop annual average ambient concentrations through the simulation of hour

- by

- hour dispersion from the emission sources into the surrounding atmosphere. Hourly emission rates used for this simulation are ge nerated by evenly dividing the total annual emission rate 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 mo del options for RTR modeling

Modeling Option Selected Parameter for chronic exposure

Type of calculations Hourly Ambient Concentration

Source type Point, area represented as pseudo point source

Receptor orientation Polar (13 rings and 16 radials) Discrete (census block centroids) and user

- supplied receptors

Terrain characterization Actual from USGS 1

- degree DEM data

Building downwash Not Included

Plume deposition/depletion Not Included

Urban source option No

Meteorology 1 year representative NWS from nearest site ( over 200 stations)

In HEM3 , meteorological data are ordinarily selecte d from a list of over 200 National Weather Service (NWS) surface observation stations across the continental United States, Alaska, Hawaii, and Puerto Rico. In most cases the nearest station is selected as representative of the conditions at the subject f acility. Ideally, when considering off

- site meteorological 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 num ber of appropriately formatted model input files derived 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 fac ility and the applicable meteorological station was 40 miles (72 km). Appendix 2 (Meteorological Data Processing Using AERMET for HEM3 ) provides a complete listing of stations andDraft Risk Assessment for 7 Chemica l Sector Source Categories

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9 assumptions along with further details used in processing the data through AERMET. The sensitivity of model results to the selection of the nearest weather station and the use of one year of meteorological data is discussed in ― Risk and Technology Review (RTR) Risk Assessment Methodologies ‖ [ 2 ].

The HEM3 system estimates ambien t concentrations at the geographic centroids of census blocks (using the 2000 Census), and at other receptor locations that can be specified by the user. The model accounts for the effects of multiple facilities when estimating concentration impacts at ea ch 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 re side rather than receptor points at the fenceline of a facility). Chronic ambient concentrations were calculated as the annual average of all estimated short

- term (one

- hour) concentrations at each

block centroid. Possible future residential use of curren tly uninhabited areas was not considered. Census blocks, the finest resolution available in the census data, are typically comprised of approximately 40 people or about ten households. For each facility in these source categories census block locations w ere carefully evaluated for proximity to each

facilit y’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 points 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 facili ty (note that for large facilities, this

100

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

- term emission rates were needed to screen for the potential for hazard via acute exposures, and since the NEI contains only an nual 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 year. 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 bas ed 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 data set
from a nu mber of source s 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 compound s for all facilities in a heavily

industrialized 4

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

an eleven

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

- term emission rates relative to long

- term emission rates‖). Most peak emission events were less than twice the

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

acute r isks.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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10 annual average, the highest was a factor of 74 times the annua l average , and the 99 th
percentile ratio of peak hourly emission rate to the annual hourly emission rate was 9 . Based on these results, we chose a factor of ten for the initial screening

, except for several source categories where a factor of 2 was applie d for certain situations (see source category risk characterization sections) . These factors are intended to cover all possible hourly peaks

associated with routinely

- variable emissions. While there have been some documented

emission excursions above thi s level, our analysis of the data from the Texas Environmental Research Consortium suggests that th ese factor s should cover more than 99% of the short

term peak gaseous or volatile HAP emissions from typical industrial sources

. We have no data relating sp ecifically to peak short

- term emissions of particulate HAP. In the absence of

source category

- specific data, we use this same default approach for particulate emissions as

well. A list of facilities where we used the factor of two instead of ten is provi ded in Appendix 6

.

Census block elevations for HEM3 modeling were determined nationally from the US Geological S urvey 1

- degree digital elevation model (DEM) data files, which have a 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 source, the model uses the average elevation of all sectors within the innermost model ring.

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

, see Appendix 1

.



### 2.3. Estimating chronic human inhalation exposur e

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 n ot 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 microenvironment concentrations and daily activities, modeling short

- term activity would, on average, reduce risk estimates about 25% for particulate H APs; it w ould also reduce risk estimates for gaseous HAPs, but typically by much less. Second, basing exposure estimates on average ambient concentrations at census block centroids may underestimate or overestimate actual exposure concentrations at some

r esidences. Further reducing exposure estimates for the most highly exposed residents by modeling their short

- term behavior could add a systematic low bias to these results.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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11 We did not address long

- term migration or population growth or decrease over 70 y ears, and

instead bas ed the assessment on the assumption that each person’s estimated exposure is constant over the course of their lifetime which is assumed to be 70 years. In assessing cancer risk, we generally estimated three metrics; the maximum indiv idual 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 bi as the estimate of the theoretical MIR nor does it affect the estimate of cancer incidence since the total population number remains the same. It does, however, affect the shape of the distribution of individual risks across the affected population, shift ing it toward higher estimated individual risks at the upper end and reducing the number of people estimated to be at lower risks, thereby increasing the estimated number of people at specific risk levels

.

When screening for potentially significant acut e 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 f ollowed 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 Sciences in its 1993 publication ―Science and Judgment in Risk Assessment‖ and subsequently was adopted in the EPA’s ―Residual Risk Rep ort to Congress‖

in 1999.

The assessment methodology is designed to eliminate from further consideration those

facilities for which we have confidence that no acute adverse health effects of concern will occur. To do so, we use what is called a tiered, iterative approach to the asse ssment. This

means that we begin with a screening assessment, which relies on readily available data and uses conservative assumptions that in combination approximate a potential worst

- case

exposure . The result of this scre ening process is that either the facility being assessed poses

no potential acute health risks (i.e., it ―screens out‖), or that it requires further , more refined

assessment. A refined assessment could u s e industry

- or site

- specific data on the temporal

p attern of emissions, the layout of emission points at the facility, the boundaries of the facility, and /or the local meteorology. In some cases, all of these site

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

- sp ecific data c an be used to determine that acute exposures are not a concern, and significant additional data collection is

not necessary.

Acute health risk screening was 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:Draft Risk Assessment for 7 Chemica l Sector Source Categories

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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 concentrations at each receptor

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

hour.

Worst

- case meteorology (from one year of local meteorology) was assumed to occur at the same time the peak emission rates occur. The recommended EPA local

- scale dispersion model, AERMOD , is used for simulating atmospheric dispersion. A person was assumed to be located downwind at the point of maximum impact during this same 1

- hour period, but no nearer to the source than 100 meters. The maximum impact was compared to multiple short

- term health benchmarks for the chemical being assessed to determine if a possible acute health risk might exist. These benchmarks are described in section 2.6 of this report.

As mentioned above, when we identify potential worst

- case exposures which exceed rel evant
health benchmarks, we refin e our acute screening estimates to the extent possible

. In some cases, this includes the use of a refined emissions multiplier to estimate the peak hourly emission rates from the average rates (rather than the default fact or of 10) . For the source categories in th is document, we conducted a review of the layout of emission points at the facilities with the facility boundaries to determine the maximum off

- site acute impact for the facilities that did not screen out during t he initial model run. Refer to Appendix 6 for the

detailed results for these sites.



### 2.5. Multipathway human health and environmental risk screening

The potential for significant human health risks due to exposures via routes other than inhalation (i.e., multi pathway exposures) was screened by first determining whether any sources emitted any hazardous air pollutants known to be persistent and bioaccumulative in the environment (PB

- HAP) 4 . The PB

- HAP compounds or compound classes are identified

for the screeni ng 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, methoxychlo r, polychlorinated biphenyls, polycyclic organic matter (POM)

, toxaphene, and trifluralin

. There were PB

- HAP emission s identified for three of the source categories addressed in this risk document. F or the polyethylene terephthalate production

source cat egory , we identified emissions of cadmium compounds, polycyclic organic matter (POM), and lead compounds . For the pesticide active ingredient production source category

, we identified emissions of lead compounds and polychlorinated biphenyls (PCBs). F or the

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 environment. In instances where the report is specifically referring to lead, it is spelled out (i.e., the two

- letter chemical symbol for lead is not used in this document).Draft Risk Assessment for 7 Chemica l Sector Source Categories

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13 p olyether polyols production source category , we identified emissions of POM, lead compounds, and hexachlorobenzene

.

These PB

- HAP emissions were evaluated for potential non

- inhalation risks and adverse environmental impacts using our recently

- develope d 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 and scenario inputs developed for EPA’s Human Health Risk Assessment Protocols (HHRAP) for hazardous waste com bustion facilities. 6 In the development of the screening

scenario

, a sensitivity analysis was conducted to ensure that its key design parameters were established such that environmental media concentrations were not underestimated, and to

also minimize th e occurrence of false positives for human health endpoints. See Appendix 5 for a complete discussion of the development and testing of the screening scenario, as well as for the values of facility

- level emission rates developed for screening potentially s ignificant

multi

- pathway impacts. For the purpose of developing emission rates for our multi

- pathway screening, we derived emission levels for each PB

- HAP (other than lead) at which the

maximum human health risk would be 1 in a million for lifetime cancer risk or a hazard quotient of 1.0 for noncancer impacts.

In evaluating the potential multi

- pathway risks from emissions of lead compounds, rather than developing a screening emission rate for them , we compared maximum estimated chronic atmospheric conce ntrations with the current National Ambient Air Quality Standard (NAAQS) for lead. Values below the NAAQS were considered to have a low potential for

multi

- pathway risks.

Additionally, we evaluated the potential for significant ecological exposures to no n PB

- HAP

from exceedances of chronic human health inhalation thresholds in the ambient air near these

facilities. Human health dose

- response threshold values are generally derived from studies conducted on laboratory animals (such as rodents) and develope d with the inclusions of uncertainty factors that could be as high as 3000. As a result, these human threshold values are often significantly lower than the level expected to cause an adverse effect in an exposed

rodent. It should be noted that there is a scarcity of data on the direct atmospheric impact of these HAPs on other receptors, such as plants, birds, and wildlife. Thus, if the maximum inhalation hazard in an ecosystem is below the level of concern for humans, we have generally concluded that ma mmalian receptors should be at no risk of adverse effects due to inhalation exposures from non

- PB

- HAP, and have assurance that other ecological receptors are also not at any significant risk from direct atmospheric impact. In some isolated cases

where we have data indicating potential adverse impacts on plants, birds, or other wildlife due to the direct atmospheric impacts of specific HAP, we note that as an uncertainty and, where possible, refine our analysis by comparing our modeled impacts to available threshold values

from the scientific literature.

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 Ha zardous Waste Combustion Facilities; http://www.epa.gov/epaoswer/hazwaste/combust/riskvol.htm#volume1Draft Risk Assessment for 7 Chemica l Sector Source Categories

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14 

### 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 repo rted in the emissions inventories for the source categories in this document were based on the EPA Office of Air Quality Planning and Standards’ existing recommendations for HAPs [ 9 ], also used for NATA [ 10 ]. This

information has been obtained from variou s sources and prioritized according to (1) conceptual consistency with EPA risk assessment guidelines and (2) level of peer review received. The prioritization process was aimed at incorporating into our assessments the best available science with respect to dose

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

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

- response assessments for chronic exposure for many of the pollutants in this s tudy. 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 inhalation ex posure 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 ―a n estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral ex posure 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 continuous lifet ime exposure to an agent at a concentration of 1 μg/m 3 in air. ‖ The

SF is ―a n 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 proportio n (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

assess ment 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

sc heduling of current individual IRIS assessments and updates ( http://cfpub.epa.gov/ncea/iristrac/index.cfm ). EPA’s science policy approach , under the current carcinogen guidelines, is to use linear low

- dose extrapolation as a default option for carcinogens for which the mode of action (MOA) has not been identified. We expect

future EPA dose

- response assessments to identify nonlinear MOAs where appropriate, and we will use those analyses (once they are peer reviewed) in our risk assessments. AtDraft Risk Assessment for 7 Chemica l Sector Source Categories

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15 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, which is part of the US Department of Health and Human Services, develops and publishes Minimum Risk Levels (MRLs) [ 12 ] for inhalation and oral exposure to many toxic substances. As

stated on the ATSDR web site: ― Following discussions with scientists with in the 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 endpoints .‖ The MRL is defined as ―an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse effects (other than cancer) over a specified duration of exposure.‖ ATSDR describes MRLs as substance

- specif ic estimates to be used by health assessors to select environmental contaminants for further evaluation. Exposures above an MRL do not necessarily represent a threat, and MRLs are therefore not intended for use as predictors of adverse health effects or f or setting 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 othe r than cancer. The process for developing these assessments is similar to that used by EPA to develop IRIS values and incorporates significant external scientific peer review. As cited in the CalEPA Technical Support Document for developing their chronic assessments 7 : ―The guidelines for developing chronic inhalation exposure levels incorporate many recommendations of the U.S. EPA [ 13 ] and NAS [ 14 ].‖ The non

- cancer information includes available inhalation health risk guidance values expressed as chronic i nhalation reference 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 professional judgment, as follows:

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

conservative dose

- response value of the chemical category i s used as a surrogate for other compounds in the group f or which dose

- response values are not available. This i s done in order to examine, unde r conservative assumptions, whether these HAPs that lack dose

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

out from further assessment.

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

- Technical Support Document

for the Determination of Non

- cancer Chronic Reference Ex posure 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 )Draft Risk Assessment for 7 Chemica l Sector Source Categories

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16 2) Where possible

, for emissions of unspecified mixtures of HAP categories su ch as met al 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 To xicology (CIIT)

cancer dose

- response value for formaldehyde (5.5 x 10 - 9 per μg/m 3 ) was based on better

science than the IRIS cancer dose

- response value (1.3 x 10 - 5 per μg/m 3 ), and we switched from using the 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 revising the formaldehyde IRIS assessment and the National Ac ademy of Sciences (NAS) completed its review of the EPA’s draft assessment in April of 2011. 8 EPA will follow the NAS Report recommendations and will present results obtained by implementing the biologically

- based dose

- response ( BBDR ) model for formaldeh yde. 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, appropriate 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 science evolves.

4) A substantial proportion of POM emissi ons reported to EPA’s N ati onal E mission

I nventory (NEI) a re not speciated into individua l compounds. As a result, it i s necessary to apply the same simplifying assumptions to assessment s that are used in NATA. [ 17 ] The NATA approach partitions POM into eig ht different non

- overlapping ―groups‖ that

a re 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 nickel compounds, to provide a health

- protective es timate 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 subsulfide was considered a major factor for estimatin g 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 derived 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 (NTP) in their 12 th Report of the Carcinogens (ROC) 9 , International Agency for Research

8 http://www.nap.edu/catalog. php?record_id=13142

9 National Toxicology Program (NTP), 2011. Report on carcinogens. 12 th ed. Research Triangle Park, NC: US Department of Health and Human Services (DHHS), Public Health Service. Available online at http://ntp.niehs.nih.gov/ntp/roc/ twelfth/roc12.pdfDraft Risk Assessment for 7 Chemica l Sector Source Categories

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17 on Cancer (IARC) 10 , and other international agencies) 11 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 epide miological 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 consideration 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 sulfides and oxides encountered

in the nick el refining industries cause cancer in humans (these studies are summarized in a review by Grimsrud et al., 2010 12 ). The major scientific bodies mentioned above have also recognized that there are differences in toxicity and/or carcinogenic potential acros s 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 13 derived for exposure to mixtures of nickel compounds, as a group, that ar e 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 plausible range of cancer potency value s for different mixtures of nickel compounds.
6) 

### For 3 carcinogenic substances, ( captan, i sophorone and p ropylene dichloride ) that

lack inhalation assessments from the sources evaluated in this document , oral carcinogenic potency estimates were converted to i nhalation UREs. The conversion from oral risk (per mg/kg/d oral intake) to inhalation risk ( per μ g/m 3


### inhaled) was based on EPA’s standard assumptions of a 70

- kg body mass and 20

m 3 

### /d inhalation rate, as follows:

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

### )

10 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 Cancer, World Health Organization Vol. 49:256.

11 World Health Organization (WHO, 1991) and the Europea n Union’s Scientific Committee o n Health and Environmental Risks (SCHER, 2006)

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

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

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

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

13 Two UREs (other than the current IRIS values) have been derived for nickel compounds as a group : one developed by the California Department of H ealth 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 ).Draft Risk Assessment for 7 Chemica l Sector Source Categories

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18



### CPS = Carcinogenic potency slope for ingestion (risk per mg oral intake per kg body mass per day)

EPA understands that conversion of oral dose

- response information to inhalation

exposure may add significant uncertainty to the resulting risk estimates

. However, the alternative to this would have been to omit these substances from quantitative

inhalation risk estimates altogether, thereby making a de facto assumption of zero carcinogenic potency. For the purposes of the residual risk assessment, EPA prefers to use the approach described above to screen these carcinogens for their potential contributions to risk. If a substance is determined to be a potentially important contributor to risk, it will be prioritized for fur ther dose

- response development through EPA’s IRIS process

.

The emissions inventory for the source categor ies in this risk document includes emissions of

HAP with available chronic quantitative inhalation dose

- response values. These HAP, their

dose

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

- 1 (a) and ( b ).

Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcinogens

URE (unit risk estimate for cancer) 14 = cancer risk per μg/m 3 of average lifetime exposure. Sources: 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 15 URE 7

(1/μg/m 3 ) Source

1,1,2

- Trichloroethane 79005 0.000016 IRIS
1,3

- Butadiene 106990 0.00003 IRIS
1,3

- Dichloropropene 542756 0.000004 IRIS
1,4

- Dichlorobenz ene 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 0.0000 68 IRIS

14 The URE is the upper

- bound excess cancer risk e stimated to result from continuous lifetime exposure to an agent at a concentration of 1 μg/m 3 in air. URE’s are considered upper bound estimates meaning they represent a plausible upper limit to the true value.

15 Chemical Abstract Services identificatio n 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.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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19 Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcinogens

URE (unit risk estimate for cancer) 14 = cancer risk per μg/m 3 of average lifetime exposure. Sources: 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 15 URE 7

(1/μg/m 3 ) Source

Aniline 62533 0.0000016 CAL
Arsenic compounds 7440382 0.0043 IRIS

Benzene 16 71432 0.0000078 IRIS Benzyl c hloride 100447 0.0 00049 CAL Beryllium compounds 7440417 0.0024 IRIS Bis(2

- ethylhexyl)phthalate 117817 0.0000024 CAL

Bromoform 75252 0.000 0011 IRIS Cadmium compounds 7440439 0.0018 IRIS Captan 133062 0.000001 Conv. Oral

Carbon t etrachloride 56235 0.000006 IRIS Chromium (VI) compounds 18540299 0.012 IRIS Dichloroethyl e ther 111444 0.00033 IRIS Epichlorohydrin (1

- Chloro

- 2,3

- e poxypropane) 106898 0.0000012 IRIS Ethyl b enzene 100414 0.0000025 CAL Ethylene d ichloride 107062 0.000026 IRIS Ethylene o xide 75218 0.000088 CAL Formaldehyde 17 50000 0.000013 IRIS

Hexachlorobenzene 118741 0.00046 IRIS

Hexachloroethane 67721 0.000004 IRIS Hydrazi ne 302012 0.0049 IRIS Isophorone 18 7859 1 0.00000027 Conv. Oral Methyl tert

- butyl e ther 1634044 0.00000026 CAL Methylene c hloride 75092 0.00000047 IRIS Naphthalene 91203 0.000034 CAL Nickel compounds 7440020 0.00048 EPA OAQPS

o

- Toluidine 95534 0.000051 CAL
Polychlorinated b iphenyls 1336363 0.0001 IRIS
Polycyclic Organic Matter 19 (POM)

16 The EPA IRIS assessment for benzene provides a range of plausible UREs. This assessment used the highest value in that range, 7.8E

- 06 per ug/m 3 . The low end of the range is 2.2E

- 06 per ug/m 3

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

instances.

18 No inhalation unit risk estima tes were available for this compound. T herefore we c onverted from an IRIS oral potency slope of 0.00095 per mg/kg/d. UREs that are converted from the oral route to the inhalation route of exposure are considered highly uncertain, and are only used in case s where no other URE is available.

19 Assigned the URE associated with a mixture of POM compounds having a similar potency. Details of this method, also used in the National Air Toxics Assessments, are available at http://www.epa.gov/nata2002/methods.html#pomDraft Risk Assessment for 7 Chemica l Sector Source Categories

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20 Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcinogens

URE (unit risk estimate for cancer) 14 = cancer risk per μg/m 3 of average lifetime exposure. Sources: 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 15 URE 7

(1/μg/m 3 ) Source

2

- Methylnaphthalene 91576 0.000088 CAL

Fluoranthene 206440 0.000088 CAL

Fluorene 86737 0.000088 CAL

Phenanthrene 85018 0.000088 CAL Pyren e 129000 0.000088 CAL Propylene d ichloride 20 78875 0.000019 Conv. Oral
Propylene oxide 75569 0.0000037 IRIS

Tetrachloroeth ylene 127184 0.0000059 CAL Trichloroethylene 79016 0.000002 CAL Vinyl c hloride 75014 0.0000088 IRIS

Table 2.6

- 1 (b) Dose

- Resp onse 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

sensitiv e subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency

for Toxi c 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 21

1,1,1

- Trichloroethane (methyl chloroform) 71556 5 IRIS

- M
1,2

- Epoxybutane 10688 7 0.02 IRIS

- M
1,3

- Butadiene 106990 0.002 IRIS

- M
1,3

- Dichloropropene 54275 6 0.02 IRIS

- H
1,4

- Dichlorobenzene 106467 0.8 IRIS

- M
1,4

- Dioxane 12391 1 3.6 ATSDR

20 No inhalation unit risk estimates were available for this compound. T herefore we c onverted from a oral potency slope of 0.068 per mg/kg/d. UREs that are converted from the oral route to the inhalation route of exposure are considered highly uncertain, and are only used in cases where no other URE is available.

21 The descriptors L (low), M (medium), and H (high) have been added for IRIS RfC values to indicate the

overall level of confid ence in the RfC value, as reported in IRIS.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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21 Table 2.6

- 1 (b) Dose

- Resp onse 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

sensitiv e subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency

for Toxi c 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 21

2,4

- Toluene diisocyanate 58484 9 0.00007 IRIS

- M
4,4'

- Methylenedianiline 10177 9 0. 02 CAL Acetaldehyde 75070 0.009 IRIS

- L

Acrolein 107028 0.00002 IRIS

- M Acrylic a cid 79107 0.001 IRIS

- M Acrylonitrile 10713 1 0.002 IRIS

- M

Aniline 6253 3 0.001 IRIS

- L Antimony c ompounds 7440360 0.0002 IRIS

- L

Arsenic c ompounds 7440382 0.00001 5 CAL

Benzene 71432 0.03 IRIS

- M Beryllium c ompounds 7440417 0.00002 IRIS

- M Bis(2

- ethylhexyl)phthalate 11781 7 0.01 CAL

Cadmium c ompounds 7440439 0.00001 ATSDR

Carb on t etrachloride 56235 0.1 IRIS

- M

Chlorine 7782505 0.00015 ATSDR

Chlorobenzene 10 8907 1 CAL

Chloroform 67663 0.098 ATSDR Chromium (VI) compounds 18540299 0.0001 IRIS

- M

Cresol s (mixed) 1319773 0.6 CAL

Cumene 98828 0.4 IRIS

- M
Cyanide & Cyanide Compounds Cyanide compounds 22 57125 0.003 IRIS

- L Hydrogen cyanide 74908 0.003 IRIS

- L

Diethanolamine 111422 0.003 CAL Epichlorohydrin (1

- Chloro

- 2,3

-

e poxypropane ) 10689 8 0.001 IRIS

- M Ethyl b enzene 100414 1 IRIS

- L Ethyl chloride 7500 3 10 IRIS

- M Ethylene d ichloride 107062 2.4 ATSDR Ethylene g lycol 107211 0.4 C AL Ethylene o xide 75218 0.03 CAL Formaldehyde 50000 0.0098 ATSDR

22 The value for hydrogen cyanide was used as a surrogate for all cyanide compounds without an RfC.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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22 Table 2.6

- 1 (b) Dose

- Resp onse 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

sensitiv e subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency

for Toxi c 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 21

Glycol Ethers 23

2

- (Hexyloxy)e thanol 11225 4 0.02 IRIS

- M

2

- Butoxyethyl a cetate 11207 2 0.02 IRIS

- M Butyl Carbitol a cetate 12417 4 0.02 IRIS

- M Diethylene glycol monobutyl

ether 11234 5 0.02 HEAST Diethylene glycol monoethyl

ether 11190 0 0.02 IRIS

- M Ethoxytriglycol 11250 5 0.02 IRIS

- M Ethylene glycol ethyl ether 11080 5 0.2 IRIS

- M Ethylene glycol methyl ether 10986 4 0.02 IRIS

- M

Gl ycol e thers 171 0.02 IRIS

- M Methoxytriglycol 11235 6 0.02 IRIS

- M Propyl c ellosolve 280730 9 0.02 IRIS

- M Triglycol monobutyl ether 14322 6 0.02 IRIS

- M

Hexachlorobenzene 11874 1 0.003 CAL

Hexachloroethane 67721 0.08 CAL

Hexane 11054 3 0.7 IRIS

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

- L Hydrof luori c acid (hydrogen fluoride) 766439 3 0.014 CAL Isophorone 7859 1 2 CAL Lead compounds 743992 1 0.00015 EPA OAQPS Maleic anhydride 10831 6 0.00 07 CAL Manganese c ompounds 7439965 0.00005 IRIS

- M

Methanol 67561 4 CAL Methyl b romide 74839 0.005 IRIS

- H Methyl c hloride 74873 0.09 IRIS

- M

Met hyl isobutyl k etone 108101 3 IRIS

- L/M Methyl isocyanate 62483 9 0.001 CAL Methyl m ethacrylate 80626 0.7 IRIS

- M/H Methyl tert

- butyl e ther 1634044 3 IRIS

- M

23 The RfC value for ethylene glycol methyl ether was used as a surrogate for all glycol ethers without an RfC.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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23 Table 2.6

- 1 (b) Dose

- Resp onse 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

sensitiv e subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency

for Toxi c 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 21

Methylene c hloride 75092 1 ATSDR Naphthalene 91203 0.003 IRIS

- M

Nickel c ompounds 7440020 0.00009 ATSDR

Phenol 108952 0.2 CAL Phosgene 7544 5 0.0003 IRIS

- M Phthalic anhydride 8544 9 0.02 CAL Propionaldehyde 123386 0.008 IRIS

– L/M Propylene d ichloride 78875 0.004 IRIS

- M Propylene oxide 7556 9 0.03 IRIS

- M

Selenium c ompounds 7782492 0.02 CAL Styrene 100425 1 IRIS

- M Tetrachloroethylene 12718 4 0.27 ATSDR

Titanium tetrachloride 755045 0 0.0001 ATSDR

Toluene 108883 5 IRIS

- H Trichloroethylene 79016 0.6 CAL Triethylamine 12144 8 0.007 IRIS

- L Vinyl a cetate 108054 0.2 IRIS

- H Vinyl c hloride 75014 0.1 IRIS

- M Xylenes (mixed) 1330207 0.1 IRIS

- M

m

- Xylene 1 8 108383 0.1 IRIS

- M

o

- Xylene 24 95476 0.1 IRIS

- M

p

- Xylene 1 8 106423 0.1 IRIS

- M

2.6.2. Sources of acute dose

- response information

Hazard identification and dose

- response assessment information for preliminary acute
inhalation exposure assessments are based on the exi sting recommendations of OAQPS for HAPs [ 18 ]

. Depending on availability, the results from screening acute assessments are compared to both ―no effects‖ reference levels for the general public, such as the California Reference Exposure Levels (RELs), as wel l as emergency response levels, such as Acute Exposure Guideline Levels (AEGLs) and Emergency Response Planning Guidelines (ERPGs), with the recognition that the ultimate interpretation of any potential risks associated

24 The RfC for mixed xylene was used as a surrogate.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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24 with an estimated exceedance of a pa rticular reference level depends on the definition of that level and any limitations expressed therein. Comparisons among different available inhalation health effect reference values (both acute and chronic) for selected HAPs can be

found in a n EPA docum ent [ 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 Leve ls (RELs).

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

― t he concentration level at or below which no adverse health effects are anticipated for a specifi ed 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 margin s of safety. Since margins of safety are incorporated to address data gaps and uncertainties, exceeding the REL does not automatically indicate an adverse health impact. ‖ Acute RELs are developed for 1

- hour (and 8

- hour) exposures. The values incorporate uncertainty factors similar to those used in deriving EPA’s Inhalation Reference Concentrations (RfCs) for chronic exposures (and, in fact, California also has developed chronic RELs).

Acute Exposure Guideline Levels (AEGLs ). AEGLs are developed by the N ational Advisory

Committee (NAC) on Acute Exposure Guideline Levels (NAC/AEGL) f or Hazardous

Substances , and then reviewed and published by the National Research Council A s described

in the Committee’s ―Standing Operating Procedures (SOP) ‖ ( http://www.epa.gov/opptintr/aegl/pubs/sop.pdf ), AEGLs ―represent threshold exposure limits for the general public and are applicable to emergency exposures ranging from 10 min to 8 h.‖ Their intended applicati on 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

docume nt 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 emerg ency response, planning, and prevention programs. More specifically, the AEGL values will be used for conducting various risk assessments to aid in the development of emergency preparedness and prevention plans, as well as real

- time emergency response act ions, 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 ge neral population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic nonsensory effects.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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25 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 can produce mild and progressively increasing but transient and nondisabling odor, taste, and sensory irritation or certain asymptomatic, nonsensory effects

. With increasing airborne concentrations above each AEGL, there is a progressive increase in the likelihood of occurrence and the severity of effects described for each corresponding AEGL. Although the AEGL values represent threshold levels for the gene ral 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 des cribed at concentration s below the corresponding AEGL.‖

Emergency Response Planning Guidelines (ERPGs). The American Industrial Hygiene Association (AIHA) has developed Emergency Response Planning Guidelines (ERPGs) [ 21 ] for acute exposures at three diffe rent levels of severity. These guidelines represent concentrations for exposure of the general population (but not particularly sensitive persons) for up to 1 hour associated with effects expected to be mild or transient (ERPG

- 1),

irreversible or serious (ERPG

- 2), and potentially life

- threatening (ERPG

- 3).

ERPG values ( http://www.aiha.org/1documents/Committees/ERP

- erpglevels.pdf ) are described in their supporting documentation as follows: ― Emergency Response Planning Guidelines (ERPGs) were developed for emergency planning and are intended as health based guideline concentrations for single exposures to chemicals. These guidelines (i.e., the ERPG

Documents and ERPG values) are int ended for use as planning tools for assessing the adequacy of accident prevention and emergency response plans, including transportation

emergency planning and for developing comm unity emergency response plans. The emphasis

is on ERPGs as planning values: When an actual chemical emergency occurs there is seldom

time to measure airborne concentrations and then to take action. ‖

ERPG

- 1 and ERPG

- 2 values are defined by AIHA as follows:

― ERPG

- 1 is the maximum airborne concentration below which it is believ ed that nearly all individuals could be exposed for up to 1 hour without experiencing other than mild

transient adverse health effects or without perceiving a clearly defined, objectionable

odor. ‖

― ERPG

- 2 is the maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing or developingDraft Risk Assessment for 7 Chemica l Sector Source Categories

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26 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 Tab le 2.6

- 2.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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27

Table 2.6

- 2 Dose

- Response Values for Acute Exposure

Pollutant CAS

Number AEGL

- 1

(1

- hr) (mg/m 3 ) AEGL

- 2

(1

- hr) (mg/m 3 ) ERPG

- 1

(1

- hr) (mg/m 3 ) ERPG

- 2

(1

- hr) (mg/m 3 ) REL
1,1,1

- Trichloroethane (methyl chloroform) 7155 6 1300 3300 1900 3800 68

1 ,2

- Epoxybutane 10688 7 210 410

1,3

- Butadiene 10699 0 1500 12000 22 440
1,4

- Dioxane 12391 1 61 1200 3

2,4

- Toluene diisocyanate 58484 9 0.14 0.59 0.071 1.1 Acetaldehyde 75070 81 490 18 360 0.47

Acetonitrile 7505 8 22 540

Acrolein 107028 0.069 0.23 0.11 0.34 0.0025 Acrylic a cid 79107 4.4 140 3 150 6 Acrylonitrile 10713 1 10 130 22 77

Aniline 6253 3 30 46
Arsenic compounds 744038 2 0.0002

Benzene 71432 170 2600 160 480 1.3
Benzyl chloride 10044 7 5.2 52 0.24
Beryllium c ompounds 7440417 0.025
Biphenyl 92524 61

Carbon t etrachloride 56235 280 1200 130 630 1.9

Chlorine 7782505 1.5 5.8 2.9 8.7 0.21

Chloroacetic a cid 79118 26

Chlorobenzene 108907 46 690

Chloroform 67663 310 240 0.15
Chloromethyl methyl ether 10730 2 1.6 3.3

Cumene 98828 250 1500 Hydrogen cyanide 7490 8 2.2 7.8 11 0.34
Dimethyl formamide 6812 2 270 6 300
Dimethyl sulfate 7778 1 0.12 0.62 Epichlorohydrin ( 1

- Chloro

- 2,3

-

e poxypropane) 106898 22 91 19 76 1.3
Ethyl a crylate 140885 34 150 0.041 120
Ethyl b enzene 100414 140 4800
Ethylene d ichloride 107062 200 810
Ethylene o xide 75218 81 90 Formaldehyde 50000 1.1 17 1.2 12 0.055
Glycol Ethers 25

2

- (Hexyloxy)e thanol 112 25 4 0.093

2

- Butoxyethyl a cetate 11207 2 0.093

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

an acute REL.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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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 a cetate 12417 4 0.093
Ethoxytriglycol 11250 5 0.093
Ethylene glycol ethyl ether 11080 5 0.37
Ethylene glycol methyl ether 10986 4 0.093
Glycol ethers 171 0.093
Methoxytriglycol 11235 6 0. 093
Propyl c ellosolve 280730 9 0.093
Triglycol monobutyl ether 14322 6 0.093

Hexane 110543 12000
Hydrazine 302012 0.13 17 0.65 6.5 Hydrochloric a cid 7647010 2.7 33 4.5 30 2.1 Hydrogen f

luoride 7664393 0.82 20 1.6 16 0.24

Maleic anhydride 10831 6 0.8 8

Methanol 67561 690 2700 260 1300 28
Methyl b romide 74839 820 190 3.9
Methyl c hloride 74873 1900 830
Methyl hydrazine 6034 4 3.2
Methyl isocyanate 62483 9 0.16 0.058 0.6
Methyl m ethacrylate 80626 70 490
Methyl te rt

- butyl e ther 1634044 180 2100 Methylene c hloride 75092 690 1900 1000 2600 14

Nickel c ompounds 7440020 0.006

Phenol 108952 58 89 38 190 5.8
Phosgene 7544 5 1.2 2 0.004
Propionaldehyde 123386 110 620 Propylene oxide 7556 9 170 690 120 1100 3.1 Styrene 100425 85 550 210 1100 21

Tetrachloroeth ylene 127184 240 1600 680 1400 20

Titanium tetrachloride 755045 0 0.54 7.8 5 20

Toluene 108883 750 4500 190 1100 37
Trichloroethylene 79016 700 2400 540 2700
Triethylamine 12144 8 2.8
Vinyl a ce tate 108054 24 630 18 260 Vinyl c hloride 75014 640 3100 1300 13000 180 Xylenes (mixed) 1330207 560 4000 22

m

- Xylene 26 108383 22

o

- Xylene 20 95476 22

p

- Xylene 20 106423 22

26 The REL for mixed xylenes was used as a surrogate.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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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 general, 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. F urther, the EPA Administrator’s March

1995 Policy for Risk Characterization [ 22 ] specifies that a risk characterization ―be prepared in a manner that is clear, transparent, reasonable, and consistent with other risk characterizations of similar scope prepar ed 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 September 2007 Mem orandum on Updated Principles for Risk Analysis 27 , and are incorporated in these assessments.

Estimates of health risk are presented in the context of uncertainties and limitations in the data and methodology. Through our tiered, iterative analytical appr oach, 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 cancer risks and n oncancer 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 H AP included in an assessment that has a potency estimate available,

individu al and population cancer risks we re calculated by multiplying the corresponding lifetime average exposure estimate by the appropriate URE. This calculated cancer risk is

defined a s the upper

- bound probability of developing cancer over a 70

- y r period (i.e., the assumed human lifespan) at that exposure. Because UREs for most HAPs are upper

- bound estimates, actual risks at a given exposure level may be lower than estimated , and could be

zero.

For EPA’s list of carcinogenic HAPs that act 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 adjusting the URE b y 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

27 Memorandum f

or t he Heads o f Ex ecutive Departments a nd 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 D eputy Director for Science, Office of Science and Technology Policy ( http://www.whitehouse.gov/omb/memoranda/fy2007/m07

- 24.pdf )Draft Risk Assessment for 7 Chemica l Sector Source Categories

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30 estimated life time risks for these pollutants 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 equivalence, based on evidence that carcinogenic POM have the same mutagenic mechanism

of action as does benzo[a]pyrene. For this reason

, EPA implem entation policy [ 27 ] recommends applyi ng the Supplemental Guidance to all carcinogenic PAHs for which risk estimates are based on relative pote ncy. Accordingly, we applied the Supplemental Guidance to all unspeciated POM mixtures.

Increased cancer incidence for the entire receptor population within the area of analysis wa s estimated by multiplying the estimated lifetime cancer risk for each cen sus block by the number of people residing in that block, then summing the results for the entire modeled

domain. This lifetime population incidence estimate wa s divided by 70 years to obtain an estimate of the number of cancer cases per year.

In the cas e 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 than use of the equally plausible low end value. If the estimated benzene

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

results.

Unlike linear dose

- response assessments for cancer, noncance r 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 divi ded 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 impa ct 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 ge nerally 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

- ter m threshold value to develop an array of HQ values relative to the various acute endpoints and thresholds. In general, when none of these HQ values are greater than one, there is no potential for acute risk. In those cases where HQ values above one are s een, additional information is used to determine if there is a potential for significant acute risks.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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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 aggre gate health risks associated with all the exposures from a particular source category combined.

To combine risks across multiple carcinogens, our assessments use the mixtures guidelines’
[ 28

, 29 ] default assumption of additivity of effects, and combine risks by summing them using the independence formula in the mixtures guidelines.

In assessing noncancer hazard from chronic exposures, in cases where different pollutants cause adverse health effects via completely different modes of action, it may be inapprop riate 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 th at act by similar toxic modes of action, or (where this information is absent) that affect the same target organ. This process creates, for each target organ, a target

- organ

- specific hazard index (TOSHI), defined as the sum of hazard quotients for individ ual HAP that affect the same organ or organ system. A ll TOSHI calculations presented here were based exclusively on effects occurring

at the ― critical dose‖ (i.e., the lowest dose that produces adverse health effects). Although HQs associated with some p ollutants have been aggregated into more than one TOSHI, this has been done only in cases where the critical dose affects more than one target organ

. Because impacts on organs or systems that occur above the critical dose have not been

included in the TOS HI calculations, some TOSHIs may have been underestimated. As with the HQ, the TOSHI should not be interpreted as a probability of adverse effects, or as strict delineation of ―safe‖ and ―unsafe‖ levels. Rather, the TOSHI is another measure of the

potent ial for adverse health outcomes associated with pollutant exposure, and needs to be interpreted carefully by health scientists and risk managers.

Because of the conservative nature of the acute inhalation screening and the variable nature of

emissions and potential exposures, acute impacts were screened on an individual pollutant basis, not using the TOSHI approach.

2.7.3. Facility

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

- wide‖ risks using

2005 NEI data and modeling as described in Section 2.2. For the facilities in these source categories, we estimated the maximum inhalation cancer and chronic noncancer risks associated with all HAP emissions sources at the facility, including emissions sources that are

not part of the source categories but are located within a contiguous area and are under common control. We analyzed risks due to the inhalation of HAP for the populations residing within 50 kilometers of each facility. The results of these facility

- wide as sessments are summarized below in the Risk Characterization sections of this document. The complete results of the facility

- wide assessments are provided in Appendix 4

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32 2.7.4. MACT

- Allowable Risks

The emissions data in the data sets for these seven source cat egories are estimates 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 memo randum 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 doc ket for this action. 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 Emis sions 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 Ingredie nt Manufacturing

3.1 Source Category Description and Results

The pesticide active ingredient (PAI) production source category consists of major source facilities that manufacture active ingredients in insecticides, herbicides, fungicides, an d related products. The HAP emission sources at PAI production facilities include storage vessels, process vents, equipment leaks, wastewater systems, heat exchange systems, and bag dumps and product dryers. The primary HAP emitted by these facilities include toluene,

meth anol, methylene chloride, and 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 NPRM.

We currently estimate that there are 17 pesticide active ingredient production facilities operating in the U.S. The data set contains all 17 facilities identified with a pesticide active ingredient production MACT cod e in the 2005 NEI. The 2005 NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and emission locations. All 17 of these facilities are identified as major sources in the NEI.

The emissions for the pesticide active ingredient production source category data set (of 17 facilities) are summarized in Table 3.1

- 1 . The total HAP emissions for the source category are approximately 350 tons per year. Based on these data, the HAP emitted in the la rgest quantities across these 17 facilities are: toluene, methanol, methylene chloride, hydrochloric acid, methyl isobutyl ketone, ethylene glycol ethyl ether (a.k.a. cellosolve solvent), hexane, chlorine, formaldehyde, tetrachloroethylene, xylenes (mixed ), triethylamine, trichloroethylene, and ethylene glycol. These 1 4 HAP account for 9 0 percent of the total emissions by mass. Persistent and bioaccumulative HAP (PB

- HA P) 28 in the data set for the

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

EPA

- 453K

- 04

- 001A, a s 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

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33 pesticide active ingredient production source category inclu de lead compounds

, hexachlorobenzene, and polychlorinated biphenyls (PCBs). 29

Table 3.1

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

- Response Values

HAP a Emissions (tpy) Number of

Facilities Reporting

HA P ( 1 7

facilities in data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

- HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer?

Toluene 79 7

Methanol 58 12
Methylene chloride 40 5
Hydrochloric Acid 3 3 10
Methyl Isobutyl Ketone 21 3
Glycol Ethers Ethylene glycol ethyl

ether (Cellosolve) 17 1 Ethylene glycol methyl

ether 0.5 1
Glycol Ethe rs 0.01 1

Hexane 16 5

Chlorine 1 1 7
Formaldehyde 10 4
Tetrachloroethylene 6 5 Xylenes (Mixture of o, m, and p Isomers) 6 7
Triethylamine 5 5
Trichloroethylene 5 2
Ethylene Glycol 4 5
Ethylene dichloride 3 3

Phenol 3 3

Chloroform 3 6
Naphthalene 3 4

Chlorobenzene 2 4

m

- Xylene 2 1

Carbon tetrachloride 2 5

o

- Xylene 2 1
Ethyl Benzene 2 4

Benzene 2 6
Ethyl chlor ide 1 4
Phosgene 2 4 0.8 4

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

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34 Table 3.1

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

- Response Values

HAP a Emissions (tpy) Number of

Facilities Reporting

HA P ( 1 7

facilities in data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

- HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer?
Methyl bromide 0.8 2

1,4

- dioxane 0.8 1
N,N’

- dimethylaniline 0.8 1

1,3

- butadiene 0.7 2
Cyanide Compounds
Hydrogen Cyanide 0.6 2
Cyanide & Compounds 0.3 2

Acetonitrile 0.5 4
Methyl Chloride 0.5 3
Captan 0.5 1
Carbaryl 0.4 1

Aniline 0.4 1
Acrylonitrile 0.2 2
Methyl isocyanate 0.2 2
Biphenyl 0.2 2
Isophorone 0.1 1
Dimethyl formamide 0.1 2
Acetaldehyde 0 .1 2

1,1,1

- Trichloroethane 0.08 2
Benzyl chloride 0.07 2

Lead & Compounds 0.04 1 c

Cumene 0.04 3 Arsenic & Compounds (Inorganic Including Arsine) 0.04 1 30

Nickel & Compounds 0.04 1
Propionaldehyde 0.04 1

Acrolein 0.03 1

Titanium tetrachloride 0.02 1
Methyl hydrazine 0.02 1
Vinyl Chloride 0.02 1
Hydrazine 0.009 1
Propoxur 0.009 1

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

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35 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

HA P ( 1 7

facilities in data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

- HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer?

Hexachlorobenzene 2 4 0.006 2

1,3

- Dichloropropene 0.006 1

Maleic a nhydride 0.00 5 1

Bromoform 0.004 1
Methyl tert

- butyl ether 0.004 1

Hexachloroethane 0.003 2
Styrene 0.002 1
Beryllium & Compounds 0.002 1
Methyl methacrylate 0.002 1
Hydrogen Fluoride 0.002 1

Vin yl acetate 0.0008 1
Polychlorinated Biphenyls 0.00004 1

a Notes for how HAP were speciated for risk assessment: For most metals, emissions reported as the elemental metal are combined with metal compound emissions (e.g.,

―cadmium‖ emissions modeled as ―cadmium & compounds‖). In the absence of speciation information, we assume the reported mass is 100 percent metal. For emissions reported generically as ―Glycol Ethers‖ or specific glycol ethers not found on EPA’s Technology

Transfer network f

or air toxics (see footnote b), emissions will be treated as ethylene glycol methyl ether.

b Specific dose

- response values for each chemical are identified on EPA’s Technology Transfer Network website for air

toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html

.

c There is no reference concentration for lead. In considering noncancer hazards for lead in this assessment, we compared maximum annual ambient exposure estimates to the Nati onal 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 (hea lth

- based) standard is a maximum or not

- to

- be

- exceeded, rolling

three

- month average, measured as total suspended particles (TSP). The secondary (welfare

- based) standard is identical to the primary standard.



### 3.2 Risk Characterization

This section presents the results of the risk assessment for the pesticide active ingredient production source category. The basic chronic inhalation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients, as well as the results of our preliminary screen for 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 t he maximum allowed emissions under the current MACT standards. A detailed summary of the facility

- specific risk assessment results is available in Appendix 4

.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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36 Table s 3 .2

- 1 and 3.2

- 2 summarize the chronic and acute inhalation risk results for this sou rce category. The results for the p esticide a ctive i ngredient m anufacturing source category

indicate that maximum lifetime individual ca ncer risks could be as high as 7 in a million. The major contributor s to this r isk are naphthalene and nickel compound s

. 31 Approximately 11,000 people (this does not reflect the updated emissions information received after the risk modeling was done) were estimated to have cancer risks above 1 in a million as a result of the

emissions from 6 facilities . The maximum chron ic non

- cancer target organ specific hazard index ( TOSHI ) value for the sou rce category could be up to 0.7 associated with emissions of

chlorine , indicating no significant potential for chronic noncancer impacts.

Worst

- case a cute HQs were calculated f or every emitted HAP that has an acute benchmark

. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that might occur outside facility boundaries. Analysis of potential off

- site im pacts for the PAI source category identified four facilities with the potential to exceed the acute REL for s ix pollutants (ethylene glycol ethyl ether (one facility)

, acrolein (one facility) , chloroform (one facility) , nickel compounds (one facility) , chl orine (one facility) , and formaldehyde (one facility) ) . One facility has HQs greater than 1 for three pollutants: ethylene glycol ethyl ether, acrolein, and nickel compounds. Table 3.2

- 2 provides

more information on the acute risk estimates for HAP that had an acute HQ greater than 1 for any benchmark. The highest refined worst

- case acute HQ value is 8 (based on the ethylene glycol ethyl ether REL). 32

All other HAP emissions at all other facilities indicated no potential to cause acute impacts of

conc ern. 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 value does not necessarily indicate that adverse effects will occur, only that they cannot be ruled out. Further, in characterizing the potential for acute noncancer impacts of concern, it is important to remember the upward bias of these worst

- case exposure estimates and to consider the results along with the rather large uncertainties related t o the emissions estimates and screening methodology.

In our refined screening analysis we adjusted the multiplier of 10 to 2 for emissions associated with equipment leaks for one facility (see Appendix 7 of this document and the memorandum

―Emission Data and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active Ingredients, Polyether Polyols, Polymers and Resins IV‖ in the docket for this action ). W e

31 After the risk assessment was completed, we learned that the arsenic emissions from the facility, Bayer Crop Science in WV (NEIWV0390007), should not have been included in the data set for PAI production. The MIR for this facility based on the incorrect emissions in the risk modeling was 20 and the acute result was 80 (REL ) associated with arsenic emissions. Arsenic was not emitted from any other facilities in the source category. We will update the data set with this information, and any additional information received during the comment period, before the final rule.

32 Additionally, we learned that the phosgene emissions at facility 01097NEI18596 were incorrect. Based on the emissions as modeled this facility had an acute value for phosgene of 4 for the REL. The emissions should have been 0.02tpy. With the smaller em issions the acute value is less than 1. We will update the data set with this information, and any additional information received during the comment period, before the final rule.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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37 reviewed 2 facilities with the highest HQ values and determined equipment leaks were primari ly responsible for the high acute HQ values of 4 and 8 and that they were modeled assuming that they all emanate from a single emission location rather than from numerous physical locations throughout the processing area. We note that this assumption furt her 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 and bias associated with them suggest that there may be no real acute issues

at all.

We conducted a screening

- level evaluation of the potential human health risks associated with

emissions of PB

- HAP . Reported emissions of PB

- HAP were compared to emission thresholds established by EPA for the purposes of the RTR risk assessments. 33 The PB

- HAP emitted from this category are lead , hexachlorobenzene, and polychlorinated biphenyls (PCBs). Lead is a PB

- H AP, 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 lead emissions from these facilities. In addition, there is currently not a screening value for PCBs and they wer e not evaluated for potential non

- inhala tion risks. We do not currently have a multipathway screening value for hexachlorobenzne and so it was not evaluated for potential non

- inhalation

risks

. As shown in Table 3.1

- 1, these HAP are not emitted in appreci able quantities. 34

33 ICF International. TRIM

- Based Multipathway Screening Scenario . Prepare d for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.

34 After the risk assessment was completed, we learned that the emissions of hexachlorobenzene in the data set for polyether polyols production should have been assigned to the pesticide active ingredient MACT code.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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38 Table 3.2

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

Production

Result HAP “Drivers”
Facilities in Source Category

Number of Facilities Estimated to be i n Source Category 17 n/a

Number of Facilities Identified in NEI and

Modeled in Preliminary Risk Assessment 17 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 35 7 naphthalene, nickel compounds

Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 10 0 in 1 million 0 n/a Greater than or equal to 10 in 1 million 0 n/a

Greater than or equal to 1 in 1 million 6 naphthalene, nickel compounds, ethylene dichloride, acrylonitrile, formaldehyde, hydrazine, trichloroethylene, 1,4

- dioxane,
1,3

- butadiene

Chr onic Noncancer Risks

Maximum Respiratory Hazard Index 0.7 chlorine Number of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Refined Screening Results

Maximum Acute Hazard Quotient 3 5 8

4

2

2

2

2 ethylene glycol ethyl ether (REL)

acrolein (REL) nickel compounds (REL)

chloroform (REL)

chlorine (REL) formaldehyde (REL)

Number of Facilities With Potential for Acute

Effects 4 ethylene glycol ethyl ether, acrolein, nickel compounds, chlorine, chloroform

, formaldehyde Population Exposure 35
Number of People Living Within 50 Kilometers

of Facilities Modeled 14,000,000 n/a

35 After the risk assessment was completed, we learned that the arsenic emissions from the facility, Bayer Crop Science in WV (NEIWV0390007), should not have been included in the data set for PAI production. The MIR for this facility based on the incorrect emissions in the risk modeling was 20 and the acute result was 80 (REL) associated with arsenic emissions. Arsenic was not emitted from any other facilities in the source category. We

also learned that the emissions of phosgene were incorrect and are much less than in our data. The refined screening acute risk for phosgene based on the incorrect emissions was 4, but with the adjusted emissions the acute value is below 1. The population exposed to cancer ri sk is less than presented in the table due to the adjusted emissions. We will update the data set with this information, and any additional information received during the comment period, before completing the final rule. There were no AEGL

- 1, AEGL

- 2, ER PG

- 1, or

ERPG

- 2 values above 1. See table 3.2

- 2 for these values.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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39 Table 3.2

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

Production

Result HAP “Drivers” Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a Greater than or equal to 10 in 1 million 900 n/a

Great er than or equal to 1 in 1 million 11,000 n/a Number of People Exposed to Noncancer Respiratory Hazard Index:

Greater than 1 0 n/a

Estimated Cancer Incidence (excess cases per year) 0.001 n/a

Contribution of HAP to Cancer Incidence naphthalene 30% n /a formaldehyde 18% n/a methylene chloride 10% n/a tetrachloroethylene 9% n/a ethylene dichloride 6% n/a
1,3

- butadiene 5% n/a nickel compounds 4% n/a

Table 3.2

- 2 Summary of Refined Screening Acute Results for Pesticide Active Ingredient

Production Faci lities

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 35 Max. 1

- hr.

Air Conc. ( mg/m 3 )

Ethylene glycol ethyl ether 0.3 8 0.37

Acrolein 0.01 4 0.1 /0.09 0.04 /0.03 0.0025 0.069 0.11 0.23 0.34

Nickel Cpds 0.012 2 0.006

Chloroform 0.3 2 0.001 / 0.001 0.15 310 240

Chlorine 0.42 2 0.3 /0.1 0.07 /0.05 0.21 1.5 2.9 5.8 8.7

Formaldehyde 0.1 2 0.1 /0.08 0.0 06/0.008 0.055 1.1 1.2 17 12

Notes on Refined Process: 1) The screening was performed for all emitted HAP with available acute dose

- response values. Only those pollutants whose screening HQs were greater than 1 for at l east 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 A cute 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 publi c. AEGL

- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience effects t hat are notable discomfort, but which are transient and reversible upon cessation of exposure.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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40

AEGL

- 2 is t he 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 Pr ogram 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 adver se 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 ind ividual’s ability to take protective action.

The facility

- wide MIR and TOSHI, available in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility

- wide assessment for cancer risks are summarized in Table 3.2

- 3. The results indicate

that 12 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

fo r the source category is 20 in a million , and it occurs at 2 facilities . At one of these

facilit ies , the risk is driven by ethylene dichloride from a mercury cell chlor

- alkali process and the PAI source category contributes less than one percent to the fa cility

- wide risk . At the other facility, the risk is almost 100 percent from an unidentified source category due to

arsenic emissions . The maximum facility

- wide TOSHI for the source category is 2, driven by

emissions of chlorine from inorganic chemical m anufacturing, synthetic organic chemical manufacturing, and mercury cell chlor

- alkali processes. The source category contributes less than 5 percent to the facility

- wide TOSHI.

Table 3.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

– Pe sticide Active Ingredient

Pesticide Active Ingredient Manufacturing Number of Facilities Binned by Facility

- Wide MIR (in 1 million) Source Category MIR Contribution to Facility

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

> 90% 1 3 0 0 4

50

- 90% 1 1 0 0 2

10

- 50% 2 4 0 0 6

< 10% 1 0 4 0 5

Total 5 8 4 0 17



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

4.1 Source Category Description and Results

The p olyether polyols pr oduction 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 re active hydrogens. Polyether polyols do not have significant uses of their own,

but rather are used to mak e a variety of other products. Polyether polyols can be produced byDraft Risk Assessment for 7 Chemica l Sector Source Categories

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41 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, h exane, toluene, and other HAP. P otential sources of emissions for this category, regardless of the specific process employed, include process vents, storage vessels, equipment leaks, wastewater operations, and heat ex changers/cooling towers . A complete description of the polyether polyols production sou rce category can be found in the text of the NPRM.

We currently estimate that there are 2 3 polyether polyols production facilities operating in the

U.S. 36 The data set contains all 2 3 facilities identified with a polyether polyols production

MACT code i n the 2005 NEI. The 2005 NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and emission locations. All 2 3 of these facilities are identified as major sources in the NEI.

The emissions fo r the polyether polyols production source category data set (of 2 3 facilities)

are summarized in Table 4.1

- 1 . The total HAP emissions for the source category are approximately 440 tons per year. Based on these data, the HAP emitted in the largest quantit ies across these 2 3 facilities are: ethylene glycol, ethylene oxide, propylene oxide, acetaldehyde, methanol, ethyl benzene, benzene, chlorobenzene, glycol ethers, hexane, propionaldehyde, and p

- dioxane. These 12 HAP account for 9 0 percent of the total em issions by mass. PB

- HA P 37 reported as emissions from these facilities include POM and lead compounds. 38

36 After the risk assessment was completed, we learned that two facilities included in the data set for polyether polyols production should not have been included. These facilities, Emeral d Carolina Chemical (NEINC0595) and Port Neches Operations C4 Plant (NEI12483), are still included in the emissions summary, but risk results have been removed from the risk summary. We will update the data set with this information, and any additional

in formation received during the comment period, before the final rule.

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

EPA

- 453K

- 04

- 001A, as referenced in the ANPRM and provided on the EPA’s Technolo gy Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html

. 38 After the risk assessment was completed, we learned that two facilities included in the data set for PEPOs production should not have been included. These facilities, Emerald Carolina Chemical (NEINC0595) and Port Neches Operations C4 Plant (NEI12483) are still included in the emissions summary. Additionally, after the risk assessment was completed, we learned that the emissions of hexachlorobenzene in the data set for polyether polyols production should have been assigned to the PAI MACT code. These emissions are still included in the emissions summary, but risk results ha ve been removed from the risk summary. We will update the data set with this information, and any additional information received during the comment period, before the final rule.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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42 Table 4.1

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

- Response Values

HAP a Emission s (tpy) Number

of

Facilities Reporting

HAP (25

facilities

in data set) 36 Prioritized I nhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for A cute
Noncancer?

Ethylene Glycol 17 8 9
Ethylene Oxide 57 2 5
Propylene Oxide 3 4 19
Acetaldehyde 27 12

Methanol 25 11
Ethyl Benzene 19 4

Benzene 16 8

Chlorobenzene 12 4
Glycol Ethers
Glycol Ethers 9 5

2

- Butoxyethyl Acetate 2 1
Methoxytriglycol 1 2 Diethylene Glycol Monoethyl Ether 0.6 1 Ethylene glycol ethyl ether ( Cellosolve ) 0.5 1
Propyl Cellosolve 0.4 1 Ethylene Glycol Methyl

Ether 0. 3 1 Diethylene Glycol Monobutyl Ether 0.07 1

2

- (Hexyloxy)Ethanol 0.05 1
Butyl Carbitol Acetate 0.004 1
Ethoxytriglycol 0.0009 1
Triglycol Monobutyl Ether 0.0003 1

Hexane 6 6
Propionaldehyde 6 5

1,4

- Dioxane (p

- Dioxane) 5 7

1,3

- Butadiene 5 3

Chlorine 4 3
Styrene 4 6
Acrylic Acid 4 2

Toluene 3 7
Formaldehyde 3 1 0
Hydrochloric Acid 2 4
Vinyl Acetate 1 3

Diethanolamine 1 5Draft Risk Assessment for 7 Chemica l Sector Source Categories

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43 Table 4.1

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

- Response Values

HAP a Emission s (tpy) Number

of

Facilities Reporting

HAP (25

facilities

in data set) 36 Prioritized I nhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for A cute
Noncancer?

Xylenes (Mixture of o, m, and p Isomers) 1 7

Ethyl Acrylate 1 2
Methyl Tert

- Butyl Ether 1 3
Propylene Dichloride 1 1

Acrolein 1 3
Ethyl Chloride 1 6
Ethylene Dichloride 0.9 5

Phenol 0.8 7

1,2

- Epoxybutane 0.8 2
Naphthalene 0.7 4
Acetophenone 0.6 3
Acrylonitrile 0. 2 3
Trichloroethylene 0. 2 1

Cumene 0. 2 5
Phosgene 0. 2 2
Vinyl Chloride 0.2 4

N,N

- Dimethylformamide 0.1 1
2,4

- Dichlorophenoxy Acetic

Acid 0.1 1
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
Methyl ene Chloride 0.04 3

Chloroacetic Acid 0.03 2

Fluoranthene 0.03 1

Chloroform 0.03 4
Triethylamine 0.02 3

Hexachlorobenzene 3 3 0.0 2 1
Methyl Isobutyl Ketone 0.02 3

m

- Xylene 0.01 1

Acetonitrile 0.01 2

Dieth yl Sulfate 0.0 1 1
Methyl Methacrylate 0.008 1Draft Risk Assessment for 7 Chemica l Sector Source Categories

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44 Table 4.1

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

- Response Values

HAP a Emission s (tpy) Number

of

Facilities Reporting

HAP (25

facilities

in data set) 36 Prioritized I nhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for A cute
Noncancer?

Hydroquinone 0.006 1
Tetrachloroethylene 0. 00 6 1

2,4,6

- Trichlorophenol 0.006 1
Phthalic Anhydride 0.004 1

Cresol 0.003 2

1,3

- Dichloropropene 0.002 1

4,4 '

- Methylenedianiline 0.001 1
Dichloroethyl Ether 0.00 1 1

p

- Xylene 0.0009 1

2,4

- Toluene Diisocyanate 0.0005 1
Bis(2

- Ethylhexyl)Phthalate 0.0005 1
Dibutyl Phthalate 0.0005 1

Lead 0.0005 1 c Quinoline 0.0005 1

o

- Toluidine 0.0005 1

1,1,2

- Trichloroethane 0.0001 1

Carbon Tetrachloride 0.0001 1

a Notes for how HAP were speciated for risk assessment: For most metals, emissions reported as the elemental metal are combined with metal c ompound emissions (e.g., ―cadmium‖ emissions modeled as ―cadmium & compounds‖). In the absence of speciation information, we assume the reported mass is 100 percent metal. For emissions of any chemicals or chemical groups classified as POM, emissions were grouped into POM subgroups as found on EPA’s Technology Transfer Network website for the 200 5 National

- Scale Air Toxics

Assessment at http://www.epa.gov/ttn/atw/nata2005/methods.html#p om ( Approach to Modeling POM)

. These POM subgroups (e.g., POM 7 2 002, not shown above) all have unit risk estimates for cancer, and are considered

PB

- HAP. For emissions reported generically as ―Glycol Ethers‖ or specific glycol ethers not found on EPA’s Te chnology Transfer network for air toxics (see footnote b), emissions will be treated as ethylene glycol methyl ether.

b Specific dose

- response values for each chemical are identified on EPA’s Technology Transfer Network website for air

toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html

.

c There is no reference concentration for lead. In considering noncancer hazards for lead in this preliminary assessment, we compared the maximum ann ual ambient exposure estimates to the National Ambient Air Quality 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). Th e secondary (welfare

- based) standard is identical to the primary standard. These NAAQS for lead were reviewed with revisions adopted in October 2008 ( http://www.epa.gov/air/lead/actions.html ).Draft Risk Assessment for 7 Chemica l Sector Source Categories

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45 

### 4.2 Risk Characterization

This section presents the results of the risk assessment for the polyether polyols production source category. The basic chronic inhalation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chroni c hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients, as well as the results of our preliminary screen for potential non

- inhalation

ris ks from PB

- HAP. Also pr esented are the HAP ―drivers,‖ which are the HAP that collectively contribute 90 percent of the maximum cancer risk or maximum hazard index at the highest exposure location , as well as a summary of the results of our facility

- wide assessments and our analy sis of risks associated with the maximum allowed emissions under the current MACT standards. A detailed summary of the facility

- specific risk assessment results is available in Appendix 4

.

Table s 4.2

- 1 and 4.2

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

category. The results indicate that maximum lifetime individual cancer risks could be as high

as 3 0 in a million, with ethylene oxide as the major contributor to the risk. The total

estimated cancer incidence from the so urce category is 0.02 excess cancer cases per year, or one case in every 50 years. Approximately 6,800 people are estimated to have cancer risks at or above 10 in a million, and approximately 160,000 people are estimated to have cancer risks

at or above 1 in a million as a result of the emissions from 17 facilities ; however these estimates are biased high due to the mistake s with the emissions data . The maximum chronic noncancer TOSHI value for the source category could be up to 0.8 from emissions of acro lein

.

Worst

- case a cute HQs were calculated f or every HAP that has an acute benchmark

. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries. Additionally

, for the facility with the highest acute HQ value the multiplier of 10 was adjusted to 2 resulting in a

reduction of the acute risk for one facility (see Appendix 7 of this document and the

memorandum ―Emission Data and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active Ingredients, Polyether Polyols, Polymers and Resins IV‖ in the docket for

th is action ). T he highest acute HQ value of 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 two facilities with the potential to exceed the acute REL for two pollutants (glycol ethers (1 facility) and acrolein (1 facility ) ). Table 4.2

- 2 provides more information on the acute risk

estimates for HA P that had an acute HQ greater than 1 for any benchmark.

The highest refined worst

- case acute HQ value is 6 (based on the REL for glycol ethers )

. In characterizing the potential acute noncancer risks from glycol ethers, it is important to

consider the uncertainties related to the emission inventory as it relates to a lack of speciation data for glycol ethers for this source category.

A ll other HAP emissions at all other facilities indicated no potential to cause acute impacts of

concern. While these estimated worst

- case exceedances indicate that there is some potential for such acute exposures to occur, we note that exceeding the modeled REL values does not necessarily indicate that adverse effects will occur, only that they cannot be ruled out.

Furt her, 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 theDraft Risk Assessment for 7 Chemica l Sector Source Categories

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46 results along with the rather large uncertainties related to the emissions e stimates and screening methodology.

We reviewed the two facilities with potential off

- site acute HQ values greater than one and determined equipment leaks were primarily responsible and that they were modeled assuming that they all emanate from a single e mission 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 e ach of these facilities. Taking all of this into consideration, these acute impact screening results indicate only the potential for acute impacts of concern, while the uncertainties and bias associated with them suggest that there may be no real acute is sues at all. Nonetheless, the emission points and pollutants identified by this evaluation should be

examined to see if further cost

- effective emission reductions are achievable.

We conducted a screening

- level evaluation of the potential human health ris ks associated with

emissions of PB

- HAP. Reported emissions of PB

- HAP w ere compared to emission thresholds established by EPA for the purposes of the RTR risk assessments. 39 The PB

- HAP emitted by facilities in this category include POM as benzo(a)pyrene T E Q ( 1 facility) and lead compounds (1 facility). 40 The one facility with POM emissions above the threshold

level exceed s the screening emission level by a factor of 4

. Lead is a PB HAP, but the NAAQS value (which was used for the chronic noncancer risk as sessment) 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 multipathw ay exposure and risk due to lead

emissions from these facilities.

39 ICF International. TRIM

- Based Multipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.

40 After the risk assessment was completed, we learned that the emissions of hexachlorobenzene in the data set for the PEPOs production should have been assigned to the PA I MACT code. These emissions are still included in the PEPOs emissions summary, but have been removed from the risk summary. We will update the data set with this information, and any additional information received during the comment period, before the final rule.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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47 Table 4.2

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

Production

Result HAP “Drivers”
Facilities in Source Category 41

Number of Facilities Estimated to be i n Source Category 2 3 n/a

Number of Facilities Identified in NEI and

Modeled in Preliminary Risk Assessment 25 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 3 0 ethylene oxide

Number of Facilities with Maximum Individual Li fetime Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a

Greater than or equal to 10 in 1 million 5 ethylene oxide, acetaldehyde, acrylonitrile, 1,3

- butadiene, benzene, 1,4

- dioxane

Greater than or equal to 1 in 1 million 17 ethylene oxide, acetaldehyde, acrylonitrile, 1,3

- butadiene, benzene, 1,4

- dioxane, propylene oxide, ethyl benzene, propylene dichloride, ethylene dichloride, naphthalene, benzyl chloride

Chronic Noncancer Risks

Maximum Respiratory Hazard Index 0.8 acrolein Number of F

acilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Refined Screening Results

Maximum Acute Hazard Quotient 6

4/0.1 g lycol ethers (REL)

acrolein (REL/AEGL

- 1)

Number of Facilities With Potential for Acute

Effects 3 acr olein, glycol ethers

Population Exposure 41
Number of People Living Within 50 Kilometers

of Facilities Modeled 18,000,000 n/a

Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a Greater than or equal to 10 in 1 mi llion 6,800 n/a Greater than or equal to 1 in 1 million 160,000 n/a

41 After the risk assessment was completed, we learned that two facilities included in the data set for polyether polyols production should not have been included. These facilities, Emerald Carolina Chemical (NEINC0595) and Port Neches Operatio ns C4 Plant (NEI12483), are still included in the emissions summary but risk results have been removed from the risk summary. One of the facilities does not have any of the maximum risks. The other, is responsible for the maximum cancer risk, the maximum respiratory hazard index, and the maximum facility

- wide MIR and TOSHI. The risk results with these 2 facilities in the data set were 60 for the MIR and 1 for the maximum HI. The risks presented in the summary table represent the results based on the upd ated information. The population exposed to cancer risk would be less than presented in the table due to the adjusted emissions. We will update the data set with this information, and any additional information received during the comment period, before t he final rule.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

48 Table 4.2

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

Production

Number of People Exposed to Noncancer Respiratory Hazard Index:

Greater than 1 0 n/a

Estimated Cancer Incidence (excess cases per year) 0.02 n/a

Contribution of HAP to Cancer Incide nce ethylene oxide 87% n/a propylene oxide 4% n/a

benzene 3% n/a

Table 4.2

- 2 Summary of Acute Refined Sce ening Results for Polyether Polyols Production

Facilities

Results MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE

- RESPONSE VALUES

Based on RE L 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 )

Glycol Ethers 0.56 6 0.093

Acrolein 0.0 1 4 0.1 4 /0.09 0.04 /0.03 0.0025 0.069 0.11 0.23 0.34

Notes on Refined Process: 1) The screening was performed for all emitted HAP with available acute dose

- response values. Only those pollutants whose screening HQs were greater than 1 for at least one acute threshold value are shown in the table. 2) HAP with available acute dose

- response values which are not in the table do not carry any potential for posing acute health risks, based on an analysis of currently available emissions data.

Notes on Acute Dose

- Response Values:

REL

– Californi a 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 experience effects t hat are notable discomfort, but which are transient and reversible upon cessation of exposure.

AEGL

- 2 is the exposure level above which it is predicte d 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 exposur e (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 exp osure 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.

The facility

- wide MIR and TOSHI, available in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility

- wide assessment are summarized in Table 4.2

- 3. The results indicate that 18 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 30 in a million, with the polyether polyol production source category contri buting 100 percent of the risk, driven by emissions of ethylene oxide from proc ess vents and equipment leaks. The maximum facility

- wide TOSHIDraft Risk Assessment for 7 Chemica l Sector Source Categories

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49 for the source category is 2 , driven by emissions of chlorine from industrial inorganic chemical manufacturing an d HON process units . T he source category contributes approximately 1 3 percent to the facility

- wide TOSHI. 42

Table 4.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

– Polyether Polyols Production

Polyether Polyols

Production Number of Facilities Binned by Facility

- Wide MIR (in 1 million) 4 2

Source Category MIR Contribution to Facility

- Wide

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

> 90% 3 3 4 0 1 0

50

- 90% 0 3 2 0 5

10

- 50% 1 2 1 0 4

< 10% 0 2 2 0 4

Total 4 10 9 0 2 3



### 5. Risk Resu lts 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 copoly mers of styrene and acrylonitrile. Styrene

- acrylonitrile resins 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 suspension 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, process 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

42 After the risk assessment was completed, we learned that two facilities included in the data set for polyether polyols production should not have been included. These facilities, Emerald Carolina Chemical (NEINC0595) and Port Neches Opera tions C4 Plant (NEI12483), are still included in the emissions summary, but risk results have been removed from the risk summary . One of the facilities does not have any of the maximum risks. The other, is responsible for the maximum cancer risk, the ma ximum respiratory hazard index, and the maximum facility

- wide MIR and TOSHI. The risk results with these 2 facilities in the data set were 60 for the MIR and 1 for the maximum HI. We will update the data set with this information, and any additional info rmation received during the comment period, before the final rule.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

50 description of the styrene

- acrylonitrile production source category can be found in the text of

the NPRM.

We currently estimate that there are two styrene

- acrylonitrile production facilities operating in

the U.S. The data set contains two facilities identified with a styrene

- acrylonitrile production MACT code in the 2005 NEI. The 2005 NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and emission locations. Both of these facilities are identified as major sources in the NEI.

The emissions for the styrene

- acrylonitrile production source categor y data set (of two facilities) are summarized in Table 5.1

- 1 . The total HAP emissions for the source category are approximately 2 tons per year. Based on these data, the HAP emitted in the largest quantities

for these 2 facilities are: ethyl benzene, styre ne, methylene chloride and acrylonitrile. T hese

four HAP account for 100 percent of the total emissions by mass. No PB

- HA P 43 are reported

in the data set for the styrene

- acrylonitrile production source category

.

Table 5. 1

- 1 Summary of Emissions from the Styrene

- Acrylonitrile Production Source Category and Availability of Dose

- Response Values

HAP Emissions (tpy) Number of

Facilities Reporting

HAP (2

facilities in data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS a

PB

- HAP? Un it Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer?
Ethyl Benzene 1 1
Styrene 1 2
Methylene chloride 0. 4 2
Acrylonitrile 0. 04 2

a Specific dose

- respon se values for each chemical are identified on EPA’s Technology Transfer Network website for air

toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html

.



### 5.2 Risk Characterization

This secti on 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 preliminary screen for potenti al non

- inhalation

risks from PB

- HAP. Also presented are the HAP ―dri vers,‖ 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

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

EPA

- 453K

- 04

- 001A, as referenced in the ANPRM and provided on the EPA’s Technology Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html

.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

51 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 4

.

Table 5.2

- 1 summarizes the chronic and acute inhalation risk results for this source category. The results indicate that maximum lifetime individual cancer risks could be as high as 0.03 in a million, with acrylonitrile and ethyl benzene as the major contributors to the risk. The total estimated cancer incidence from the source category is 0.000006 excess cancer cases per year, or one case in every 167,000 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 0.0002 , ba sed primarily on emissions of acrylonitrile, indicating no significant potential for chronic noncancer impacts.

Worst

- case a cute HQs were calculated f or every HAP that has an acute benchmark, and the highest acute HQ value of 0.007 (based on the methyle ne chloride REL) is shown in Table

5.2

- 1. There were no screening acute HQs greater than 1, so further refinement was not performed. A screening

- level evaluation of the potential human health risks associated with

emissions of PB

- HAP was not necessary fo r this source category since no PB

- HAP are

emitted

.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

52 Table 5.2

- 1 Summary of Source Category Level Risks for Styrene

- Acrylonitrile

Production

Result HAP “Drivers”
Facilities in Source Category

Number of Facilities Estimated to be i n Source Catego ry 2 n/a

Number of Facilities Identified in NEI and

Modeled in Preliminary Risk Assessment 2 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 0.03 acrylonitrile, ethyl benzene

Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1

million 0 n/a

Greater than or equal to 10 in 1

million 0 n/a

Greater than or equal to 1 in 1 million 0 n/a

Chronic Noncancer Risks

Maximum Respiratory Hazard Index 0.0002 acrylonitrile Number of Faci lities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a Acute Noncancer Screening Results Maximum Acute Hazard Quotient 0.007 methylene chloride (REL)

Number of Facilities With Potential for Acute

Effects 0 n/a

Population Exposure

Numbe r of People Living Within 50

Kilometers of Facilities Modeled 680,000 n/a

Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1

million 0 n/a

Greater than or equal to 10 in 1

million 0 n/a

Greater than or equal to 1 in 1 million 0 n/a Number of People Exposed to Noncancer Respiratory Hazard Index:

Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.000006 n/a

Contribution of HAP to Cancer Incidence ethyl benzene 52% n/a acrylonitrile 44% n/a

The facility

- wide MIR and TOSHI, available in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility

- wide assessment are summarized in Table 5.2

- 2 . The results indicate that both

facilities with styrene

- acrylonitrile production processes have a facility

- wide cancer MIRDraft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

53 greater than or equal to 1 in a million. The maximum facility

- wide cancer MIR is 20 in a million for 1 facility. At this facility, the source c ategory contributes less than one percent t o the facility

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

cell chlor

- alkali process. The other facility has a cancer risk of 10 in a million. Again, the

styrene

- acrylonitrile so urce 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 TOSHI for the source category is 2, 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 So urce 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≤ M IR<10 10≤ MIR<100 > 100 Total

> 90% 0 0 0 0 0

50

- 90% 0 0 0 0 0

10

- 50% 0 0 0 0 0

< 10% 0 0 2 0 2

Total 0 0 2 0 2



### 6. Risk Results for the P&R IV 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 process (operated in

a conti nuous 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 the 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 polystyrene 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 polyst yrene resins, including disposable dinnerware,Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

54 shower doors, light diffusers, soap dishes, insulation board, food containers, drain pipes, audio and video tape, picnic coolers, loose fill packaging, and tubing. A complete description of the polystyrene pro duction source category can be found in the text of the NPRM.

We currently believe that there are 11 polystyrene production facilities operating in the U.S.

, and t he data set contains those 11 facilities identified with a polystyrene production MACT

cod e in the 2005 NEI. The 2005 NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and emission locations. All 11 of these facilities are identified as major sources in the NEI.

The emissions for the polystyrene production source category data set (of 11 facilities) are

summarized in Table 6.1

- 1 . The total HAP emissions for the source category are approximately 90 tons per year. Based on these data, the HAP emitted in the largest quantities

fo r these 11 facilities is s tyrene, which accounts for 94 percent of the total emissions by mass.

No PB

- HA P 44 are reported in the data set for the polystyrene production source category

.

Table 6.1

- 1 Summary of Emissions from the Polystyrene Production S ource Category and Availability

of Dose

- Response Values

HAP Emissions

(tpy) Number of

Facilities Reporting HAP (11 facilities in data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS a

PB

- HAP? Unit Risk

Estimate for

Cancer? Referenc e

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer?
Styrene 85 10

Toluene 2 5
Ethyl Benzene 1 7

Tetrachloroeth ylene 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 chemica l 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 o f 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 cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum

44 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Ri sk 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.ep a.gov/ttn/fera/risk_atra_vol1.html

.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

55 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

e xposure location , as well as a summary of the results of our facility

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

- specific risk assessment re sults is available in Appendix 4

.

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 could be as high as 2 in a million, with tetrachloroet h ylene as the major contributor to risk. The total estimated cancer incidence from the source category is 0.00003 excess cancer cases per year, or one case in every 33,000 years. Approximately 180 people are estimated to have cancer risks at or above

1 i n a million as a result of the emissions from one facility. The maximum chronic noncancer TOSHI value for the source category could be up to 0.004 from emissions of xylenes and styrene, 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 screening acute HQs greater than 1, indicating no potential concerns about acute impacts , and further refinement was not performed

. A screening

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

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

- HAP are emitted

.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

56 Table 6.2

- 1 Summ ary of Source Category Level Risks for Polystyrene Production

Result HAP “Drivers”
Facilities in Source Category

Number of Facilities Estimated to be i n Source Category 11 n/a

Number of Facilities Identified in NEI and

Modeled in Preliminary Risk Asse ssment 11 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 2 tetrachloroeth yl ene

Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1

million 0 n/a

Greater than or equal to 10 in 1 million 0 n/a Greater than or equal to 1 in 1 million 1 tetrachloroeth yl ene Chronic Noncancer Risks

Maximum Neurological Hazard Index 0.004 xylenes (mixed), styrene Number of Facilities with Maximum Neurological Hazard Index:

Greater than 1 0 n/a Acute Noncancer Screening Results Maximum Acute Hazard Quotient 0.3 styrene (REL)

Number of Facilities With Potential for Acute

Effects 0 n/a

Population Exposure Number of People Living Within 50

Kilometers of Facilities Modeled 9,000,000 n/a

Num ber of People Exposed to Cancer Risk: Greater than or equal to 100 in 1

million 0 n/a

Greater than or equal to 10 in 1 million 0 n/a Greater than or equal to 1 in 1 million 180 n/a Number of People Exposed to Noncancer Neurological Hazard Index:

G reater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.00003 n/a

Contribution of HAP to Cancer Incidence

tetrachloroeth yl ene 74% n/a ethyl benzene 25% n/a

The facility

- wide MIR and TOSHI, available in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility

- wide assessment are summarized in Table 6.2

- 2. The results indicate that two
facilities with polystyrene production processes ha ve a facility

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

- wide cancer MIR for the source category is

1 0 in a million at one facility. At this facility, the source category contributes less than oneDraft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

57 percent to the facilit y

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

- butadiene

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

cancer risk of 2 in a million. The polystyrene production source category contributes over 95

perc ent to the facility

- wide MIR, which is driven by emissions of tetrachloroeth ylene from storage vessels. The maximum facility

- wide TOSHI for the source category is less than 1.

Table 6.2

- 2 Source Category Contribution to Facility

- Wide Cancer Risks

– Pol ystyrene Production

Polystyrene

Production Number of Facilities Binned by Facility

- Wide MIR (in 1 million) Source Category MIR Contribution to Facility

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

> 90% 3 1 0 0 4

50

- 90% 1 0 0 0 1

10

- 50% 0 0 0 0 0

< 10% 5 0 1 0 6

Total 9 1 1 0 11



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

7.1 Source Category Description and Results

Three different t ypes of resins are made by sources covered by the polyethylene ter e phthalate ( PET ) source category: solid

- state resins (PET bottle grade resins)

, polyester film

, and engineering resins. They are all thermoplastic linear condensation polymers based on

dime thyl terephthalate (DMT) or terephthalic acid (TPA). PET production can occur via either a batch or continuous process. PET solid

- state resin is produced in a two

- step process.
The most common use of PET solid

- state resins is in soft drink bottles, some industrial fiber

graded polyester (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 most common uses of PET film are photogr aphic film and magnetic media. PET is used e xtensively in the manufacture of synthetic fibers (i.e., polyester fibers), which compose the largest segment of the synthetic fiber industry. The most common uses of polyester fibers are apparel, home furnishings, carpets, fiberfill, and other industrial processes. Emissions sources present at PET production processes include raw material storage tanks, mix tanks, prepolymerization and polymerization reaction vents and process tanks, equipment leaks and ancillary systems, and wastewater operations. A co mplete description of the polyethylene terephthalate production source category can be found in the text of the NPRM.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

58 We curr ently estimate that there are 12 PET production facilities operating in the U.S. 45 The

data set contains 15 facilities identified with a PET production MACT code in the 2005 NEI. The 2005 NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and emission locations. All 15 of these facilities are identified as major sources in the NEI.

The emissions for the PET production source category data set (of 15 facilities) are

summarized in Table 7.1

- 1 . The total HAP emissions for the source category are approximately 1,200 tons per year. Based on these data, the HAP emitted i n the largest quantities across these 1 5 facilities are ethylene glycol, acetaldehyde, methanol, and biphenyl.

These four HAP account for over 90 percent of the total emissions by mass. PB

- HA P 46 in the

data set for the PET production source category inclu de cadmium compounds, polycyclic organic matter (POM), and lead compounds

.

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

Fac ilities Reporting

HAP ( 1 5

facilities in data set) 45 Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

- HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer?

Eth ylene Glycol 500 15
Acetaldehyde 278 15

Methanol 270 11
Biphenyl 59 7

1,4

- dioxane 18 14
Methyl bromide 12 1

o

- Xylene 9 2

m

- Xylene 8 1

p

- Xylene 7 2
Hydrochloric acid 5 1

Toluene 4 2

Benzene 4 3
Formaldehyde 3 4
Glycol Ethers 3 1
Antimony & compounds 0.5 2
Trichloroethylene 0. 5 1

45 After the risk assessment was completed, we learned that three facilities included in the data set for polyethylene terephthalate production have been shut down or closed the PET production process. These

facilities , Dupont in Florence, SC (NEI41302), Dupont in Old Hickory, TN (NEI45591), and Wellman in Darlington, SC (NEI43310), are still included in the emissions summary but risk results have been removed from the risk summary. We will update the data set with thi s information, and any additional information received during the comment period, before the final rule.

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

EPA

- 453K

- 04

- 001A, as referenced in the NPRM and provided on the EPA’s Technology Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html

.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

59 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

Fac ilities Reporting

HAP ( 1 5

facilities in data set) 45 Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

- HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer? Xylenes (Mixture of o, m, and p Isomers) 0.4 3
Ethylene oxide 0.4 2
Selenium & compounds 0.1 1
Manganese & co mpounds 0.09 2

Hexane 0.03 2

Chlorine 0.01 1

Acrolein 0.0 1 1
Nickel compounds

Nickel 0.0003 1
Nickel & compounds 0.0 0002 1

Cadmium compounds

Cadmium 0.0002 1
Cadmium & compounds 0.00001 1
Propylene Oxide 0.0001 1

1,4

- Dichlorobenzene 0.00001 1

Lead compounds (Inorganic) 0.000005 1 c Naphthalene 0.000004 1 Arsenic & Compounds (Inorganic Including Arsine) 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 assum e 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 et her. For emissions of any chemicals or chemical groups classified as POM, emissions were grouped into POM subgroups as found on EPA’s Technology Transfer Network website for the 2005 National

- Scale Air Toxics

Assessment at http://www.epa.gov/ttn/atw/nata2005/methods.html#pom ( Approach to Modeling POM) . These POM subgroups (e.g., POM 7 2 002, not shown above) all have unit risk estimates for cancer, and are considered

PB

- HAP.

b Specific d ose

- response values for each chemical are identified on EPA’s Technology Transfer Network website for air

toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html

.

c There is no reference concentration for lead. In considering noncancer hazards for lead in this assessment, we compared maximum annual ambient exposure estimates to the National Ambient Air Quality Standards (NAAQS) for leadDraft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

60 (0.15 μg/m 3 ). These NAAQS for lead were reviewed wi th 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 s uspended 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 maxim um hazard quotients, as well as the results of our preliminary screen for potenti al non

- inhalation risks from PB

- HAP. Also presented are the HAP ―drivers,‖ which are the HAP that collectively contribute 90 percent of the maximum cancer risk or maximum

haz ard 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

- s pecific risk assessment results is available in Appendix 4

.

Table s 7.2

- 1 and 7.2

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

category. The results indicate that maximum lifetime individual cancer risks could be as high

a s 9 in a million, with acetaldehyde and 1,4

- dioxane as major contributors to the risk. The total estimated cancer incidence from the source category is 0.002, or one case in every 500

years. Approximately 4,200 people are estimated to have cancer risks a t 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 categ ory could be up to 0.5, indicating no significant potential for chronic noncancer impacts.

Worst

- case a cute HQs were calculated f or every HAP that has an acute benchmark

. For cases where the screening acute HQ was greater than 1, we further refined the e stimates 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 o u r approach as described in the me morandum ―Emission Data and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active Ingredients, Polyether Polyols, Polymers and Resins IV‖ available in the docket for this action . Other facility multiplier s were adjusted from 10 to 2 since t he 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: Pesticid e Active Ingredients, Polyether Polyols, Polymers

and Resins IV‖ in the docket for this action ). Using these adjustments to the multiplier of 10

resulted in t he highest acute refined screening HQ value of 8 (based on the acetaldehyde REL)

as shown in Tabl e 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 acetaldehyde. Table

7.2

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

- hour

AEGL

- 1 value is 0.2 , and the maximum HQ for acetaldehyde based on the 1

- hour ERPG

- 1Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

61 value is 1 . The ERPG

- 1 value is a no effect level which is expect ed to be pro tective 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 irritation in the general population.

All other HAP emissions at all other facilities indicat ed no potential to cause acute impacts of

concern. While these estimated worst

- case exceedances indicate that there is some potential for such acute exposures to occur, we note that exceeding the modeled REL or ERPG

- 1 values does not necessarily indicate that adverse effects will occur, 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 re sults along with the rather large uncertainties related to the emissions estimates and screening methodology.

Upon further evaluation, we identified that, for 2 facilities with the highest HQ values ( based

on both the 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 throughout the processing area. We note that this assumption further biases the HQ values high, but to an unknown extent, given that we do not know the actual size of the processing areas at each of these

facilities

. W e also identified that one of the high HQ values was associated with acetaldehyde

emissions from w astewater treatment operations which w ere modeled from a single emission location versus being modeled as emissions emanating across a large area , again biasing the HQ estimate high . Taking all of this into consideration, these acute impact screening resu lts indicate only the potential for acute impacts of concern, while the uncertainties and bias associated with them suggest that there may be no real acute issues.

We conducted a screening

- level evaluation of the potential human health risks associated with

emissions of PB

- HAP. Reported emissions of PB

- HAP were compared to emission thresholds established by EPA for the purposes of the RTR risk assessments. 47 The PB

- HAP

emitted by facilities from this category are cadmium compounds (2 facilities), polycy clic 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 signifi cant 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 m ultipathway 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.

47 ICF International. TRIM

- Based Multi pathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

62 Table 7.2

- 1 Summary of Source Category Level Risks for Polyethylene Terephthalate

Production

Result HAP “Drivers”
Facilities in Source Category 48

Number of Facilities Estimated to be i n Source Category 1 2 n/a

Number of Facilities Identified in NEI and

Modeled in Preliminary Risk Assessment 15 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 9 acetaldehyde, 1,4

- dioxane

Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1

million 0 n/a

Greater than or equal to 10 in 1

million 0 n/a

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

- dioxane, ethylene

oxide

Chronic Noncancer Risks

Maximum Respiratory Hazard Index 0.5 acetaldehyde, acrolein, ethylene glycol

Num ber of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Refined Screening Results

Maximum Acute Hazard Quotient 8

1

0. 2 acetaldehyde (REL)

acetaldehyde (ERPG

- 1) acetaldehyde (AEGL

- 1 )

Number of Facilities With Pote ntial for Acute

Effects 9 acetaldehyde

Population Exposure Number of People Living Within 50

Kilometers of Facilities Modeled 4 8 7,700,000 n/a

Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1

million 0 n/a

Greater than or e qual to 10 in 1

million 0 n/a

Greater than or equal to 1 in 1 million 4,200 n/a

48 After the risk assessment was completed, we learned that three facilities included in the data set for polyethylene terephthalate p roduction have been shut down or closed the PET production process. These facilities, Dupont in Florence, SC (NEI41302), Dupont in Old Hickory, TN (NEI45591), and Wellman in Darlington, SC (NEI43310), are still included in the emissions summary but risk r esults have been removed from the risk summary. All three facilities have acute HQs greater than 1 based on the acetaldehyde REL, and one of them has the maximum value. The risks presented in the summary table represent the results based on the updated i nformation. The population exposed to cancer risk would be less than presented in the table due to the adjusted emissions. We will update the data set with this information, and any additional information received during the comment period, before comple ting the final rule.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

63 Table 7.2

- 1 Summary of Source Category Level Risks for Polyethylene Terephthalate

Production

Result HAP “Drivers” Number of People Exposed to Noncancer Respiratory Hazard Index:

Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.002 n/a

Contribution of HAP to Cancer Incidence acetaldehyde 74% n/a
1,4

- dioxane 16% n/a

Table 7.2

- 2 Summary of Acute Refined Screening Results for Polyethylene Terephthalate

Production

Results MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE

- RESPONSE VALUES

Based on REL B ased 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 19.3 8 0.2/ 1 0.04/ 0.05 0.47 81 18 490 360

Notes on Refined Proce ss: 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

- respo nse 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, i ncluding susceptible individuals, could experience effects t hat 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 susce ptible individuals, could experience irreversible or other serious, long

- lasting adverse health effects of an impaired ability to escape.

EPRG

– Emergency Removal Program guidelines represent emergency exposure (1

- hour) limits for the general public.

ERPG

- 1 is the maximum level below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing other than mild, transient adverse health effects.

ERPG

- 2 is the maximum exposure below which it is believed that nearly a ll 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.

The facility

- wide MIR and TOSHI, available i n Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility

- wide assessment are summarized in Table 7 .2

- 3 . The results indicate that eight

facilities with PET produc tion 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 9

in a million , and it occurs at two facilit ies . At one of these facilit ies , the source category

contr ibutes less than ten percent to the facility

- wide MIR, which is driven by emissions of arsenic and chromium from hazardous waste incineration. At the other facility, the PET production source category contributes almost 100 percent to the facility

- wide MI R, which isDraft Risk Assessment for 7 Chemica l Sector Source Categories

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64 driven by emissions of acetaldehyde and 1,4

- dioxane from wastewater treatment operations

. The maximum facility

- wide TOSHI for the source category is 1, driven mainly by emissions

of chlorine from hazardous waste incineration. T he source categ ory contributes approximately five percent to the facility

- wide TOSHI.

Table 7.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

–

Polyethylene Terephthalate Production

Polyethylene Terephthalate

Production Number of Facilities Binne d 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 4 0 0 9

50

- 90% 1 0 0 0 1

10

- 50% 0 1 0 0 1

< 10% 0 1 0 0 1

Total 6 6 0 0 12



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

- Butadiene

Styrene Source Category

8.1 Source Category Description and Results

Methyl m ethacrylate

- 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, equi pment 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 NPRM.

We currently estimate that there are two MBS production facilit ies operating in the U.S. The

data set contains two facilities identified with a MBS production MACT code in the 2005 NEI. The 2005 NEI was updated for this category with more recent data from industry and enhanced quality assurance of facility and emiss ion locations. Both of these facilities are identified as major sources in the NEI.

The emissions for the MBS production source category data set (of two facilities) are

summarized in Table 8.1

- 1

. The total HAP emissions for the source category are approximately five tons per year. Based on these data, the HAP emitted in the largest quantities for these two facilities are: methyl methacrylate, 1,3

- butadiene, ethyl acrylate,Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

65 methanol, and styrene. T hese five HAP account for over 99 percent of the to tal emissions by

mass. No PB

- HA P 49 are reported in the data set for the MBS production source category

.

Table 8.1

- 1 Summary of Emissions from the Methyl Methacrylate

- Butadiene

- Styrene Production

Source Category and Availability of Dose

- Response Valu es

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

Benchmar k

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 identif ied 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 ass essment 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 a lso 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 the maximum cancer risk or maximum

hazard index at t he 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 M A CT standards. A detailed summary of the facility

- specific

risk a ssessment results is available in Appendix 4

.

Table 8.2

- 1 summarizes the chronic and acute inhalation risk results for this source category. The results indicate that maximum lifetime individual cancer risks could be as high as 0.4 in a million, with 1,3

- butadiene as the major contributor to the risk. The total estimated cancer incidence from the source category is 0.00003 excess cancer cases per year or one case in every 33,000 years. There are no people with an estimated cancer risk greater than 1 in a million. The maximum chronic noncancer TOSHI value for the source category could be up to 0.007 from emissions of 1,3

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

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

EPA

- 453K

- 04

- 001A, as referenced in the EPA’s Technology Transfer Network website for Fate, Exposure, and

Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html

.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

66 Worst

- case acute HQs were calculated f or every HAP that has an acute benchmark

. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries. Analysis of potential

off

- site acute impacts for this sourc e category identified one facility with the potential to

exceed the acute ERPG

- 1 value for ethyl acrylate. Table 8.2

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

After these refine ments, t he highest worst

- case acute HQ value is 9 (based on the ethyl acrylate ERPG

- 1). Th is 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

recogn ition threshold, while the AEGL

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

- case exposure level, a person might smell the pollutant, but not experience any eye irritation.

All other HAP emissio ns 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 expo sure estimates and to consider the results along with the rather large uncertainties related to the emissions estimates and screening methodology.

Upon further evaluation, we identified that at the facility with the highest HQ values ( based

on the ERPG

- 1) equipment leaks were primarily responsible for the high acute HQ values, and that they were modeled assuming that they all emanate from a single emission location, rather than from numerous physical locations throughout the processing area. We note th at 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 indi cate only the potential for acute impacts of concern, while the uncertainties and bias associated with them suggest that there may be no real acute issues at all.

A screening

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

PB

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

- HAP are emitted

.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

67 Table 8.2

- 1 Summary of Source Category Level Risks for Methyl Methacrylate

Butadiene

- Styrene Production

Result HAP “Drivers”
Facilities in Source Category

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

Number of Facilities Identified in NEI and

Modeled in Preliminary Risk Assessment 2 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 0.4 1,3

- butadiene

Number of Facilities w ith Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1

million 0 n/a

Greater than or equal to 10 in 1

million 0 n/a

Greater than or equal to 1 in 1 million 0 n/a

Chronic Noncancer Risks

Maximum Reproductive Hazard Index 0.00 7 1,3

- butadiene Number of Facilities with Maximum Reproductive Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Refined Screening Results

Maximum Acute Hazard Quotient 9

0.0 1 ethyl acrylate (ERPG

- 1)

ethyl acrylate (AEGL

- 1 )

Number of Facilities Wit h Potential for Acute

Effects 1 ethyl acrylate

Population Exposure Number of People Living Within 50

Kilometers of Facilities Modeled 1,600,000 n/a

Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1

million 0 n/a

Greater tha n or equal to 10 in 1

million 0 n/a

Greater than or equal to 1 in 1 million 0 n/a Number of People Exposed to Noncancer Reproductive Hazard Index:

Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.00003 n/a

Contributio n of HAP to Cancer Incidence
1,3

- butadiene 100% n/aDraft Risk Assessment for 7 Chemica l Sector Source Categories

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68 Table 8 .2

- 2 Summary of Acute Refined Screening Results for Methyl Methacrylate

- Butadiene

Styrene Production Facilities

Results MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE

- RESPONSE VALUES

Based on REL Based on

AEGL

- 1/

ERPG

- 1 Based on

AEGL

- 2/

ERPG

- 2 REL

(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/ 9 0. 002/ 0.0 03 34 0.041 150 120

Notes on Refi ned 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 d ose

- 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 popu lation, including susceptible individuals, could experience effects t hat 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, includ ing 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 pub lic.

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.

The facility

- wide MIR and TOSHI, a vailable in Appendix 4 , are based on emissions, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility

- wide assessment are summarized in Table 8.2

- 3 . The results indicate that one facility

with MBS production processes has a facility

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

- wide cancer MIR for the source category is 2 in a million

, driven by emissions of acrylonitrile from a source without a MACT code assigned to it in the

NEI. T he source category does not contribute to the facility

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

- response values

. At the other facility, with a facility

- wide cancer MIR of 0.4 in a million, the f acility

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

- butadiene from equipme nt leaks from the MBS process. The maximum facility

- wide TOSHI for the source category is less than 1.

Table 8.2

- 3 Source Category Contribution to Facili ty

- Wide Cancer Risks

– Methyl

Methacrylate

- Butadiene

- Styrene Production

Methyl Methacrylate

- Butadiene

Styrene Production Number of Facilities Binned by Facility

- Wide MIR (in 1 million) Source Category MIR Contribution to Facility

- Wide MIR < 1 1≤

MIR<10 10≤

MIR<100 > 100 Total

> 90% 1 0 0 0 1Draft Risk Assessment for 7 Chemica l Sector Source Categories

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69

50

- 90% 0 0 0 0 0

10

- 50% 0 0 0 0 0

< 10% 0 1 0 0 1

Total 1 1 0 0 2



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

- Butadiene

- Styrene Source Category

9.1 

### Source Category Description and Results

Acrylonitrile

- butadien e

- styrene ( ABS ) resins consist of a terpolymer of acrylonitrile, butadiene, and styrene and can be synthesized by emulsion, suspension, and continuous mass polymerization. The majority of ABS resin production is by batch emulsion. In emulsion polymerizati on, monomers are dispersed in water using a soap solution or an emulsifier. The emulsion process involves three distinct polymerizations: polymerization 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, susp ending agents, salts or waters. The primary HAP emissions during the ABS production process occur via equipment leaks and process vents. Typical products made from ABS resins are piping, refrigerator door liners and food compartments, automotive components , telephones, luggage and cases, toy s, mobile homes, and margarine t ubs

. A complete description of the acrylonitrile

- butadiene

- styrene production source category can be found in the text of the

NPRM.

We currently estimate that there are five acrylonitrile

- butadiene

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

butadiene

- styrene production MACT code in the 2005 NEI

. The 2005 NEI was updated for this category with more recent data f rom industry and enhanced quality assurance of facility and emission locations. All 5 of these facilities are identified as major sources in the NEI.

The emissions for the acrylonitrile

- butadiene

- styrene production source category data set (of

five fa cilities) are summarized in Table 9.1

- 1 . The total HAP emissions for the source category are approximately 200 tons per year. Based on these data, the HAP emitted in the largest quantities across these five facilities are: styrene, acrylonitrile, 1,3

- buta diene, cumene, methyl methacrylate, and xylenes (mixed). These six HAP account for over 90 percent of the total emissions by mass. No PB

- HA P 50 are reported in the data set for the acrylonitrile

butadiene

- styrene production source category.

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

EPA

- 453K

- 04

- 001A, as referenced in the NPRM and provided on the EPA’s Technology Transfer Network website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html

.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

70 Table 9. 1

- 1 Summary of Emissions from the Acrylonitrile

- Butadiene

- Styrene Production Source Category and Avai lability of Dose

- Response Values

HAP a Emissions (tpy) Number of

Facilities Reporting HAP (5 facilities in data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

- HAP? Unit Risk

Estimate for

Cancer? Reference

Concentration

for Chronic

Noncancer? Health

Benchmark

Values for Acute

Noncancer?
Styrene 92 4
Acrylonitrile 32 5

1,3

- Butadiene 32 5

Cumene 14 4
Methyl Methacrylate 11 3 Xylenes (Mixture of o, m, and p Isomers) 10 2
Ethyl Benzene 7 4

Aniline 2 1
Ethylene Glycol 2 1
Triethylamine 0.9 1
Propylene Oxide 0.8 1
Acrylic Acid 0.7 2
Chloromethyl Me thyl Ether 0.5 1
Acetaldehyde 0.5 1

o

- Xylene 0.3 1
Vinyl Acetate 0.2 1

2,4

- Dichlorophenoxy Acetic Acid 0.03 1

Chloroacetic Acid 0.02 1
Glycol Ethers 0.02 1
Ethyl Acrylate 0.01 1

2,4,6

- Trichlorophenol 0.00 7 1

N,N

- Dimethylformamide 0.004 1
Phosgene 0.003 1
Hydroquinone 0.002 1
Naphthalene 0.002 1
Ethylene Oxide 0 1

a Notes for how HAP were speciated for risk assessment: For emissions reported generically as ―Glycol E thers‖ 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 Technolog y Transfer Network website for air

toxics at http://www.epa.gov/ttn/atw/toxsource/summary.html

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71 9.2 

### Risk Characterization

This section presents the results of the risk assessment for the acr ylonitrile

- 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 fro m 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 the maximum cancer risk or maximum hazard index at the highest exposure loca tion , 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 ava ilable in Appendix 4

.

Table s 9.2

- 1 and 9.2

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

category. The results indicate that maximum individual lifetime cancer risks could be as high as 30 in a million, with acrylonitrile and 1,3

- butadiene as the major contributors to the risk. The total estimated cancer incidence from the source category is 0.003 excess cancer cases per year, or one case in every 333 years. Approximately 530 people are estimated to have

cancer risks at or above 10 in a million and approximately 32,000 people are estimated to

have cancer risks at or above 1 in a million as a result of the emissions from 4 facilities. The maximum chronic noncancer TOSHI value for the source category could be up to 0.2 fro m emissions of 1,3

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

Worst

- case a cute HQs were calculated f or every HAP that has an acute benchmark, and the highest acute HQ value of 2 (based on the acetaldehyde REL) is show n in Table 9.2

- 1. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries. Table 9.2

- 1 provides

more information on the acute risk estimates for HA P that had an acute HQ greater than 1 for any benchmark. The highest refined worst

- case acute HQ value remains 2 based on the acetaldehyde REL , with only one facility showing the potential to exceed the REL . Th is

estimated worst

- case acute impact corresp ond s to an acute HQ of 0. 0 4 based on the

a cetaldehyde ERPG

- 1. Refer to Table 9.2

- 2 for further information on the refined acute risk

estimate.

All other HAP emissions at all other facilities indicated no potential to cause acute impacts of

concern. Whil e these estimated worst

- case exceedances indicate that there is some potential for such acute exposures to occur, we note that exceeding the modeled REL or ERPG

- 1 values does not necessarily indicate that adverse effects will occur, only that they cannot b e ruled out. Further, in characterizing the potential for acute noncancer impacts of concern, it is important to remember the upward bias of these worst

- case exposure estimates and to consider the results along with the rather large uncertainties related to the emissions estimates and screening methodology.

A screening

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

PB

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

- HAP are emitted.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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72 Table 9.2

- 1 Summa ry of Source Category Level Risks for Acrylonitrile

- Butadiene

Styrene Production

Result HAP “Drivers”
Facilities in Source Category

Number of Facilities Estimated to be i n Source Category 5 n/a

Number of Facilities Identified in NEI and

Modeled in Pr eliminary Risk Assessment 5 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 30 acrylonitrile, 1,3

- butadiene

Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1

million 0 n/a

Gr eater than or equal to 10 in 1

million 3 acrylonitrile, 1,3

- butadiene

Greater than or equal to 1 in 1 million 4 acrylonitrile, 1,3

- butadiene, ethyl

benzene

Chronic Noncancer Risks

Maximum Reproductive Hazard Index 0.2 1,3

- butadiene Number of Facilitie s with Maximum Reproductive Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Screening Results

Maximum Acute Hazard Quotient 2

0. 0 4 acetaldehyde (REL)

acetaldehyde (ERPG

- 1)

Number of Facilities With Potential for Acute

Effects 1 acetaldehyde

Popu lation Exposure Number of People Living Within 50

Kilometers of Facilities Modeled 3,900,000 n/a

Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1

million 0 n/a

Greater than or equal to 10 in 1

million 530 n/a

Greater than or equal to 1 in 1 million 32,000 n/a Number of People Exposed to Noncancer Reproductive Hazard Index:

Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.003 n/a

Contribution of HAP to Cancer Incidence acrylonitrile 66% n/a
1,3

- butadiene 32% n/aDraft Risk Assessment for 7 Chemica l Sector Source Categories

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73 Table 9.2

- 2 Summary of Acute Screening Results for Acrylonitrile

- Butadiene

- Styrene

Production

Results MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE

- RESPONSE VALUES

Based on REL Based on

AEGL

- 1/

ERPG

- 1 Based on

AEGL

- 2/

ERPG

- 2 REL

(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 )

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

Notes on Screening Process: 1) The screening was performed fo r 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 ta ble 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 ar e 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, co uld 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 or an impaired ability

to escape.
ERPG

– Emergency Removal Program guidelines represent emergency exposure (1

- hour) limits for the general public.

ERPG

- 1 is the maximum level below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing other than mild, transient adverse health effects.

ERPG

- 2 is the maximum exposure below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual’s ability to take protective ac tion.

The facility

- wide MIR and TOSHI, available in Appendix 4 , are based on emission s, as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility

- wide assessment are summarized in Table 9.2

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

- wide cancer 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, with the source category contributing almost 100 percent of the facility

- wide risk, driven by emissions of acrylonitrile a nd 1,3

- butadiene from process vents. The maximum facility

- wide TOSHI for the source category is less than 1.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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74 Table 9.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

–

Acrylonitrile

- Butadiene

- Styrene Production

Acrylonitrile

- B utadiene

- Styrene

Production Number of Facilities Binned by Facility

- Wide MIR (in 1 million) Source Category MIR Contribution to Facility

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

> 90% 0 0 3 0 3

50

- 90% 0 0 1 0 1

10

- 50% 1 0 0 0 1

< 10% 0 0 0 0 0

Total 1 0 4 0 5



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

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 uncertainties in our exposure

mod eling 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 meteorology. 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 the maximum individual risk ( MIR) contain uncertainty , because they are deriv ed at census block centroid locations rather than actual

residences. This uncertainty is known to create potential underestimates and overestimates of the actual MIR values for individual facilities, but, ov erall, 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 p erformed 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 than 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.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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75 We have purposely biased the acute screening results high, co nsidering 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 scientifically acceptable we h ave 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 thresholds, we have refined o ur 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 f

ollow, 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 chroni c exposures (up to a lifetime), bu t may also be derived for acute (

- term (>24 hours up to 30 days), and subchronic (>30 days up to 10% of lifetime) exposure durations, all of which are derived based on an assumption of continuous exposure throughout the duration specified. For the purposes of assessing all potential health risks associated wit h the

emissions included in an assessment, we rely on both chronic (cancer and noncancer) and acute ( noncancer ) benchmarks, which are described in m ore detail below.

Although every effort is made to identify peer

- review ed dose

- response values for all HAPs

emitted by the sources included in an assessment, some HAP have no peer

- reviewed cancer potency values or reference values for chronic non

- cancer o r 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

- res ponse 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 result of these

revi ews, 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 focuses

on the unce rtainties 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 factor s 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 p rotection 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 healthDraft Risk Assessment for 7 Chemica l Sector Source Categories

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76 protective.‖ The approach adopted in this document is cons istent 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

develo ping cancer given long

- term exposures to the pollutant. Depending on the pollutant being evaluated, EPA relies on both animal bioassay and epidemiological studies to characterize cancer risk. As a science policy approach, consistent with the Cancer

Guide lines , 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 s cientific 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 estimate s developed following the procedures described in the Cancer Guidelines and outlined below generally provide an upper bound estimate of risk. That is, EPA’s upper bound estimates represent a ―plausible upper limit to the true value of a quantity‖ (althoug h this is usually not a true statistical confidence limit). 51 In some circumstances, the true risk could be as low as zero; however, in other circumstances the risk could also be greater. 52
When developing an upper bound estimate of risk and to provide ri sk values that do not underestimate risk, EPA generally relies on conservative default approaches. 53 EPA also uses the upper bound (rather than lower bound or central) estimates in its assessments, although it is noted that this approach can have limitatio ns 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 actua l biological processes for

the assessed substance. EPA’s Risk Characterization Handbook also recommends that risk characterizations present estimates demonstrating the impact on the assessment of alternative

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

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

53 According to the NRC report Science and Judgment in Risk Assessment (NRC, 1994) ―[Default] options are generic approaches, based on 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). 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 ch emicals is not underestimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An Examination of EPA Risk Assessment Principles and Practices,

EPA/100/B

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

- final.pdf.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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77 choices, data, models and assumptions [ 31 ]. Som e 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. 54 However, unless scientific support is available to show otherwise, EPA assumes that tumors in animals are relevant in humans, regardless of target organ concordance. For a specific pollutant, qualitative differences in species responses can

lead to either under

- es timation or over

- estimation of human cancer risks.

(2) Uncertainties regarding the most appropriate dose metric for an assessment can also lead

to differences in risk estimates . For example, the measure of dose is commonly expressed in units of mg/kg/d ingested or the inhaled concentration of the pollutant. However, data may support development of a pharmacokinetic model for the absorption, distribution, metabolism and excretion of an agent, which may result in improved dose metrics (e.g., average bloo d 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 either over or underestimation of risk.

(3) For the quantitative extrapolation of cancer risk estimates from experimental animals to humans, EPA uses scaling methodologies (relating expected response to differences in physical size of the species), which introduce another source of uncertainty. These methodologies are based on both biological data on differences in rates of process according

to sp ecies size and empirical comparisons of toxicity between experimental animals and humans. For a particular pollutant, the quantitative difference in cancer potency between experimental animals and humans may be either greater than or less than that estima ted by baseline scientific scaling predictions due to uncertainties associated with limitations in the

test data and the correctness of scaled estimates.

(4) EPA cancer risk estimates, whether based on epidemiological or experimental animal data,

are ge nerally 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 dose at which the specified excess risk occurs (the BMDL), decreasing the likelihood of understating risk. EPA has generally utilized the multistage model for estimation of the BMDL using cancer bioassay data (see further discussion below).

54 Per t he EPA Cancer Guidelines: ―The default option is that positive effects in animal cancer studies indicate that the agent under study can have carcinogenic potential in humans.‖ and ―Target organ concordance is not a prerequisite for evaluating the implicat ions of animal study results for humans.‖Draft Risk Assessment for 7 Chemica l Sector Source Categories

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78 (5) Extrapolation from high to low doses is an important, and potentially large, source of uncertainty in cancer risk assessment. EPA uses different a pproaches to low dose risk assessment (i.e., developing estimates of risk for exposures to environmental doses of an agent from observations in experimental or epidemiological studies at higher dose) depending on the available data and understanding of a p ollutant’s mode of action (i.e., the manner in which a pollutant causes cancer). EPA’s Cancer Guidelines express a preference for the use of reliable, compound

- specific, biologically

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

for low

- dose exposure. A reference value is calculated when the available mode of action

data show the response to be nonlinear (e.g., as in a threshold response). A linear low

- dose (straight line from POD) approach is used when available mode of action data support a linear (e.g., nonthreshold response) or as the most common default approach whe n a compound’s mode of action is unknown. Linear extrapolation can be supported by both pollutant

- specific data and broader scientific considerations. For example, EPA’s Cancer Guidelines generally

consider a linear dose

- response to be appropriate for po llutants that interact with DNA and induce mutations. Pollutants whose effects are additive to background biological processes in cancer development can also be predicted to have low

- dose linear responses, although the slope of this relationship may not b e the same as the slope estimated by the straight line approach.

EPA most frequently utilizes a linear low

- dose extrapolation approach as a baseline science

policy choice (a ―default‖) when available data do not allow a compound

- specific

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

- response models, when appropriately applied as part of EPA’s cancer risk assessment process, provide an upper bound estimate of risk and 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 populations. Another National Research Council (NRC) report [ 32 ] suggests that

models based on distributions of individual thre sholds 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, c oincident exposures, nutritional status, and various other susceptibility factors...‖ Thus, if a distribution of thresholds approach is considered for a carcinogen risk assessment, application would depend on ability of modeling to reflect the degree of variability in response in human populations (as opposed to responses in bioassays with genetically more uniform rodents). Note also that low dose linearity in risk can arise for reasons separate from population variability: due to the nature of a mode of action and additivity of a chemical’s effect on top of background chemical exposures and biological

processes.

As noted above, EPA’s current 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 lineDraft Risk Assessment for 7 Chemica l Sector Source Categories

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79 risk estimates can be quantified by comparing risk estimates using the BMDL value to central estimate BMD values, alth ough these differences are generally not a large contributor to uncertainty in risk assessment (Subramaniam et. al., 2006) [ 33 ]. It is important to note that earlier EPA assessments, including the majority of those for which risk values exist today,

were g enerally developed using the multistage model to extrapolate down to environmental dose levels and did not involve the use of a POD. Subramaniam et. al. (2006) also provide comparisons indicating that slopes based on straight line extrapolation from a POD do not show large differences from those based on the upper confidence limit of the multistage

model.

(6) Cancer risk estimates do not generally make specific adjustments to reflect the variability in response within the human population

— resulting in a nother 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 gene rally 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 a ssessments do not generally quantitatively address life stage differences. However, one approach used commonly in EPA assessments that may help address variability in response is to extrapolate human response from results observed in the most sensitive

sp ecies and sex tested, resulting typically in the highest URE which can be supported by reliable data, thus supporting estimates that are designed not to underestimate risk in the face of uncertainty and variability.

Chronic noncancer assessment

Chronic n oncancer reference values represent chronic exposure levels that are intended to be

health

- protective. That is, EPA and other organizations which develop noncancer reference values (e.g., the Agency for Toxic Substances and Disease Registry

– ATSDR) utiliz e an approach that is intended not to underestimate risk in the face of uncertainty and variability. When there are gaps in the available information, uncertainty factors (UFs) are applied to derive reference values that are intended to be protective agai nst appreciable risk of

deleterious effects . Uncertainty factors are commonly default values 55 e.g., factors of 10 or 3, used in the absence of compound

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

- speci fic information. When data are limited, more

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

e lements of the risk

- assessment process when the correct scientific model is unknown or uncertain.‖ The 1983 NRC report Risk Assessment in the Federal Government: Managing the Process defined default option as ―the option chosen on the basis of risk assess ment policy that appears to be the best choice in the absence of data to the contrary‖ (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the agency may depart from them in evaluating the risks posed by a specific s ubstance when it believes this to be appropriate. In keeping with EPA’s goal of protecting public health and the environment, default assumptions are used to ensure that risk to chemicals is not underestimated (although defaults are not intended to overtl y overestimate risk). See EPA 2004 An examination of EPA Risk Assessment Principles and Practices,

EPA/100/B

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

- final.pdf.Draft Risk Assessment for 7 Chemica l Sector Source Categories

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80 assumptions are needed and more default factors are used. Thus there may be a greater tendency to overestimate risk

— in the sense that further study might support development of reference values that are higher (i.e., less potent) because fewer default assumptions are needed. However, for some pollutants it is possible that risks may be underestimated.

For non

- cancer endpoints related to chronic exposures, EPA derives a Reference Dose (RfD) for exposures via i ngestion and a Reference Concentration (RfC) for inhalation exposures.

These values provide an estimate (with uncertainty spanning perhaps an order of magnitude)

of a daily oral exposure (RfD) or a continuous inhalation exposure (RfC) to the human populat ion (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. 56 To derive values that are intended to be ―without appreciable risk,‖ EPA’s methodology relies upon an uncertainty factor (UF) a pproach
[ 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 using statistical modeling of the available data, and then determines the appropriate point of departure (POD) for derivation of the reference value. A POD is determined by (in order of preference): (1) a statistical estimation using the benchmark dose (BMD) approach; (2) use of the dose or concentration at which the toxic response was not significantly elevated (no

observed adverse effect level

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

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

the reference value [ 36 ] . While collectively termed ―UFs‖, these factors account for a

number of different quantitative considerations when utilizing observed animal (usually rodent) or human toxicity data in a risk assessment. The UFs are intended to account for: (1) variation in susceptibility among the members of the human population (i.e., inter

- individual variability); (2) uncertainty in extrapolating from experimental animal data to humans (i.e., interspecies differences); (3) uncertainty in extrapolating from data obtained in a study with

less

- than

- lifetime exposure (i.e., extrapolating from s ubchronic 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 there are problems with applicability of available studies

. When scientifically sound, peer

- rev iewed 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 lead ing 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 dat a 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 h uman variation is considered in extrapolating doses from a subset or

56 See IRIS glossaryDraft Risk Assessment for 7 Chemica l Sector Source Categories

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81 smaller

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

po llutant

- 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; however, data to examine the potential magnitude of human variability are often unavailabl e. 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 ass essments . When interpreting animal data, the concentration at the POD (e.g. NOAEL, BMDL) in an animal model (e.g. rodents) is extrapolated to estimate the human response. While there is long

- standing scientific support

for the use of animal studies as in dicators of potential toxicity to humans , there are uncertainties in such extrapolations. In the absence of data to the contrary, the typical approach is to use the most relevant endpoint from the most sensitive species and the most

sensitive sex in asses sing risks to the average human. Typically

, compound specific data to evaluate relative sensitivity in humans versus rodents are lacking, thus leading to uncertainty in this extrapolation. Size

- related differences (allometric relationships) indicate that typically humans are more sensitive than rodents when compared on a mg/kg/day basis. The default choice of 10 for the interspecies UF is consistent with these differences. For a s pecific chemical, differences in species responses may be greater or less than this value

.

Pharmacokinetic models are useful to examine species differences in pharmacokinetic processing and associated uncertainties; however, such dosimetric adjustments are not 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 unc ertainty in extrapolating from laboratory animals to humans in the derivation of a reference value. If information on one or the other of these components is available and accounted for in the cross

- species extrapolation, a UF of 3 may be used for the rem aining 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 addit ional UF of 3 or 10

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

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

- fold is often applied.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

82 5) The database UF is intended to account for the potential for deriving an underprotective RfD/RfC due to a data gap preventing complete character ization 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 typically applied.

Acute noncancer assessment

Many of the UFs used to account for variability and uncertainty in the deve lopment of acute reference values are quite similar to those developed for chronic durations, but more often using individual UF values that may be less than 10. UFs are applied based on chemical

specific or health effect

- specific information (e.g., simpl e 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) uncertainty in accounting for an incomplete database on toxic effects of potential concern. Additional adjustments are often applied to account for uncertainty in extrapolation from observations at one exposure duration (e.g., 4 hours) to arrive at a POD for derivation of an acute reference value at another exposure duration (e.g., 1 hour).

Not all acute reference valu es are developed for the same purpose and care must be taken when interpreting the results of an acute assessment of human health effects relative to the reference value or values being exceeded. W here relevant to the estimated exposures, the

lack of thre shold values at different levels of severity should be factored into the risk characterization as potential uncertainties.Draft Risk Assessment for 7 Chemica l Sector Source Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

83 

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