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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 Terephthalate

Polymers and Resins IV -- Methyl Methacrylate-Butadiene Styrene

Polymers and Resins IV -- Acrylic Butadiene Styrene

by

EPA’s Office of Air Quality Planning and Standards

Office of Air and Radiation

November 2011
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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 Acrylonitrile 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 Methacrylate-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................................ 8
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Table 2.6-1 (a) Dose-Response Values for Chronic Inhalation Exposure to Carcinogens.... 18

Table 2.6-1 (b) Dose-Response Values for Chronic Inhalation Exposure to Noncarcinogens

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

Table 2.6-2 Dose-Response Values for Acute Exposure........................................................ 27

Table 3.1-1 Summary of Emissions from the Pesticide Active Ingredients Source 

Category and Availability of Dose-Response Values.............................................................. 33

Table 3.2-1 Summary of Source Category Level Risks for Pesticide Active Ingredient 

Production 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 Cancer 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 Polyether 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 for Styrene-Acrylonitrile 

Production 52

Table 5.2-2 Source Category Contribution to Facility-Wide Cancer Risks – StyreneAcrylonitrile 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 Polyethylene 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 MethacrylateButadiene-Styrene Production ................................................................................................. 67

Table 8.2-2 Summary of Acute Refined Results for Methyl Methacrylate-ButadieneStyrene Production Facilities................................................................................................... 68
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Table 8.2-3 Source Category Contribution to Facility-Wide Cancer Risks – Methyl

Methacrylate-Butadiene-Styrene Production........................................................................... 68

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-ButadieneStyrene 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 – AcrylonitrileButadiene-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 

rates

Appendix 4 Detailed Risk Modeling Results

Appendix 5 Technical Support Document for TRIM-Based Multipathway Screening 

Scenario for RTR: Summary of Approach and Evaluation

Appendix 6 Acute Impacts Refined Analysis 

Appendix 7 Dispersion Model Receptor Revisions and Additions

Index of Acronyms

AERMOD American Meteorological Society/EPA Regulatory Model

AEGL Acute exposure guideline level

ASTDR US Agency for Toxic Substances and Disease Registry

CalEPA California Environmental Agency

ERPG Emergency Response Planning Guideline

HAP Hazardous Air Pollutant

HEM Human Exposure Model

HI Hazard index

HQ Hazard quotient

IRIS Integrated Risk Information System

MACT Maximum Achievable Control Technology

MIR Maximum Individual Risk

MOA Mode of action

NAC National Advisory Committee

NATA National Air Toxics Assessment

NEI National Emissions Inventory

NPRM Notice of Proposed Rulemaking

PB-HAP Persistent and Bioaccumulative - HAP

POM Polycyclic organic matter
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REL Reference exposure level

RfC Reference concentration

RfD Reference dose

RTR Risk and Technology

TOSHI Target-organ-specific hazard index

URE Unit risk estimate
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1. Introduction

Section 112 of the Clean Air Act (CAA) establishes a two-stage regulatory process for 

addressing emissions of hazardous air pollutants (HAPs) from stationary sources. In the first 

stage, section 112(d) requires the Environmental Protection Agency (EPA, or the Agency) to 

develop technology-based standards for categories of sources (e.g., petroleum refineries, pulp 

and paper mills, etc.) [1]. EPA has largely completed the initial Maximum Achievable 

Control Technology (MACT) standards as required under this provision. Under section 

112(d)(6), EPA must review each of these technology-based standards at least every eight 

years and revise a standard, as necessary, “taking into account developments in practices, 

processes and control technologies.” In the second stage, EPA is required under section 

112(f)(2) to assess the health and environmental risks that remain after implementation of the 

MACT standards. If additional risk reductions are necessary to protect public health with an 

ample margin of safety or to prevent an adverse environmental effect, EPA must develop 

standards to address these remaining risks. This second stage of the regulatory process is 

known as the residual risk stage. For each source category for which EPA issued MACT 

standards, the residual risk stage must be completed within eight years of promulgation of the 

initial technology-based standard.

In December of 2006 we consulted with a panel from the EPA's Science Advisory Board 

(SAB) on the “Risk and Technology Review (RTR) Assessment Plan” and in June of 2007, 

we received a letter with the results of that consultation. Subsequent to the consultation, in 

July of 2009 a meeting was held with an SAB panel for a formal peer review of the “Risk and 

Technology Review (RTR) Assessment Methodologies” [2]. We received the final SAB 

report on this review in May of 2010 [3]. Where appropriate, we have responded to the key

messages from this review in developing our current risk assessments and we will be 

continuing our efforts to improve our assessments by incorporating updates based on the SAB 

recommendations as they are developed and become available. Our responses to the key

recommendations of the SAB are outlined in the memo entitled, “EPA’s Actions in Response 

to Key Recommendations from the SAB Review of RTR Risk Assessment Methodologies” 

[4].

This document contains the methods and the results of baseline risk assessments (i.e., after the 

implementation of the respective MACT standards) performed for seven chemical industry

source categories. Five of the source categories were 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 Acrylonitrile,

Polymers and Resins IV-- Polystyrene,

Polymers and Resins IV-- Polyethylene Terephthalate,

Polymers and Resins IV-- Methyl Methacrylate-Butadiene Styrene, and

Polymers and Resins IV-- Acrylic Butadiene Styrene.

The methods discussion includes descriptions of the methods used to develop refined 

estimates of chronic inhalation exposures and human health risks for cancer and noncancer 
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endpoints, as well as descriptions of the methods used to screen for acute health risks, chronic 

non-inhalation health risks, and adverse environmental effects. Since the screening 

assessments indicated low potential for chronic non-inhalation health effects or environmental 

impacts, including effects to threatened and endangered species, no further refinement of 

these assessments was performed.

2. Methods

2.1. Emissions and source data

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

Toxics Assessment (NATA)1served as the starting point for these 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 contains facility, process, and 

emissions data for each facility in these seven source categories. Next, we performed an 

engineering review of the information using EPA engineers who were directly involved in the 

development of the MACT standards for these source categories, and/or who have extensive 

knowledge of the characteristics of this industry. The goal of the engineering review was to 

identify 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 facility

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 the 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 exposure 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 modeling system. The approach used in applying this 

modeling system is outlined below, and further details are provided in Appendix 1. The 

HEM3 performs three main operations: atmospheric dispersion modeling, estimation of 

individual human exposures and health risks, and estimation of population risks. 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 attributable to the MACT program. The 

NEI associates MACT codes corresponding to MACT source categories with stationary major and area source 

data.
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The dispersion model in the HEM3 system, AERMOD version 11103, is a state-of-thescience Gaussian plume dispersion model that is preferred by EPA for modeling point, area, 

and volume sources of continuous air emissions from facility applications [5]. Further details 

on AERMOD can be found in the AERMOD Users Guide [6]. The model is used to develop 

annual average ambient concentrations through the simulation of hour-by-hour dispersion 

from the emission sources into the surrounding atmosphere. Hourly emission rates used for 

this simulation are generated by 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 model options for RTR modeling

Modeling Option Selected Parameter for chronic exposure

Type of calculations Hourly Ambient Concentration

Source type Point, area represented as pseudo point source

Receptor orientation Polar (13 rings and 16 radials)

Discrete (census block centroids) and user-supplied receptors

Terrain characterization Actual from USGS 1-degree DEM data

Building downwash Not Included

Plume deposition/depletion Not Included

Urban source option No

Meteorology 1 year representative NWS from nearest site (over 200 

stations)

In HEM3, meteorological data are ordinarily selected from a list of over 200 National 

Weather Service (NWS) surface observation stations across the continental United States, 

Alaska, Hawaii, and Puerto Rico. In most cases the nearest station is selected as 

representative of the conditions at the subject facility. 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 number 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 facility 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 and 
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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 ambient concentrations at the geographic centroids of census

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

user. The model accounts for the effects of multiple facilities when estimating concentration 

impacts at each block centroid. Typically we combined only the impacts of facilities within 

the same source category, and assessed chronic exposure and risk only for census blocks with 

at least one resident (i.e., locations where people may reasonably be assumed to reside rather 

than receptor points at the fenceline of a 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 currently uninhabited areas was not 

considered. Census blocks, the finest resolution available in the census data, are typically 

comprised of approximately 40 people or about ten households. For each facility in these 

source categories census block locations were carefully evaluated for proximity to each 

facility’s property line (see Appendix 7). 

In contrast to the development of ambient concentrations for evaluating long-term exposures, 

which was performed only for occupied census blocks, worst-case short-term (one-hour) 

concentrations were estimated both at the census block centroids and at 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 facility (note that for large facilities, this 

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

emission rates were needed to screen for the potential for hazard via acute exposures, and 

since the NEI contains only annual emission totals, we generally apply the assumption to all 

source categories that the maximum one-hour emission rate from any source is ten times the 

average annual hourly emission rate for that source.3

The average hourly emissions rate is defined as the total emissions for a year divided by the 

total number of operating hours in the 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 based on an engineering judgment. To develop a more robust peak-tomean emissions factor, and in response to one of the key messages from the SAB consultation 

on our RTR Assessment Plan, we performed an analysis using a short-term emissions dataset

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

that report, the Texas Environmental Research Consortium Project compared hourly and 

annual emissions data for volatile organic compounds for all facilities in a heavilyindustrialized 4-county area (Harris, Galveston, Chambers, and Brazoria Counties, TX) over 

an eleven-month time period in 2001. We obtained the dataset and performed our own 

analysis, focusing that analysis on sources which reported emitting high quantities of HAP 

over short periods of time (see Appendix 3, “Analysis of data on short-term 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 risks.
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annual average, the highest was a factor of 74 times the annual average, and the 99th

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 applied 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 this level, our analysis of the data from the Texas Environmental 

Research Consortium suggests that these factors should cover more than 99% of the shortterm peak gaseous or volatile HAP emissions from typical industrial sources. We have no 

data relating specifically to peak short-term emissions of particulate HAP. In the absence of 

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

well. A list of facilities where we used the factor of two instead of ten is provided in 

Appendix 6.

 

Census block elevations for HEM3 modeling were determined nationally from the US 

Geological Survey 1-degree digital elevation model (DEM) data files, which have a spatial 

resolution of about 90 meters. Elevations of polar grid points used in estimating short- and 

long-term ambient concentrations were assumed to be equal to the highest elevation of any

census block falling within the polar grid sector corresponding to the grid point. If a sector 

does not contain any blocks, the model defaults the elevation to that of the nearest block. If 

an elevation is not provided for the emission source, the model uses the average elevation of 

all sectors within the innermost model ring.

In addition to using receptor elevation to determine plume height, AERMOD adjusts the 

plume’s flow if nearby elevated hills are expected to influence the wind patterns. For details 

on how hill heights were estimated and used in the AERMOD modeling, see Appendix 1. 

2.3. Estimating chronic human inhalation exposure

We used the estimated annual average ambient air concentration of each HAP at each census 

block centroid as a surrogate for the lifetime inhalation exposure concentration of all the 

people who reside in the census block. That is, the risk analysis did not consider either the 

short-term or long-term behavior (mobility) of the exposed populations and its potential 

influence on their exposure.

 

We did not address short-term human activity for two reasons. First, our experience with the 

NATA assessments (which modeled daily activity using EPA’s HAPEM model) suggests 

that, given our current understanding of microenvironment concentrations and daily activities, 

modeling short-term activity would, on average, reduce risk estimates about 25% for 

particulate HAPs; it would also reduce risk estimates for gaseous HAPs, but typically by 

much less. Second, basing exposure estimates on average ambient concentrations at census 

block centroids may underestimate or overestimate actual exposure concentrations at some 

residences. Further reducing exposure estimates for the most highly exposed residents by 

modeling their short-term behavior could add a systematic low bias to these results.
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We did not address long-term migration or population growth or decrease over 70 years, and 

instead based the assessment on the assumption that each person’s estimated exposure is 

constant over the course of their lifetime which is assumed to be 70 years. In assessing cancer 

risk, we generally estimated three metrics; the maximum individual risk (MIR), which is 

defined as the risk associated with a lifetime of exposure at the highest concentration; the 

population risk distribution; and the cancer incidence. The decision not to consider short or 

long-term population mobility does not bias the estimate of the theoretical MIR nor does it 

affect the estimate of cancer incidence since the total population number remains the same. It 

does, however, affect the shape of the distribution of individual risks across the affected 

population, shifting it toward higher estimated individual risks at the upper end and reducing 

the number of people estimated to be at lower risks, thereby increasing the estimated number 

of people at specific risk levels. 

When screening for potentially significant acute exposures, we used an estimate of the highest 

hourly ambient concentration at any off-site location as the surrogate for the maximum 

potential acute exposure concentration for any individual.

2.4. Acute Risk Screening and Refined Assessments

In establishing a scientifically defensible approach for the assessment of potential health risks 

due to acute exposures to HAP, we followed 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 Report to Congress” 

in 1999. 

The assessment methodology is designed to eliminate from further consideration those 

facilities for which we have confidence that no acute adverse health effects of concern will 

occur. To do so, we use what is called a tiered, iterative approach to the assessment. This 

means that we begin with a screening assessment, which relies on readily available data and 

uses conservative assumptions that in combination approximate a potential worst-case 

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

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

assessment. A refined assessment could use industry- or site-specific data on the temporal 

pattern of emissions, the layout of emission points at the facility, the boundaries of the 

facility, and/or the local meteorology. In some cases, all of these site-specific data would be 

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

determine that acute exposures are not a concern, and significant additional data collection is

not 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:
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 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 relevant 

health benchmarks, we refine 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 factor of 10). For the source 

categories in this document, we conducted a review of the layout of emission points at the 

facilities with the facility boundaries to determine the maximum off-site acute impact for the 

facilities that did not screen out during the initial model run. Refer to Appendix 6 for the 

detailed results for these sites.

2.5. Multipathway human health and environmental risk screening

The potential for significant human health risks due to exposures via routes other than 

inhalation (i.e., multipathway exposures) was screened by first determining whether any 

sources emitted any hazardous air pollutants known to be persistent and bioaccumulative in 

the environment (PB-HAP) 4. The PB-HAP compounds or compound classes are identified 

for the screening from the EPA’s Air Toxics Risk Assessment Library [8]. Examples of PBHAP are cadmium compounds, chlordane, chlorinated dibenzodioxins and furans, DDE, 

heptachlor, hexachlorobenzene, hexachlorocyclohexane, lead compounds, mercury

compounds, methoxychlor, polychlorinated biphenyls, polycyclic organic matter (POM), 

toxaphene, and trifluralin. There were PB-HAP emissions identified for three of the source 

categories addressed in this risk document. For the polyethylene terephthalate production 

source category, we identified emissions of cadmium compounds, polycyclic organic matter 

(POM), and lead compounds. For the pesticide active ingredient production source category, 

we identified emissions of lead compounds and polychlorinated biphenyls (PCBs). For the 

 

4 Although the two-letter chemical symbol for lead is Pb, in this assessment PB-HAP refers to the many air 

pollutants known to be persistent and bioaccumulative in the 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). 
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polyether 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-developed screening scenario which was developed 

for use with the TRIM.FaTE5 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 combustion 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 the 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 significant 

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

screening, we derived emission levels for each PB-HAP (other than lead) at which the 

maximum human health risk would be 1 in a million for lifetime cancer risk or a hazard 

quotient of 1.0 for noncancer impacts. 

In evaluating the potential multi-pathway risks from emissions of lead compounds, rather than 

developing a screening emission rate for them, we compared maximum estimated chronic 

atmospheric concentrations with the current 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 non 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 developed 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 mammalian receptors should be at no risk of adverse effects due to 

inhalation exposures from non-PB-HAP, and have assurance that other ecological receptors 

are also not at any 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 Hazardous Waste Combustion Facilities;

http://www.epa.gov/epaoswer/hazwaste/combust/riskvol.htm#volume1
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2.6. Dose-Response Assessment

2.6.1. Sources of chronic dose-response information 

Dose-response assessment (carcinogenic and non-carcinogenic) for chronic exposure (either 

by inhalation or ingestion) for the HAPs reported in the emissions inventories for the source

categories in this document were based on the EPA Office of Air Quality Planning and 

Standards’ existing recommendations for HAPs [9], also used for NATA [10]. This 

information has been obtained from various sources and prioritized according to (1) 

conceptual consistency with EPA risk assessment guidelines and (2) level of peer review 

received. The prioritization process was aimed at incorporating into our assessments the best 

available science with respect to dose-response information. The recommendations are based 

on the following sources, in order of priority: 

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

assessments for chronic exposure for many of the pollutants in this study. These 

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 exposure to the human population (including 

sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects 

during a lifetime.” The RfD is “an estimate (with uncertainty spanning perhaps an order 

of magnitude) of a daily oral exposure to the human population (including sensitive 

subgroups) that is likely to be without an appreciable risk of deleterious effects during a 

lifetime.” The URE is defined as “the upper-bound excess cancer risk estimated to result 

from continuous lifetime exposure to an agent at a concentration of 1 μg/m3in air.” The 

SF is “an upper bound, approximating a 95% confidence limit, on the increased cancer 

risk from a lifetime exposure to an agent. This estimate, [is] usually expressed in units of 

proportion (of a population) affected per mg/kg-day...” EPA disseminates dose-response 

assessment information in several forms, based on the level of review. The Integrated 

Risk Information System (IRIS) [11] is an EPA database that contains scientific health 

assessment information, including dose-response information. All IRIS assessments since 

1996 have also undergone independent external peer review. The current IRIS process 

includes review by EPA scientists, interagency reviewers from other federal agencies, and 

the public, and peer review by independent scientists external to EPA. New 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 

scheduling of current individual IRIS assessments and updates 

(http://cfpub.epa.gov/ncea/iristrac/index.cfm). EPA’s science policy approach, under the 

current carcinogen guidelines, is to use linear low-dose extrapolation as a default option 

for carcinogens for which the mode of action (MOA) has not been identified. We expect 

future EPA dose-response assessments to identify nonlinear MOAs where appropriate, 

and we will use those analyses (once they are peer reviewed) in our risk assessments. At 
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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 within 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-specific estimates to be 

used by health assessors to select environmental contaminants for further evaluation. 

Exposures above an MRL do not necessarily represent a threat, and MRLs are therefore 

not intended for use as predictors of adverse health effects or for setting cleanup levels.

3) California Environmental Protection Agency (CalEPA). The CalEPA Office of 

Environmental Health Hazard Assessment has developed dose-response assessments for 

many substances, based both on carcinogenicity and health effects other than cancer. The 

process for developing these assessments is similar to that used by EPA to develop IRIS 

values and incorporates significant external scientific peer review. As cited in the 

CalEPA Technical Support Document for developing their chronic assessments7: “The 

guidelines for developing chronic inhalation exposure levels incorporate many

recommendations of the U.S. EPA [13] and NAS [14].” The non-cancer information 

includes available inhalation health risk guidance values expressed as chronic inhalation 

reference exposure levels (RELs) [15]. CalEPA defines the REL as “the concentration 

level at or below which no health effects are anticipated in the general human population.” 

CalEPA's quantitative dose-response information on carcinogenicity by inhalation 

exposure is expressed in terms of the URE [16], defined similarly to EPA's URE. 

 

In developing chronic risk estimates, we adjusted dose-response values for some HAP based 

on professional judgment, as follows: 

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

conservative dose-response value of the chemical category is used as a surrogate for other 

compounds in the group for which dose-response values are not available. This is done in 

order to examine, under conservative assumptions, whether these HAPs that lack doseresponse 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 Exposure Levels. Air Toxicology and Epidemiology 

Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. 

February 2000 (http://www.oehha.ca.gov/air/chronic_rels/pdf/relsP32k.pdf)
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2) Where possible, for emissions of unspecified mixtures of HAP categories such as metal 

compounds and POM, we apply category-specific chemical speciation profiles appropriate 

to the source category to develop a composite dose-response value for the category. 

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

cancer dose-response value for formaldehyde (5.5 x 10-9per μg/m3) was based on better 

science than the IRIS cancer dose-response value (1.3 x 10-5per μg/m3), 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 Academy of Sciences 

(NAS) completed its review of the EPA’s draft assessment in April of 2011.8 EPA will 

follow the NAS Report recommendations and will present results obtained by

implementing the biologically-based dose-response (BBDR) model for formaldehyde. 

EPA will compare these estimates with those currently presented in the 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 emissions reported to EPA’s National Emission 

Inventory (NEI) are not speciated into individual compounds. As a result, it is necessary

to apply the same simplifying assumptions to assessments that are used in NATA.[17] 

The NATA approach partitions POM into eight different non-overlapping “groups” that 

are modeled as separate pollutants. Each POM group comprises POM species of similar 

carcinogenic potency, for which we can apply the same URE. 

5) In the case of nickel compounds, to provide a health-protective estimate of potential 

cancer risks, we used the IRIS URE value for nickel subsulfide in this assessment. Based 

on past scientific and technical considerations, the determination of the percent of nickel 

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

risks of cancer due to nickel-containing emissions. Nickel speciation information for 

some of the largest nickel-emitting sources (including oil combustion, coal combustion, 

and others) suggested that at least 35 percent of total nickel emissions may be soluble 

compounds and that the URE for the mixture of inhaled nickel compounds (based on 

nickel subsulfide, and representative of pure insoluble crystalline nickel) could be 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 12th 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. 12th 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.pdf
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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 epidemiological studies, mechanistic studies, and carcinogenic 

studies in rodents support the concept that nickel compounds generate nickel ions in target 

cells at sites critical for carcinogenesis, thus allowing 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 nickel refining industries cause cancer in humans (these studies are summarized in a 

review by Grimsrud et al., 201012). The major scientific bodies mentioned above have 

also recognized that there are differences in toxicity and/or carcinogenic potential across 

the different nickel compounds. In this 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 values13 derived 

for exposure to mixtures of nickel compounds, as a group, that are 2-3 fold lower than the 

IRIS URE for nickel subsulfide, the EPA also considers it reasonable to use a value that is 

50 percent of the IRIS URE for nickel subsulfide for providing an estimate of the lower 

end of the plausible range of cancer potency values for different mixtures of nickel 

compounds.

6) For 3 carcinogenic substances, (captan, isophorone and propylene dichloride) that 

lack inhalation assessments from the sources evaluated in this document, oral 

carcinogenic potency estimates were converted to inhalation UREs. The 

conversion from oral risk (per mg/kg/d oral intake) to inhalation risk (per μg/m3

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 μg/m3)

 

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 European Union’s Scientific Committee on 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 Health Services 

(http://www.arb.ca.gov/toxics/id/summary/nickel_tech_b.pdf) and the other by the Texas Commission on 

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

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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 further dose-response 

development through EPA’s IRIS process.

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

HAP with available chronic quantitative inhalation dose-response values. These HAP, their 

dose-response values, and the source of the values are listed in Tables 2.6-1 (a) and (b).

Table 2.6-1 (a) Dose-Response Values for Chronic Inhalation Exposure to 

Carcinogens

URE (unit risk estimate for cancer)14 = cancer risk per μg/m3of 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 

Number15

URE7

(1/μg/m3)

Source

1,1,2-Trichloroethane 79005 0.000016 IRIS

1,3-Butadiene 106990 0.00003 IRIS

1,3-Dichloropropene 542756 0.000004 IRIS

1,4-Dichlorobenzene 106467 0.000011 CAL

1,4-Dioxane 123911 0.0000077 CAL

2,4,6-Trichlorophenol 88062 0.0000031 IRIS

2,4-Toluene diisocyanate 584849 0.000011 CAL

4,4'-Methylenedianiline 101779 0.00046 CAL

Acetaldehyde 75070 0.0000022 IRIS

Acrylonitrile 107131 0.000068 IRIS

 

14 The URE is the upper-bound excess cancer risk estimated to result from continuous lifetime exposure to an 

agent at a concentration of 1 μg/m3in air. URE’s are considered upper bound estimates meaning they represent 

a plausible upper limit to the true value. 

15 Chemical Abstract Services identification number. For groups of compounds that lack a CAS number we 

have used a surrogate 3-digit identifier corresponding to the group’s position on the CAA list of HAPs.
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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/m3of 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 

Number15

URE7

(1/μg/m3)

Source

Aniline 62533 0.0000016 CAL

Arsenic compounds 7440382 0.0043 IRIS

Benzene16 71432 0.0000078 IRIS

Benzyl chloride 100447 0.000049 CAL

Beryllium compounds 7440417 0.0024 IRIS

Bis(2-ethylhexyl)phthalate 117817 0.0000024 CAL

Bromoform 75252 0.0000011 IRIS

Cadmium compounds 7440439 0.0018 IRIS

Captan 133062 0.000001 Conv. Oral

Carbon tetrachloride 56235 0.000006 IRIS

Chromium (VI) compounds 18540299 0.012 IRIS

Dichloroethyl ether 111444 0.00033 IRIS

Epichlorohydrin (1-Chloro-2,3-epoxypropane) 106898 0.0000012 IRIS

Ethyl benzene 100414 0.0000025 CAL

Ethylene dichloride 107062 0.000026 IRIS

Ethylene oxide 75218 0.000088 CAL

Formaldehyde17 50000 0.000013 IRIS

Hexachlorobenzene 118741 0.00046 IRIS

Hexachloroethane 67721 0.000004 IRIS

Hydrazine 302012 0.0049 IRIS

Isophorone18 78591 0.00000027 Conv. Oral

Methyl tert-butyl ether 1634044 0.00000026 CAL

Methylene chloride 75092 0.00000047 IRIS

Naphthalene 91203 0.000034 CAL

Nickel compounds 7440020 0.00048 EPA OAQPS

o-Toluidine 95534 0.000051 CAL

Polychlorinated biphenyls 1336363 0.0001 IRIS

Polycyclic Organic Matter19 (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/m3. The low end of the range is 2.2E-06 per ug/m3.

17 The EPA has used the CIIT URE value, 5.5X10-9

per mg/m3, to characterize formaldehyde cancer risk in some 

instances.

18 No inhalation unit risk estimates were available for this compound. Therefore we converted from an IRIS oral 

potency slope of 0.00095 per mg/kg/d. UREs that are converted from the oral route to the inhalation route of 

exposure are considered highly uncertain, and are only used in cases where no other URE is available.

19 Assigned the URE associated with a mixture of POM compounds having a similar potency. Details of this 

method, also used in the National Air Toxics Assessments, are available at 

http://www.epa.gov/nata2002/methods.html#pom 
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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/m3of 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 

Number15

URE7

(1/μg/m3)

Source

 2-Methylnaphthalene 91576 0.000088 CAL

 Fluoranthene 206440 0.000088 CAL

 Fluorene 86737 0.000088 CAL

 Phenanthrene 85018 0.000088 CAL

 Pyrene 129000 0.000088 CAL

Propylene dichloride20 78875 0.000019 Conv. Oral

Propylene oxide 75569 0.0000037 IRIS

Tetrachloroethylene 127184 0.0000059 CAL

Trichloroethylene 79016 0.000002 CAL

Vinyl chloride 75014 0.0000088 IRIS

Table 2.6-1 (b) Dose-Response Values for Chronic Inhalation Exposure to 

Noncarcinogens

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an 

order of magnitude) of a continuous inhalation exposure to the human population (including 

sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects 

during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = 

California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency

for Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables, 

EPA OAQPS = EPA Office of Air Quality Planning & Standards

Pollutant CAS Number8 RfC 

(mg/m3)

Source21

1,1,1-Trichloroethane (methyl 

chloroform) 71556 5 IRIS - M

1,2-Epoxybutane 106887 0.02 IRIS - M

1,3-Butadiene 106990 0.002 IRIS - M

1,3-Dichloropropene 542756 0.02 IRIS - H

1,4-Dichlorobenzene 106467 0.8 IRIS - M

1,4-Dioxane 123911 3.6 ATSDR

 

20 No inhalation unit risk estimates were available for this compound. Therefore we converted 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 confidence in the RfC value, as reported in IRIS.
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Table 2.6-1 (b) Dose-Response Values for Chronic Inhalation Exposure to 

Noncarcinogens

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an 

order of magnitude) of a continuous inhalation exposure to the human population (including 

sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects 

during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = 

California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency

for Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables, 

EPA OAQPS = EPA Office of Air Quality Planning & Standards

Pollutant CAS Number8 RfC 

(mg/m3)

Source21

2,4-Toluene diisocyanate 584849 0.00007 IRIS - M

4,4'-Methylenedianiline 101779 0.02 CAL

Acetaldehyde 75070 0.009 IRIS - L

Acrolein 107028 0.00002 IRIS - M

Acrylic acid 79107 0.001 IRIS - M

Acrylonitrile 107131 0.002 IRIS - M

Aniline 62533 0.001 IRIS - L

Antimony compounds 7440360 0.0002 IRIS - L

Arsenic compounds 7440382 0.000015 CAL

Benzene 71432 0.03 IRIS - M

Beryllium compounds 7440417 0.00002 IRIS - M

Bis(2-ethylhexyl)phthalate 117817 0.01 CAL

Cadmium compounds 7440439 0.00001 ATSDR

Carbon tetrachloride 56235 0.1 IRIS - M

Chlorine 7782505 0.00015 ATSDR

Chlorobenzene 108907 1 CAL

Chloroform 67663 0.098 ATSDR

 Chromium (VI) compounds 18540299 0.0001 IRIS - M

Cresols (mixed) 1319773 0.6 CAL

Cumene 98828 0.4 IRIS - M

Cyanide & Cyanide Compounds

 Cyanide compounds22 57125 0.003 IRIS - L

 Hydrogen cyanide 74908 0.003 IRIS - L

Diethanolamine 111422 0.003 CAL

Epichlorohydrin (1-Chloro-2,3-

epoxypropane) 106898 0.001 IRIS - M

Ethyl benzene 100414 1 IRIS - L

Ethyl chloride 75003 10 IRIS - M

Ethylene dichloride 107062 2.4 ATSDR

Ethylene glycol 107211 0.4 CAL

Ethylene oxide 75218 0.03 CAL

Formaldehyde 50000 0.0098 ATSDR

 

22 The value for hydrogen cyanide was used as a surrogate for all cyanide compounds without an RfC.
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Table 2.6-1 (b) Dose-Response Values for Chronic Inhalation Exposure to 

Noncarcinogens

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an 

order of magnitude) of a continuous inhalation exposure to the human population (including 

sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects 

during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = 

California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency

for Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables, 

EPA OAQPS = EPA Office of Air Quality Planning & Standards

Pollutant CAS Number8 RfC 

(mg/m3)

Source21

Glycol Ethers23

 2-(Hexyloxy)ethanol 112254 0.02 IRIS - M

 2-Butoxyethyl acetate 112072 0.02 IRIS - M

 Butyl Carbitol acetate 124174 0.02 IRIS - M

 Diethylene glycol monobutyl 

ether 112345 0.02 HEAST

 Diethylene glycol monoethyl 

ether 111900 0.02 IRIS - M

 Ethoxytriglycol 112505 0.02 IRIS - M

 Ethylene glycol ethyl ether 110805 0.2 IRIS - M

 Ethylene glycol methyl ether 109864 0.02 IRIS - M

 Glycol ethers 171 0.02 IRIS - M

 Methoxytriglycol 112356 0.02 IRIS - M

 Propyl cellosolve 2807309 0.02 IRIS - M

 Triglycol monobutyl ether 143226 0.02 IRIS - M

Hexachlorobenzene 118741 0.003 CAL

Hexachloroethane 67721 0.08 CAL

Hexane 110543 0.7 IRIS - M

Hydrazine 302012 0.0002 CAL

Hydrochloric acid (hydrogen 

chloride) 7647010 0.02 IRIS - L

Hydrofluoric acid (hydrogen 

fluoride) 7664393 0.014 CAL

Isophorone 78591 2 CAL

Lead compounds 7439921 0.00015 EPA OAQPS

Maleic anhydride 108316 0.0007 CAL

Manganese compounds 7439965 0.00005 IRIS - M

Methanol 67561 4 CAL

Methyl bromide 74839 0.005 IRIS - H

Methyl chloride 74873 0.09 IRIS - M

Methyl isobutyl ketone 108101 3 IRIS - L/M

Methyl isocyanate 624839 0.001 CAL

Methyl methacrylate 80626 0.7 IRIS - M/H

Methyl tert-butyl ether 1634044 3 IRIS - M

 

23 The RfC value for ethylene glycol methyl ether was used as a surrogate for all glycol ethers without an RfC.
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Table 2.6-1 (b) Dose-Response Values for Chronic Inhalation Exposure to 

Noncarcinogens

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an 

order of magnitude) of a continuous inhalation exposure to the human population (including 

sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects 

during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = 

California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency

for Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables, 

EPA OAQPS = EPA Office of Air Quality Planning & Standards

Pollutant CAS Number8 RfC 

(mg/m3)

Source21

Methylene chloride 75092 1 ATSDR

Naphthalene 91203 0.003 IRIS - M

Nickel compounds 7440020 0.00009 ATSDR

Phenol 108952 0.2 CAL

Phosgene 75445 0.0003 IRIS - M

Phthalic anhydride 85449 0.02 CAL

Propionaldehyde 123386 0.008 IRIS – L/M

Propylene dichloride 78875 0.004 IRIS - M

Propylene oxide 75569 0.03 IRIS - M

Selenium compounds 7782492 0.02 CAL

Styrene 100425 1 IRIS - M

Tetrachloroethylene 127184 0.27 ATSDR

Titanium tetrachloride 7550450 0.0001 ATSDR

Toluene 108883 5 IRIS - H

Trichloroethylene 79016 0.6 CAL

Triethylamine 121448 0.007 IRIS - L

Vinyl acetate 108054 0.2 IRIS - H

Vinyl chloride 75014 0.1 IRIS - M

Xylenes (mixed) 1330207 0.1 IRIS - M

 m-Xylene18108383 0.1 IRIS - M

 o-Xylene24 95476 0.1 IRIS - M

 p-Xylene18106423 0.1 IRIS - M

2.6.2. Sources of acute dose-response information 

Hazard identification and dose-response assessment information for preliminary acute 

inhalation exposure assessments are based on the existing recommendations of OAQPS for 

HAPs [18]. Depending on availability, the results from screening acute assessments are 

compared to both “no effects” reference levels for the general public, such as the California 

Reference Exposure Levels (RELs), as well 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.
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with an estimated exceedance of a particular reference level depends on the definition of that 

level and any limitations expressed therein. Comparisons among different available 

inhalation health effect reference values (both acute and chronic) for selected HAPs can be 

found in an EPA document [19].

California Acute Reference Exposure Levels (RELs). The California Environmental 

Protection Agency (CalEPA) has developed acute dose-response reference values for many 

substances, expressing the results as acute inhalation Reference Exposure Levels (RELs). 

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

“the concentration level at or below which no adverse health effects are anticipated for a 

specified exposure duration [20]. RELs are based on the most sensitive, relevant, adverse 

health effect reported in the medical and toxicological literature. RELs are designed to 

protect the most sensitive individuals in the population by the inclusion of margins of 

safety. Since margins of safety are incorporated to address data gaps and 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 National Advisory

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

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

in the Committee’s “Standing Operating Procedures (SOP)”

(http://www.epa.gov/opptintr/aegl/pubs/sop.pdf), AEGLs “represent threshold exposure limits 

for the general public and are applicable to emergency exposures ranging from 10 min to 8 h.” 

Their intended application is “for conducting risk assessments to aid in the development of 

emergency preparedness and prevention plans, as well as real time emergency response 

actions, for accidental chemical releases at fixed facilities and from transport carriers.” The 

document states that “the primary purpose of the AEGL program and the NAC/AEGL 

Committee is to develop guideline levels for once-in-a-lifetime, short-term exposures to 

airborne concentrations of acutely toxic, high-priority chemicals.” In detailing the intended 

application of AEGL values, the document states, “It is anticipated that the AEGL values will 

be used for regulatory and nonregulatory purposes by U.S. Federal and State agencies, and 

possibly the international community in conjunction with chemical emergency response, 

planning, and prevention programs. More specifically, the AEGL values will be used for 

conducting various risk assessments to aid in the development of emergency preparedness and 

prevention plans, as well as real-time emergency response actions, for accidental chemical 

releases at fixed facilities and from transport carriers.” 

The NAC/AEGL defines AEGL-1 and AEGL-2 as:

“AEGL-1 is the airborne concentration (expressed as ppm or mg/m3) of a substance above 

which it is predicted that the general population, including susceptible individuals, could 

experience notable discomfort, irritation, or certain asymptomatic nonsensory effects. 
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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/m3) 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 general public, including susceptible 

subpopulations, such as infants, children, the elderly, persons with asthma, and those with 

other illnesses, it is recognized that individuals, subject to unique or idiosyncratic 

responses, could experience the effects described at concentrations below the 

corresponding AEGL.”

Emergency Response Planning Guidelines (ERPGs). The American Industrial Hygiene 

Association (AIHA) has developed Emergency Response Planning Guidelines (ERPGs) [21] 

for acute exposures at three different levels of severity. These guidelines represent 

concentrations for exposure of the general 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 intended for use as planning tools for assessing the 

adequacy of accident prevention and emergency response plans, including transportation 

emergency planning and for developing community emergency response plans. The emphasis 

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

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

ERPG-1 and ERPG-2 values are defined by AIHA as follows:

“ERPG-1 is the maximum airborne concentration below which it is believed that nearly all 

individuals could be exposed for up to 1 hour without experiencing other than mild 

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

odor.”

“ERPG-2 is the maximum airborne concentration below which it is believed that nearly all 

individuals could be exposed for up to 1 hour without experiencing or developing 
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irreversible or other serious health effects or symptoms which could impair an individual's 

ability to take protective action.”

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

HAP with relevant and available quantitative acute dose-response threshold values. These 

HAP, their acute threshold values, and the source of the value are listed below in Table 2.6-2.
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Table 2.6-2 Dose-Response Values for Acute Exposure

Pollutant

CAS 

Number

AEGL-1

(1-hr)

(mg/m3)

AEGL-2

(1-hr)

(mg/m3)

ERPG-1

(1-hr)

(mg/m3)

ERPG-2

(1-hr)

(mg/m3) REL 

1,1,1-Trichloroethane (methyl 

chloroform) 71556 1300 3300 1900 3800 68

1,2-Epoxybutane 106887 210 410

1,3-Butadiene 106990 1500 12000 22 440

1,4-Dioxane 123911 61 1200 3

2,4-Toluene diisocyanate 584849 0.14 0.59 0.071 1.1

Acetaldehyde 75070 81 490 18 360 0.47

Acetonitrile 75058 22 540

Acrolein 107028 0.069 0.23 0.11 0.34 0.0025

Acrylic acid 79107 4.4 140 3 150 6

Acrylonitrile 107131 10 130 22 77

Aniline 62533 30 46

Arsenic compounds 7440382 0.0002

Benzene 71432 170 2600 160 480 1.3

Benzyl chloride 100447 5.2 52 0.24

Beryllium compounds 7440417 0.025

Biphenyl 92524 61

Carbon tetrachloride 56235 280 1200 130 630 1.9

Chlorine 7782505 1.5 5.8 2.9 8.7 0.21

Chloroacetic acid 79118 26

Chlorobenzene 108907 46 690

Chloroform 67663 310 240 0.15

Chloromethyl methyl ether 107302 1.6 3.3

Cumene 98828 250 1500

Hydrogen cyanide 74908 2.2 7.8 11 0.34

Dimethyl formamide 68122 270 6 300

Dimethyl sulfate 77781 0.12 0.62

Epichlorohydrin (1-Chloro-2,3-

epoxypropane) 106898 22 91 19 76 1.3

Ethyl acrylate 140885 34 150 0.041 120

Ethyl benzene 100414 140 4800

Ethylene dichloride 107062 200 810

Ethylene oxide 75218 81 90

Formaldehyde 50000 1.1 17 1.2 12 0.055

Glycol Ethers25

 2-(Hexyloxy)ethanol 112254 0.093

 2-Butoxyethyl acetate 112072 0.093

 

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

an acute REL.
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Table 2.6-2 Dose-Response Values for Acute Exposure

Pollutant

CAS 

Number

AEGL-1

(1-hr)

(mg/m3)

AEGL-2

(1-hr)

(mg/m3)

ERPG-1

(1-hr)

(mg/m3)

ERPG-2

(1-hr)

(mg/m3) REL 

 Butyl carbitol acetate 124174 0.093

 Ethoxytriglycol 112505 0.093

 Ethylene glycol ethyl ether 110805 0.37

 Ethylene glycol methyl ether 109864 0.093

 Glycol ethers 171 0.093

 Methoxytriglycol 112356 0.093

 Propyl cellosolve 2807309 0.093

 Triglycol monobutyl ether 143226 0.093

Hexane 110543 12000

Hydrazine 302012 0.13 17 0.65 6.5

Hydrochloric acid 7647010 2.7 33 4.5 30 2.1

Hydrogen fluoride 7664393 0.82 20 1.6 16 0.24

Maleic anhydride 108316 0.8 8

Methanol 67561 690 2700 260 1300 28

Methyl bromide 74839 820 190 3.9

Methyl chloride 74873 1900 830

Methyl hydrazine 60344 3.2

Methyl isocyanate 624839 0.16 0.058 0.6

Methyl methacrylate 80626 70 490

Methyl tert-butyl ether 1634044 180 2100

Methylene chloride 75092 690 1900 1000 2600 14

Nickel compounds 7440020 0.006

Phenol 108952 58 89 38 190 5.8

Phosgene 75445 1.2 2 0.004

Propionaldehyde 123386 110 620

Propylene oxide 75569 170 690 120 1100 3.1

Styrene 100425 85 550 210 1100 21

Tetrachloroethylene 127184 240 1600 680 1400 20

Titanium tetrachloride 7550450 0.54 7.8 5 20

Toluene 108883 750 4500 190 1100 37

Trichloroethylene 79016 700 2400 540 2700

Triethylamine 121448 2.8

Vinyl acetate 108054 24 630 18 260

Vinyl chloride 75014 640 3100 1300 13000 180

Xylenes (mixed) 1330207 560 4000 22

 m-Xylene26 108383 22

 o-Xylene20 95476 22

 p-Xylene20 106423 22

 

26 The REL for mixed xylenes was used as a surrogate.
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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. Further, the EPA Administrator’s March 

1995 Policy for Risk Characterization [22] specifies that a risk characterization “be prepared 

in a manner that is clear, transparent, reasonable, and consistent with other risk 

characterizations of similar scope prepared across programs in the Agency.” These principles 

of transparency and consistency have been reinforced by the Agency’s Risk Characterization 

Handbook [23], in 2002 by the Agency’s information quality guidelines [24], and in the 

OMB/OSTP September 2007 Memorandum on Updated Principles for Risk Analysis27, and 

are incorporated in these assessments.

Estimates of health risk are presented in the context of uncertainties and limitations in the data 

and methodology. Through our tiered, iterative analytical approach, we have attempted to 

reduce both uncertainty and bias to the greatest degree possible in these assessments, within 

the limitations of available time and resources. We provide summaries of risk metrics 

(including maximum individual cancer risks and noncancer hazards, as well as cancer 

incidence estimates) along with a discussion of the major uncertainties associated with their 

derivation to provide decision makers with the fullest picture of the assessment and its 

limitations.

For each carcinogenic HAP included in an assessment that has a potency estimate available, 

individual and population cancer risks were calculated by multiplying the corresponding 

lifetime average exposure estimate by the appropriate URE. This calculated cancer risk is 

defined as the upper-bound probability of developing cancer over a 70-yr period (i.e., the 

assumed human lifespan) at that exposure. Because UREs for most HAPs are upper-bound 

estimates, actual risks at a given exposure level may be lower than 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 by factors of 10 (for 

children aged 0-1), 3 (for children aged 2-15), or 1.6 (for 70 years of exposure beginning at 

birth), as needed in risk assessments. In this case, this has the effect of increasing the 

 

27Memorandum for the Heads of Executive Departments and Agencies - Updated Principles for Risk Analysis

(September 19, 2007), From Susan E. Dudley, Administrator, Office of Information and Regulatory Affairs, 

Office of Management and Budget; and Sharon L. Hays, Associate Director and Deputy Director for Science, 

Office of Science and Technology Policy (http://www.whitehouse.gov/omb/memoranda/fy2007/m07-24.pdf)
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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 implementation policy [27] 

recommends applying the Supplemental Guidance to all carcinogenic PAHs for which risk 

estimates are based on relative potency. Accordingly, we applied the Supplemental Guidance 

to all unspeciated POM mixtures.

Increased cancer incidence for the entire receptor population within the area of analysis was 

estimated by multiplying the estimated lifetime cancer risk for each census block by the 

number of people residing in that block, then summing the results for the entire modeled 

domain. This lifetime population incidence estimate was divided by 70 years to obtain an 

estimate of the number of cancer cases per year.

In the case of benzene, the high end of the reported cancer URE range was used in our 

assessments to provide a conservative estimate of potential cancer risks. Use of the high end 

of the range provides risk 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 evaluated the impact of using the low end of the URE range on our risk 

results.

Unlike linear dose-response assessments for cancer, noncancer health hazards generally are 

not expressed as a probability of an adverse occurrence. Instead, “risk” for noncancer effects 

is expressed by comparing an exposure to a reference level as a ratio. The “hazard quotient” 

(HQ) is the estimated exposure divided by a reference level (e.g., the RfC). For a given HAP, 

exposures at or below the reference level (HQ≤1) are not likely to cause adverse health 

effects. As exposures increase above the reference level (HQs increasingly greater than 1), 

the potential for adverse effects increases. For exposures 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 impact of 

this on possible health interpretations. 

The risk characterization for chronic effects other than cancer is expressed in terms of the HQ 

for inhalation, calculated for each HAP at each census block centroid. As discussed above, 

RfCs incorporate generally conservative uncertainty factors in the face of uncertain 

extrapolations, such that an HQ greater than one does not necessarily suggest the onset of 

adverse effects. The HQ cannot be translated to a probability that adverse effects will occur, 

and is unlikely to be proportional to adverse health effect outcomes in a population.

Screening for potentially significant acute inhalation exposures also followed the HQ 

approach. We divided the maximum estimated acute exposure by each available short-term 

threshold value to develop an array of HQ values relative to the various acute endpoints and 

thresholds. In general, when none of these HQ values are greater than one, there is no 

potential for acute risk. In those cases where HQ values above one are seen, additional 

information is used to determine if there is a potential for significant acute risks.
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2.7.2. Mixtures

Since most or all receptors in these assessments receive exposures to multiple pollutants 

rather than a single pollutant, we estimated the aggregate 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 inappropriate 

to aggregate HQs. In consideration of these mode-of-action differences, the mixtures 

guidelines support aggregating effects of different substances in specific and limited ways. 

To conform to these guidelines, we aggregated non-cancer HQs of HAP that act by similar 

toxic modes of action, or (where this information is absent) that affect the same target organ. 

This process creates, for each target organ, a target-organ-specific hazard index (TOSHI), 

defined as the sum of hazard quotients for individual HAP that affect the same organ or organ 

system. All TOSHI calculations presented here were based exclusively on effects occurring 

at the “critical dose” (i.e., the lowest dose that produces adverse health effects). Although 

HQs associated with some pollutants 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 TOSHI calculations, some TOSHIs may have been underestimated. As with 

the HQ, the TOSHI should not be interpreted as a probability of adverse effects, or as strict 

delineation of “safe” and “unsafe” levels. Rather, the TOSHI is another measure of the 

potential for adverse health outcomes associated with pollutant exposure, and needs to be 

interpreted carefully by health scientists and risk managers.

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

emissions and potential exposures, acute impacts were screened on an individual pollutant 

basis, not using the TOSHI approach.

1.1.1. 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 assessments 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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1.1.2. MACT-Allowable Risks

The emissions data in the data sets for these seven source categories are estimates of actual 

emissions on an annual basis. The risk results presented in the following sections are based 

on these actual emissions. For these seven source categories, the MACT-allowable emissions 

are estimated to be equivalent to the actual emissions except for certain emission sources. See

the memorandum titled “MACT Allowable Emissions and Risks for the Pesticide Active 

Ingredient (PAI), Polyether Polyols, and Polymers and Resins IV Production Source 

Categories” available in the docket for this 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 MACTAllowable Emissions and Risks for the Pesticide Active Ingredient, Polyether Polyols, and 

Polymers and Resins IV Production Source Categories (available in the docket for this action) 

for details on the MACT-allowable risk. 

3. Risk Results for Pesticide Active Ingredient 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, and 

related products. The HAP emission sources at PAI production facilities include storage 

vessels, process vents, equipment leaks, wastewater systems, heat exchange systems, and bag 

dumps and product dryers. The primary HAP emitted by these facilities include toluene, 

methanol, methylene chloride, 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 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 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 largest 

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 14 HAP account for 90 percent of the total 

emissions by mass. Persistent and bioaccumulative HAP (PB-HAP)28 in the data set for the 

 

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

EPA-453K-04-001A, as referenced in the ANPRM and provided on the EPA’s Technology Transfer Network 

website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html. 
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pesticide active ingredient production source category include lead compounds, 

hexachlorobenzene, and polychlorinated biphenyls (PCBs).29 

Table 3.1-1 Summary of Emissions from the Pesticide Active Ingredients Source Category 

and Availability of Dose-Response Values

HAPa Emissions

(tpy)

Number of 

Facilities 

Reporting 

HAP (17 

facilities in 

data set)

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

Unit Risk PB-HAP?

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 33 10  

Methyl Isobutyl Ketone 21 3 

Glycol Ethers

Ethylene glycol ethyl 

ether (Cellosolve) 17 1

 

Ethylene glycol methyl 

ether 0.5 1

 

Glycol Ethers 0.01 1  

Hexane 16 5  

Chlorine 11 7  

Formaldehyde 10 4   

Tetrachloroethylene 6 5   

Xylenes (Mixture of o, m, 

and p Isomers) 6 7

 

Triethylamine 5 5  

Trichloroethylene 5 2   

Ethylene Glycol 4 5 

Ethylene dichloride 3 3   

Phenol 3 3  

Chloroform 3 6  

Naphthalene 3 4  

Chlorobenzene 2 4  

m-Xylene 2 1  

Carbon tetrachloride 2 5   

o-Xylene 2 1  

Ethyl Benzene 2 4   

Benzene 2 6   

Ethyl chloride 1 4 

Phosgene 240.8 4  

 

29 After the risk assessment was completed, we learned that the emissions of hexachlorobenzene in the data set 

for polyether polyols production should have been assigned to the pesticide active ingredient MACT code. We 

will update the data set with this information, and any additional information received during the comment 

period, before the final rule.
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Table 3.1-1 Summary of Emissions from the Pesticide Active Ingredients Source Category 

and Availability of Dose-Response Values

HAPa Emissions

(tpy)

Number of 

Facilities 

Reporting 

HAP (17 

facilities in 

data set)

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

Unit Risk PB-HAP?

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. Additionally, 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 are much lower than in our reported data. We will update the data set 

with this information, and any additional information received during the comment period, before the final rule. 
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Table 3.1-1 Summary of Emissions from the Pesticide Active Ingredients Source Category 

and Availability of Dose-Response Values

HAPa Emissions

(tpy)

Number of 

Facilities 

Reporting 

HAP (17 

facilities in 

data set)

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

Unit Risk PB-HAP?

Estimate for 

Cancer?

Reference 

Concentration 

for Chronic 

Noncancer?

Health 

Benchmark 

Values for Acute 

Noncancer?

Hexachlorobenzene240.006 2  

1,3-Dichloropropene 0.006 1  

Maleic anhydride 0.005 1  

Bromoform 0.004 1 

Methyl tert-butyl ether 0.004 1   

Hexachloroethane 0.003 2  

Styrene 0.002 1  

Beryllium & Compounds 0.002 1   

Methyl methacrylate 0.002 1  

Hydrogen Fluoride 0.002 1  

Vinyl acetate 0.0008 1  

Polychlorinated Biphenyls 0.00004 1  

a Notes for how HAP were speciated for risk assessment:

 For most metals, emissions reported as the elemental metal are combined with metal compound emissions (e.g., 

“cadmium” emissions modeled as “cadmium & compounds”). In the absence of speciation information, we assume 

the reported mass is 100 percent metal.

 For emissions reported generically as “Glycol Ethers” or specific glycol ethers not found on EPA’s Technology 

Transfer network for air toxics (see 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 National Ambient Air Quality Standards (NAAQS) for lead 

(0.15 μg/m3). These NAAQS for lead were reviewed with revisions adopted in October 2008 

(http://www.epa.gov/air/lead/actions.html). The primary (health-based) standard is a maximum or not-to-be-exceeded, rolling 

three-month average, measured as total suspended particles (TSP). The secondary (welfare-based) standard is identical to the 

primary standard. 

3.2 Risk Characterization

This section presents the results of the risk assessment for the pesticide active ingredient 

production source category. The basic chronic inhalation risk estimates presented here are the 

maximum individual lifetime 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 noninhalation risks from PB-HAP. Also presented are the HAP “drivers,” which are the HAP 

that collectively contribute 90 percent of the maximum cancer risk or maximum hazard index 

at the highest exposure location, as well as a summary of the results of our facility-wide 

assessments and our analysis of risks associated with the maximum allowed emissions under 

the current MACT standards. A detailed summary of the facility-specific risk assessment 

results is available in Appendix 4. 
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Tables 3.2-1 and 3.2-2 summarize the chronic and acute inhalation risk results for this source 

category. The results for the pesticide active ingredient manufacturing source category

indicate that maximum lifetime individual cancer risks could be as high as 7 in a million. The 

major contributors to this risk are naphthalene and nickel compounds.

31

 Approximately

11,000 people (this does not reflect the updated emissions information received after the risk 

modeling was done) were estimated to have cancer risks above 1 in a million as a result of the 

emissions from 6 facilities. The maximum chronic non-cancer target organ specific hazard 

index (TOSHI) value for the source category could be up to 0.7 associated with emissions of 

chlorine, indicating no significant potential for chronic noncancer impacts. 

Worst-case acute HQs were calculated for every emitted HAP that has an acute benchmark. 

For cases where the screening acute HQ was greater than 1, we further refined the estimates 

by determining the highest HQ value that might occur outside facility boundaries. Analysis of 

potential off-site impacts for the PAI source category identified four facilities with the 

potential to exceed the acute REL for six pollutants (ethylene glycol ethyl ether (one facility), 

acrolein (one facility), chloroform (one facility), nickel compounds (one facility), chlorine

(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 

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 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 to 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). We 

 

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 emissions the acute value is less than 1. We will update the data set with this 

information, and any additional information received during the comment period, before the final rule.
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reviewed 2 facilities with the highest HQ values and determined equipment leaks were 

primarily responsible for the high acute HQ values of 4 and 8 and that they were modeled 

assuming that they all emanate from a single emission location rather than from numerous 

physical locations throughout the processing area. We note that this assumption further biases 

the HQ values high, but to an unknown extent, given that we do not know the actual size of 

the processing areas at each of these facilities. Taking all of this into consideration, these 

acute impact screening results indicate only the potential for acute impacts of concern, while 

the uncertainties and bias associated with them suggest that there may be no real acute issues 

at all. 

We conducted a screening-level evaluation of the potential human health risks associated with 

emissions of PB-HAP. Reported emissions of PB-HAP were compared to emission 

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

emitted from this category are lead, hexachlorobenzene, and polychlorinated biphenyls 

(PCBs). Lead is a PB-HAP, but the National Ambient Air Quality Standards (NAAQS) value 

(which was used for the chronic noncancer risk assessment) takes into account multipathway

exposures, so a separate multipathway screening value was not developed. Since we did not 

estimate 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 were not 

evaluated for potential non-inhalation 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 appreciable quantities.34

 

33 ICF International. TRIM-Based Multipathway Screening Scenario. Prepared 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. 
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Table 3.2-1 Summary of Source Category Level Risks for Pesticide Active Ingredient 

Production

Result HAP “Drivers”

Facilities in Source Category

Number of Facilities Estimated to be in Source 

Category 17 n/a

Number of Facilities Identified in NEI and 

Modeled in Preliminary Risk Assessment 17 n/a

Cancer Risks

Maximum Individual Lifetime Cancer Risk (in 1 

million) 35 7 naphthalene, nickel compounds

Number of Facilities with Maximum Individual Lifetime Cancer Risk:

Greater than or equal to 100 in 1 million 0 n/a

Greater than or equal to 10 in 1 million 0 n/a

Greater than or equal to 1 in 1 million 6

naphthalene, nickel compounds, 

ethylene dichloride, 

acrylonitrile, formaldehyde, 

hydrazine, trichloroethylene, 

1,4-dioxane, 1,3-butadiene

Chronic Noncancer Risks

Maximum Respiratory Hazard Index 0.7 chlorine

Number of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Refined Screening Results

Maximum Acute Hazard Quotient35

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 Exposure35

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 risk is less than presented in the table due to the 

adjusted emissions. We will update the data set with this information, and any additional information received 

during the comment period, before completing the final rule.
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Table 3.2-1 Summary of Source Category Level Risks for Pesticide Active Ingredient 

Production

Result HAP “Drivers”

Number of People Exposed to Cancer Risk:

Greater than or equal to 100 in 1 million 0 n/a

Greater than or equal to 10 in 1 million 900 n/a

Greater than or equal to 1 in 1 million 11,000 n/a

Number of People Exposed to Noncancer Respiratory Hazard Index:

Greater than 1 0 n/a

Estimated Cancer Incidence (excess cases per 

year) 0.001 n/a

Contribution of HAP to Cancer Incidence

naphthalene 30% n/a

formaldehyde 18% n/a

methylene chloride 10% n/a

tetrachloroethylene 9% n/a

ethylene dichloride 6% n/a

1,3-butadiene 5% n/a

nickel compounds 4% n/a

Table 3.2-2 Summary of Refined Screening Acute Results for Pesticide Active Ingredient 

Production Facilities

Results

MAXIMUM ACUTE HAZARD 

QUOTIENTS

ACUTE DOSE-RESPONSE VALUES

Based 

on 

REL

Based on 

AEGL-1/

ERPG-1

Based on 

AEGL-2/

ERPG-2

REL

(mg/m3)

AEGL-1 (1-

hr) (mg/m3)

ERPG-1 

(mg/m3)

AEGL-2

(1-hr)

(mg/m3)

ERPG-2 

(mg/m3)

HAP35 Max. 1-hr. 

Air Conc. 

(mg/m3)

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 0.006/0.008 0.055 1.1 1.2 17 12

Notes on Refined Process:

1) The screening was performed for all emitted HAP with available acute dose-response values. Only those pollutants whose 

screening HQs were greater than 1 for at least one acute threshold value are shown in the table.

2) HAP with available acute dose-response values which are not in the table do not carry any potential for posing acute health risks, 

based on an analysis of currently available emissions data.

Notes on Acute Dose-Response Values:

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

AEGL – Acute exposure guideline levels 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 that are notable discomfort, but which are transient and reversible upon cessation of exposure.
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AEGL-2 is the exposure level above which it is predicted that the general population, including susceptible individuals, could 

experience irreversible or other serious, long-lasting adverse health effects of an impaired ability to escape.

EPRG – Emergency Removal Program guidelines represent emergency exposure (1-hour) limits for the general public.

ERPG-1 is the maximum level below which it is believed that nearly all individuals could be exposed for up to 1 hour without 

experiencing other than mild, transient adverse health effects.

ERPG-2 is the maximum exposure below which it is believed that nearly all individuals could be exposed for up to 1 hour without 

experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual’s ability to 

take protective action.

The facility-wide 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 

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

facilities, 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 facility-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 manufacturing, 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 – Pesticide 

Active Ingredient

Pesticide Active Ingredient 

Manufacturing

Number of Facilities Binned by Facility-Wide 

MIR (in 1 million)

Source Category MIR Contribution 

to Facility-Wide MIR

<1 1≤ MIR<10 10≤ MIR<100 > 100 Total

> 90% 1 3 0 0 4

50-90% 1 1 0 0 2

10-50% 2 4 0 0 6

< 10% 1 0 4 0 5

Total 5 8 4 0 17

4. Risk Results for the Polyether Polyols Production Source 

Category

4.1 Source Category Description and Results

The polyether polyols production source category consists of major source facilities that 

produce chemical products with repeating ether linkages (i.e., -R-O-R-) formed by the 

reaction of ethylene oxide, propylene oxide, or other cyclic ethers with compounds having 

one or more reactive hydrogens. Polyether polyols do not have significant uses of their own, 

but rather are used to make a variety of other products. Polyether polyols can be produced by 
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either polymerization of epoxides (i.e., a three-membered cyclic ether, such as ethylene oxide 

or propylene oxide) or tetrahydrofuran (THF). In the production of polyether polyols, HAP 

are used primarily as reactants or extraction solvents and include ethylene oxide, propylene 

oxide, hexane, toluene, and other HAP. Potential sources of emissions for this category, 

regardless of the specific process employed, include process vents, storage vessels, equipment 

leaks, wastewater operations, and heat exchangers/cooling towers. A complete description of 

the polyether polyols production source category can be found in the text of the NPRM. 

We currently estimate that there are 23 polyether polyols production facilities operating in the 

U.S.36 The data set contains all 23 facilities identified with a polyether polyols 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 23

of these facilities are identified as major sources in the NEI. 

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

are summarized in Table 4.1-1. The total HAP emissions for the source category are 

approximately 440 tons per year. Based on these data, the HAP emitted in the largest 

quantities across these 23 facilities are: ethylene glycol, ethylene oxide, propylene oxide, 

acetaldehyde, methanol, ethyl benzene, benzene, chlorobenzene, glycol ethers, hexane, 

propionaldehyde, and p-dioxane. These 12 HAP account for 90 percent of the total emissions 

by mass. PB-HAP

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, Emerald Carolina Chemical (NEINC0595)

and Port Neches Operations C4 Plant (NEI12483), are still included in the emissions summary, but risk results 

have been removed from the risk summary. We will update the data set with this information, and any additional 

information received during the comment period, before the final rule.

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

EPA-453K-04-001A, as referenced in the ANPRM and provided on the EPA’s Technology Transfer Network 

website for Fate, Exposure, and Risk Assessment at http://www.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 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.
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Table 4.1-1 Summary of Emissions from the Polyether Polyols Production Source Category and 

Availability of Dose-Response Values

HAPa Emissions 

(tpy)

Number 

of 

Facilities 

Reporting 

HAP (25 

facilities 

in data 

set)36

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

PBUnit Risk HAP?

Estimate for 

Cancer?

Reference 

Concentration 

for Chronic 

Noncancer?

Health 

Benchmark 

Values for Acute 

Noncancer?

Ethylene Glycol 178 9 

Ethylene Oxide 57 25   

Propylene Oxide 34 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 10   

Hydrochloric Acid 2 4  

Vinyl Acetate 1 3  

Diethanolamine 1 5 
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Table 4.1-1 Summary of Emissions from the Polyether Polyols Production Source Category and 

Availability of Dose-Response Values

HAPa Emissions 

(tpy)

Number 

of 

Facilities 

Reporting 

HAP (25 

facilities 

in data 

set)36

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

PBUnit Risk HAP?

Estimate for 

Cancer?

Reference 

Concentration 

for Chronic 

Noncancer?

Health 

Benchmark 

Values for Acute 

Noncancer?

Xylenes (Mixture of o, m, and 

p Isomers) 1 7  

Ethyl Acrylate 1 2 

Methyl Tert-Butyl Ether 1 3   

Propylene Dichloride 1 1  

Acrolein 1 3  

Ethyl Chloride 1 6 

Ethylene Dichloride 0.9 5   

Phenol 0.8 7  

1,2-Epoxybutane 0.8 2  

Naphthalene 0.7 4  

Acetophenone 0.6 3

Acrylonitrile 0.2 3   

Trichloroethylene 0.2 1   

Cumene 0.2 5  

Phosgene 0.2 2  

Vinyl Chloride 0.2 4   

N,N-Dimethylformamide 0.1 1  

2,4-Dichlorophenoxy Acetic 

Acid 0.1 1

Dimethyl Sulfate 0.1 1 

Epichlorohydrin (1-Chloro-2,3-

Epoxypropane) 0.1 2

 



Benzyl Chloride 0.1 2  

Biphenyl 0.1 2 

Isophorone 0.06 1  

Aniline 0.06 4   

Methylene Chloride 0.04 3   

Chloroacetic Acid 0.03 2 

Fluoranthene 0.03 1  

Chloroform 0.03 4  

Triethylamine 0.02 3  

Hexachlorobenzene 330.02 1   

Methyl Isobutyl Ketone 0.02 3 

m-Xylene 0.01 1  

Acetonitrile 0.01 2  

Diethyl Sulfate 0.01 1

Methyl Methacrylate 0.008 1  
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Table 4.1-1 Summary of Emissions from the Polyether Polyols Production Source Category and 

Availability of Dose-Response Values

HAPa Emissions 

(tpy)

Number 

of 

Facilities 

Reporting 

HAP (25 

facilities 

in data 

set)36

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

PBUnit Risk HAP?

Estimate for 

Cancer?

Reference 

Concentration 

for Chronic 

Noncancer?

Health 

Benchmark 

Values for Acute 

Noncancer?

Hydroquinone 0.006 1

Tetrachloroethylene 0.006 1   

2,4,6-Trichlorophenol 0.006 1 

Phthalic Anhydride 0.004 1 

Cresol 0.003 2 

1,3-Dichloropropene 0.002 1  

4,4'-Methylenedianiline 0.001 1  

Dichloroethyl Ether 0.001 1 

p-Xylene 0.0009 1  

2,4-Toluene Diisocyanate 0.0005 1   

Bis(2-Ethylhexyl)Phthalate 0.0005 1  

Dibutyl Phthalate 0.0005 1

Lead 0.0005 1 c 

Quinoline 0.0005 1

o-Toluidine 0.0005 1 

1,1,2-Trichloroethane 0.0001 1  

Carbon Tetrachloride 0.0001 1   

a Notes for how HAP were speciated for risk assessment:

 For most metals, emissions reported as the elemental metal are combined with metal compound emissions (e.g., 

“cadmium” emissions modeled as “cadmium & compounds”). In the absence of speciation information, we assume 

the reported mass is 100 percent metal.

 For emissions of any chemicals or chemical groups classified as POM, emissions were grouped into POM 

subgroups as found on EPA’s Technology Transfer Network website for the 2005 National-Scale Air Toxics 

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

POM subgroups (e.g., POM 72002, not shown above) all have unit risk estimates for cancer, and are considered 

PB-HAP.

 For emissions reported generically as “Glycol Ethers” or specific glycol ethers not found on EPA’s Technology 

Transfer network for air toxics (see footnote b), 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 annual ambient exposure estimates to the National Ambient Air Quality Standards (NAAQS) for 

lead (0.15 μg/m3). The primary (health-based) standard is a maximum or not-to-be-exceeded, rolling three-month average, 

measured as total suspended particles (TSP). The secondary (welfare-based) standard is identical to the primary standard.

These NAAQS for lead were reviewed with revisions adopted in October 2008 (http://www.epa.gov/air/lead/actions.html). 
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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 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 the maximum allowed emissions under 

the current MACT standards. A detailed summary of the facility-specific risk assessment 

results is available in Appendix 4. 

Tables 4.2-1 and 4.2-2 summarize the chronic and acute inhalation risk results for this source 

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

as 30 in a million, with ethylene oxide as the major contributor to the risk. The total 

estimated cancer incidence from the source category is 0.02 excess cancer cases per year, or 

one case in every 50 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 mistakes with the emissions data. The maximum chronic 

noncancer TOSHI value for the source category could be up to 0.8 from emissions of acrolein. 

Worst-case acute HQs were calculated for every HAP that has an acute benchmark. For cases 

where the screening acute HQ was greater than 1, we further refined the estimates by

determining the highest HQ value that is outside facility boundaries. 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 

this action). The 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 HAP 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. 

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

concern. While these estimated worst-case exceedances indicate that there is some potential 

for such acute exposures to occur, we note that exceeding the modeled REL 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 
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results along with the rather large uncertainties related to the emissions estimates and 

screening methodology.

We reviewed the two facilities with potential off-site acute HQ values greater than one and 

determined equipment leaks were primarily responsible 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. 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. 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 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.39 The PB-HAP 

emitted by facilities in this category include POM as benzo(a)pyrene TEQ (1 facility) and

lead compounds (1 facility). 40 The one facility with POM emissions above the threshold 

level exceeds 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 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. 

 

39 ICF International. TRIM-Based Multipathway Screening Scenario. Prepared for U.S. Environmental 

Protection Agency, Research Triangle Park, NC. October 2008.

40 After the risk assessment was completed, we learned that the emissions of hexachlorobenzene in the data set 

for the PEPOs production should have been assigned to the PAI MACT code. These emissions are still included 

in the PEPOs emissions summary, but have been removed from the risk summary. We will update the data set 

with this information, and any additional information received during the comment period, before the final rule.
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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 Category41

Number of Facilities Estimated to be in Source 

Category 23 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) 30 ethylene oxide 

Number of Facilities with Maximum Individual Lifetime Cancer Risk:

Greater than or equal to 100 in 1 million 0 n/a

Greater than or equal to 10 in 1 million 5

ethylene oxide, acetaldehyde, 

acrylonitrile, 1,3-butadiene,

benzene, 1,4-dioxane

Greater than or equal to 1 in 1 million 17

ethylene oxide, acetaldehyde, 

acrylonitrile, 1,3-butadiene, 

benzene, 1,4-dioxane, propylene 

oxide, ethyl benzene, propylene 

dichloride, ethylene dichloride, 

naphthalene, benzyl chloride

Chronic Noncancer Risks

Maximum Respiratory Hazard Index 0.8 acrolein

Number of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Refined Screening Results

Maximum Acute Hazard Quotient 6

4/0.1

glycol ethers (REL)

acrolein (REL/AEGL-1)

Number of Facilities With Potential for Acute 

Effects 3 acrolein, glycol ethers

Population Exposure41

Number of People Living Within 50 Kilometers 

of Facilities Modeled 18,000,000 n/a

Number of People Exposed to Cancer Risk:

Greater than or equal to 100 in 1 million 0 n/a

Greater than or equal to 10 in 1 million 6,800 n/a

Greater than or equal to 1 in 1 million 160,000 n/a

 

41 After the risk assessment was completed, we learned that two facilities included in the data set for polyether 

polyols production should not have been included. These facilities, Emerald Carolina Chemical (NEINC0595) 

and Port Neches Operations C4 Plant (NEI12483), are still included in the emissions summary but risk results 

have been removed from the risk summary. One of the 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 updated 

information. The population exposed to cancer risk would be less than presented in the table due to the adjusted 

emissions. We will update the data set with this information, and any additional information received during the 

comment period, before the final rule.
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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 Incidence

ethylene oxide 87% n/a

propylene oxide 4% n/a

benzene 3% n/a

Table 4.2-2 Summary of Acute Refined Sceening Results for Polyether Polyols Production 

Facilities

Results

MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE-RESPONSE VALUES

Based on REL Based on 

AEGL-1/

ERPG-1

Based on 

AEGL-2/

ERPG-2

REL

(mg/m3)

AEGL-1 

(1-hr) 

(mg/m3)

ERPG-1 

(mg/m3)

AEG

L-2

(1-hr)

(mg/

m

3

)

ERP

G-2 

(mg/

m

3 HAP Max. 1-hr. )

Air Conc.

(mg/m3)

Glycol Ethers 0.56 6 0.093

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

Notes on Refined Process:

1) The screening was performed for all emitted HAP with available acute dose-response values. Only those pollutants whose 

screening HQs were greater than 1 for at least one acute threshold value are shown in the table.

2) HAP with available acute dose-response values which are not in the table do not carry any potential for posing acute health risks, 

based on an analysis of currently available emissions data.

Notes on Acute Dose-Response Values:

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

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

AEGL-2 is the exposure level above which it is predicted that the general population, including susceptible individuals, could 

experience irreversible or other serious, long-lasting adverse health effects of an impaired ability to escape.

EPRG – Emergency Removal Program guidelines represent emergency exposure (1-hour) limits for the general public.

ERPG-1 is the maximum level below which it is believed that nearly all individuals could be exposed for up to 1 hour without 

experiencing other than mild, transient adverse health effects.

ERPG-2 is the maximum exposure below which it is believed that nearly all individuals could be exposed for up to 1 hour without 

experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual’s ability to 

take protective action.

The facility-wide 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 contributing 100 percent of the risk, driven by emissions of 

ethylene oxide from process vents and equipment leaks. The maximum facility-wide TOSHI 
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for the source category is 2, driven by emissions of chlorine from industrial inorganic 

chemical manufacturing and HON process units. The source category contributes 

approximately 13 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) 42

Source Category MIR 

Contribution to Facility-Wide 

MIR

<1 1≤ MIR<10 10≤ MIR<100 > 100 Total

> 90% 3 3 4 0 10

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 23

 

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

Category

5.1 Source Category Description and Results

This section summary presents the risk assessment for the styrene-acrylonitrile (SA) resin 

production source category. Styrene-acrylonitrile resins are copolymers of styrene and 

acrylonitrile. Styrene-acrylonitrile 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 Operations 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. We will update the data set with this information, and any additional information received 

during the comment period, before the final rule.
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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 category data set (of two

facilities) are summarized in Table 5.1-1. The total HAP emissions for the source category are 

approximately 2 tons per year. Based on these data, the HAP emitted in the largest quantities 

for these 2 facilities are: ethyl benzene, styrene, methylene chloride and acrylonitrile. These 

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

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 OAQPSa

Unit Risk PB-HAP?

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

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

5.2 Risk Characterization

This section presents the results of the risk assessment for the 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 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 

 

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. 
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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, based primarily on emissions of acrylonitrile, indicating no 

significant potential for chronic noncancer impacts. 

Worst-case acute HQs were calculated for every HAP that has an acute benchmark, and the 

highest acute HQ value of 0.007 (based on the methylene chloride REL) is shown in Table 

5.2-1. There were no screening acute HQs greater than 1, so further refinement was not 

performed. A screening-level evaluation of the potential human health risks associated with 

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

emitted. 
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Table 5.2-1 Summary of Source Category Level Risks for Styrene-Acrylonitrile 

Production

Result HAP “Drivers”

Facilities in Source Category

Number of Facilities Estimated to be in Source 

Category 2 n/a

Number of Facilities Identified in NEI and 

Modeled in Preliminary Risk Assessment 2 n/a

Cancer Risks

Maximum Individual Lifetime Cancer Risk (in 

1 million) 0.03 acrylonitrile, ethyl benzene

Number of Facilities with Maximum Individual Lifetime Cancer Risk:

Greater than or equal to 100 in 1 

million 0 n/a

Greater than or equal to 10 in 1 

million 0 n/a

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

Chronic Noncancer Risks

Maximum Respiratory Hazard Index 0.0002 acrylonitrile

Number of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Screening Results

Maximum Acute Hazard Quotient 0.007 methylene chloride (REL)

Number of Facilities With Potential for Acute 

Effects 0 n/a

Population Exposure

Number of People Living Within 50 

Kilometers of Facilities Modeled 680,000 n/a

Number of People Exposed to Cancer Risk:

Greater than or equal to 100 in 1 

million 0 n/a

Greater than or equal to 10 in 1 

million 0 n/a

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

Number of People Exposed to Noncancer Respiratory Hazard Index:

Greater than 1 0 n/a

Estimated Cancer Incidence (excess cancer 

cases per year) 0.000006 n/a

Contribution of HAP to Cancer Incidence

ethyl benzene 52% n/a

acrylonitrile 44% n/a

The facility-wide 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 MIR 
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greater than or equal to 1 in a million. The maximum facility-wide cancer MIR is 20 in a 

million for 1 facility. At this facility, the source category contributes less than one percent to 

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

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

resins production source category. The maximum facility-wide 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 Source Category Contribution to Facility-Wide Cancer Risks – StyreneAcrylonitrile Production

Styrene-Acrylonitrile

Production

Number of Facilities Binned by Facility-Wide 

MIR (in 1 million)

Source Category MIR Contribution 

to Facility-Wide MIR

<1 1≤ MIR<10 10≤ MIR<100 > 100 Total

> 90% 0 0 0 0 0

50-90% 0 0 0 0 0

10-50% 0 0 0 0 0

< 10% 0 0 2 0 2

Total 0 0 2 0 2

6. Risk Results for the P&R IV 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 continuous mode). The mass and suspension methods are the most commercially 

significant, whereas use of the emulsion process has decreased significantly since the mid1940s. 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 polystyrene resins, including disposable dinnerware, 
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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 production 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 the data set contains those 11 facilities identified with a polystyrene 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 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 

for these 11 facilities is styrene, which accounts for 94 percent of the total emissions by mass. 

No PB-HAP

44 are reported in the data set for the polystyrene production source category. 

Table 6.1-1 Summary of Emissions from the Polystyrene Production Source Category and Availability 

of Dose-Response Values

HAP Emissions

(tpy)

Number of 

Facilities 

Reporting HAP

(11 facilities in 

data set)

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSa

Unit Risk PB-HAP?

Estimate for 

Cancer?

Reference 

Concentration 

for Chronic 

Noncancer?

Health 

Benchmark 

Values for Acute 

Noncancer?

Styrene 85 10  

Toluene 2 5  

Ethyl Benzene 1 7   

Tetrachloroethylene 1 1   

Xylenes (mixed) 1 5  

Hydrochloric acid 0.3 1  

Cumene 0.1 4  

Hexane 0.1 1  

Benzene 0.007 2   

a

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

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

6.2 Risk Characterization

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

exposure location, as well as a summary of the results of our facility-wide assessments and 

our analysis of risks associated with the maximum allowed emissions under the current 

MACT standards. A detailed summary of the facility-specific risk assessment results is 

available in Appendix 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 tetrachloroethylene 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 in 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. 
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Table 6.2-1 Summary of Source Category Level Risks for Polystyrene Production

Result HAP “Drivers”

Facilities in Source Category

Number of Facilities Estimated to be in Source 

Category 11 n/a

Number of Facilities Identified in NEI and 

Modeled in Preliminary Risk Assessment 11 n/a

Cancer Risks

Maximum Individual Lifetime Cancer Risk (in 

1 million) 2 tetrachloroethylene

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 tetrachloroethylene

Chronic Noncancer Risks

Maximum Neurological Hazard Index 0.004 xylenes (mixed), styrene

Number of Facilities with Maximum Neurological Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Screening Results

Maximum Acute Hazard Quotient 0.3 styrene (REL)

Number of Facilities With Potential for Acute 

Effects 0 n/a

Population Exposure

Number of People Living Within 50 

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

Number of People Exposed to Cancer Risk:

Greater than or equal to 100 in 1 

million 0 n/a

Greater than or equal to 10 in 1 million 0 n/a

Greater than or equal to 1 in 1 million 180 n/a

Number of People Exposed to Noncancer Neurological Hazard Index:

Greater than 1 0 n/a

Estimated Cancer Incidence (excess cancer 

cases per year) 0.00003 n/a

Contribution of HAP to Cancer Incidence

tetrachloroethylene 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 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 

10 in a million at one facility. At this facility, the source category contributes less than one 
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57

percent to the facility-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 

percent to the facility-wide MIR, which is driven by emissions of tetrachloroethylene 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 – 

Polystyrene Production 

Polystyrene 

Production

Number of Facilities Binned by Facility-Wide 

MIR (in 1 million)

Source Category MIR 

Contribution to Facility-Wide MIR

<1 1≤ MIR<10 10≤ MIR<100 > 100 Total

> 90% 3 1 0 0 4

50-90% 1 0 0 0 1

10-50% 0 0 0 0 0

< 10% 5 0 1 0 6

Total 9 1 1 0 11

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

Category

7.1 Source Category Description and Results

Three different types of resins are made by sources covered by the polyethylene terephthalate 

(PET) source category: solid-state resins (PET bottle grade resins), polyester film, and 

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

dimethyl terephthalate (DMT) or terephthalic acid (TPA). PET 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 fibergraded 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 photographic film and magnetic media. PET is used extensively 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 complete description of the polyethylene terephthalate production 

source category can be found in the text of the NPRM.
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We currently estimate that there are 12 PET production facilities operating in the U.S.45 The 

data set contains 15 facilities identified with a PET production MACT code in the 2005 NEI. 

The 2005 NEI was updated for this category with more recent data from industry and 

enhanced quality assurance of facility and emission locations. All 15 of these facilities are 

identified as major sources in the NEI. 

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

summarized in Table 7.1-1. The total HAP emissions for the source category are 

approximately 1,200 tons per year. Based on these data, the HAP emitted in the largest 

quantities across these 15 facilities are ethylene glycol, acetaldehyde, methanol, and biphenyl.

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

46 in the 

data set for the PET production source category include cadmium compounds, polycyclic 

organic matter (POM), and lead compounds. 

Table 7.1-1 Summary of Emissions from the Polyethylene Terephthalate Production Source Category

and Availability of Dose-Response Values

HAPa Emissions

(tpy)

Number of 

Facilities 

Reporting 

HAP (15 

facilities in 

data set)45

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

Unit Risk PB-HAP?

Estimate for 

Cancer?

Reference 

Concentration 

for Chronic 

Noncancer?

Health 

Benchmark 

Values for Acute 

Noncancer?

Ethylene Glycol 500 15 

Acetaldehyde 278 15   

Methanol 270 11  

Biphenyl 59 7 

1,4-dioxane 18 14   

Methyl bromide 12 1  

o-Xylene 9 2  

m-Xylene 8 1  

p-Xylene 7 2  

Hydrochloric acid 5 1  

Toluene 4 2  

Benzene 4 3   

Formaldehyde 3 4   

Glycol Ethers 3 1  

Antimony & compounds 0.5 2 

Trichloroethylene 0.5 1   

 

45 After the risk assessment was completed, we learned that three facilities included in the data set for 

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 this information, and any additional information received 

during the comment period, before the final rule.

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

EPA-453K-04-001A, as referenced in the NPRM and provided on the EPA’s Technology Transfer Network 

website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html. 
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Table 7.1-1 Summary of Emissions from the Polyethylene Terephthalate Production Source Category

and Availability of Dose-Response Values

HAPa Emissions

(tpy)

Number of 

Facilities 

Reporting 

HAP (15 

facilities in 

data set)45

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

Unit Risk PB-HAP?

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 & compounds 0.09 2 

Hexane 0.03 2  

Chlorine 0.01 1  

Acrolein 0.01 1  

Nickel compounds

 Nickel 0.0003 1   

 Nickel & compounds 0.00002 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 assume 

the reported mass is 100 percent metal.

 For emissions reported generically as “Glycol Ethers” or specific glycol ethers not found on EPA’s Technology 

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

 For emissions of any chemicals or 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 72002, not shown above) all have unit risk estimates for cancer, and are considered

PB-HAP.

b

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

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

c There is no reference concentration for lead. In considering noncancer hazards for lead in this assessment, we compared 

maximum annual ambient exposure estimates to the National Ambient Air Quality Standards (NAAQS) for lead 
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(0.15 μg/m3). These NAAQS for lead were reviewed with revisions adopted in October 2008 

(http://www.epa.gov/air/lead/actions.html). The primary (health-based) standard is a maximum or not-to-be-exceeded, rolling 

three-month average, measured as total suspended particles (TSP). The secondary (welfare-based) standard is identical to the 

primary standard.

7.2 Risk Characterization

This section presents the results of the risk assessment for the polyethylene terephthalate

(PET) production source category. The basic chronic inhalation risk estimates presented here 

are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the 

cancer incidence. We also present results from our acute inhalation impact screening in the 

form of maximum hazard quotients, as well as the results 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 the maximum allowed 

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

risk assessment results is available in Appendix 4. 

Tables 7.2-1 and 7.2-2 summarize the chronic and acute inhalation risk results for this source 

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

as 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 at or above 1 in a 

million as a result of the emissions from 6 facilities. The population exposed to cancer risk 

would be less than presented in the table below due to the adjusted emissions. The maximum 

chronic noncancer TOSHI value for the source category could be up to 0.5, indicating no 

significant potential for chronic noncancer impacts.

Worst-case acute HQs were calculated for every HAP that has an acute benchmark. For cases 

where the screening acute HQ was greater than 1, we further refined the estimates by

determining the highest HQ value that is outside facility boundaries. An additional 

adjustment to the multiplier of 10 was made for 2 facilities. The multiplier was adjusted from 

10 to a value of 2 based on our approach as described in the memorandum “Emission Data 

and Acute Risk Factor Used in Residual Risk Modeling: Pesticide Active Ingredients, 

Polyether Polyols, Polymers and Resins IV” available in the docket for this action. Other 

facility multipliers were adjusted from 10 to 2 since the emissions are from equipment leaks 

and we believe there is less variability associated with emissions from equipment leaks (see 

Appendix 7 of this document and the memorandum “Emission Data and Acute Risk Factor 

Used in Residual Risk Modeling: Pesticide Active Ingredients, Polyether Polyols, Polymers 

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

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

as shown in Table 7.2-1. Analysis of potential off-site acute impacts for this source category

identified six facilities with the potential to exceed the acute REL for acetaldehyde. Table 

7.2-2 provides more information on the acute risk estimates for HAP that had an acute HQ 

greater than 1 for any benchmark. The maximum HQ for acetaldehyde based on the 1-hour 

AEGL-1 value is 0.2, and the maximum HQ for acetaldehyde based on the 1-hour ERPG-1 
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value is 1. The ERPG-1 value is a no effect level which is expected to be protective for 

sensitive populations from eye and upper respiratory irritation. The AEGL-1 value is a level 

at which we expect to see mild eye or upper respiratory irritation in the general population.

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

concern. While these estimated worst-case exceedances indicate that there is some potential 

for such acute exposures to occur, we note 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 results along with the rather large uncertainties related to the emissions estimates 

and screening methodology. 

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

on both the 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. We also identified that one of the high HQ values was associated with acetaldehyde 

emissions from wastewater treatment operations which were modeled from a single emission 

location versus being modeled as emissions emanating across a large area, again biasing the 

HQ estimate high. Taking all of this into consideration, these acute impact screening results 

indicate only the potential for acute impacts of concern, while the uncertainties and bias 

associated with them suggest that there may be no real acute issues. 

We conducted a screening-level evaluation of the potential human health risks associated with 

emissions of PB-HAP. Reported emissions of PB-HAP were compared to emission 

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

emitted by facilities from this category are cadmium compounds (2 facilities), polycyclic 

organic matter (POM) as benzo(a)pyrene toxicity equivalence (TEQ) (1 facility), and lead 

compounds (1 facility). All cadmium and POM as benzo(a)pyrene TEQ emissions were 

below the screening threshold levels, and therefore we do not expect any significant 

multipathway exposure and risk due to these emissions. Lead is a PB-HAP, but the National 

Ambient Air Quality Standards (NAAQS) value (which was used for the chronic noncancer 

risk assessment) takes into account multipathway exposures, so a separate multipathway

screening value was not developed. Since we did not estimate any exceedances of the 

NAAQS in our chronic noncancer risk assessment, we do not expect any significant 

multipathway exposure and risk due to lead emissions from these facilities. 

 

47 ICF International. TRIM-Based Multipathway Screening Scenario. Prepared for U.S. Environmental 

Protection Agency, Research Triangle Park, NC. October 2008.
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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 in Source 

Category 12 n/a

Number of Facilities Identified in NEI and 

Modeled in Preliminary Risk Assessment 15 n/a

Cancer Risks

Maximum Individual Lifetime Cancer Risk (in 

1 million) 9 acetaldehyde, 1,4-dioxane

Number of Facilities with Maximum Individual Lifetime Cancer Risk:

Greater than or equal to 100 in 1 

million 0 n/a

Greater than or equal to 10 in 1 

million 0 n/a

Greater than or equal to 1 in 1 million 6

acetaldehyde, 1,4-dioxane, ethylene 

oxide

Chronic Noncancer Risks

Maximum Respiratory Hazard Index 0.5 acetaldehyde, acrolein, ethylene glycol

Number of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Refined Screening Results

Maximum Acute Hazard Quotient

8

1

0.2

acetaldehyde (REL)

acetaldehyde (ERPG-1)

acetaldehyde (AEGL-1)

Number of Facilities With Potential for Acute 

Effects 9 acetaldehyde

Population Exposure

Number of People Living Within 50 

Kilometers of Facilities Modeled 48 7,700,000 n/a

Number of People Exposed to Cancer Risk:

Greater than or equal to 100 in 1 

million 0 n/a

Greater than or equal to 10 in 1 

million 0 n/a

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

 

48 After the risk 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. 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 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 completing the final rule.
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Table 7.2-1 Summary of Source Category Level Risks for Polyethylene Terephthalate 

Production

Result HAP “Drivers”

Number of People Exposed to Noncancer Respiratory Hazard Index:

Greater than 1 0 n/a

Estimated Cancer Incidence (excess cancer 

cases per year) 0.002 n/a

Contribution of HAP to Cancer Incidence

acetaldehyde 74% n/a

1,4-dioxane 16% n/a

Table 7.2-2 Summary of Acute Refined Screening Results for Polyethylene Terephthalate 

Production

Results

MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE-RESPONSE VALUES

Based on REL Based on 

AEGL-1/

ERPG-1

Based on 

AEGL-2/

ERPG-2

REL

(mg/m3)

AEGL-1 

(1-hr) 

(mg/m3)

ERPG-1 

(mg/m3)

AEGL-2

(1-hr)

(mg/m3)

ERPG-2 

(mg/m3)

HAP Max. 1-hr. 

Air Conc. 

(mg/m3)

Acetaldehyde 19.3 8 0.2/1 0.04/0.05 0.47 81 18 490 360

Notes on Refined Process:

1) The screening was performed for all emitted HAP with available acute dose-response values. Only those pollutants whose 

screening HQs were greater than 1 for at least one acute threshold value are shown in the table.

2) HAP with available acute dose-response values which are not in the table do not carry any potential for posing acute health risks, 

based on an analysis of currently available emissions data.

Notes on Acute Dose-Response Values:

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

AEGL – Acute exposure guideline levels represent emergency exposure (1-hour) limits for the general public.

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

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

AEGL-2 is the exposure level above which it is predicted that the general population, including susceptible individuals, could 

experience irreversible or other serious, long-lasting adverse health effects of an impaired ability to escape.

EPRG – Emergency Removal Program guidelines represent emergency exposure (1-hour) limits for the general public.

ERPG-1 is the maximum level below which it is believed that nearly all individuals could be exposed for up to 1 hour without 

experiencing other than mild, transient adverse health effects.

ERPG-2 is the maximum exposure below which it is believed that nearly all individuals could be exposed for up to 1 hour without 

experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual’s ability to 

take protective action.

The facility-wide 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 7.2-3. The results indicate that eight

facilities with PET production processes have a facility-wide cancer MIR greater than or 

equal to 1 in a million. The maximum facility-wide cancer MIR for the source category is 9

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

contributes less than ten percent to the facility-wide MIR, which is driven by emissions of 

arsenic and chromium from hazardous waste incineration. At the other facility, the PET 

production source category contributes almost 100 percent to the facility-wide MIR, which is 
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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. The source category contributes 

approximately five percent to the facility-wide TOSHI. 

Table 7.2-3 Source Category Contribution to Facility-Wide Cancer Risks – 

Polyethylene Terephthalate Production

Polyethylene Terephthalate

Production

Number of Facilities Binned by Facility-Wide 

MIR (in 1 million)48

Source Category MIR Contribution 

to 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-ButadieneStyrene Source Category

8.1 Source Category Description and Results

Methyl methacrylate-butadiene styrene resins (MBS) are prepared by grafting methyl

methacrylate and styrene onto a styrene-butadiene rubber in an emulsion process. In 

emulsion polymerization, monomers are dispersed in water using a soap solution or an 

emulsifier. The product is a two-phase polymer used as an impact modifier for rigid 

polyvinyl chloride products. These products are used for applications in packaging, building, 

and construction. Emission points for MBS resin production include process vents, 

equipment 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 facilities operating in the U.S. The 

data set contains two facilities identified with a MBS production MACT code in the 2005 

NEI. The 2005 NEI was updated for this category with more recent data from industry and 

enhanced quality assurance of facility and emission locations. Both of these facilities are 

identified as major sources in the NEI. 

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

summarized in Table 8.1-1. The total HAP emissions for the source category are 

approximately five tons per year. Based on these data, the HAP emitted in the largest 

quantities for these two facilities are: methyl methacrylate, 1,3-butadiene, ethyl acrylate, 
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65

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

mass. No PB-HAP

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 Values

HAP Emissions

(tpy)

Number of 

Facilities 

Reporting 

HAP (2 

facilities in 

data set)

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSa

Unit Risk PB-HAP?

Estimate for 

Cancer?

Reference 

Concentration 

for Chronic 

Noncancer?

Health 

Benchmark 

Values for Acute 

Noncancer?

Methyl Methacrylate 2 1  

1,3-Butadiene 2 1   

Ethyl Acrylate 0.9 1 

Methanol 0.2 1  

Styrene 0.2 1  

Hydrochloric Acid 0.008 1  

a

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

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

8.2 Risk Characterization

This section presents the results of the risk assessment for the methyl methacrylate-butadienestyrene production source category. The basic chronic inhalation risk estimates presented 

here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, 

and the cancer incidence. We also present results from our acute inhalation impact screening 

in the form of maximum hazard quotients. Also presented are the HAP “drivers,” which are 

the HAP that collectively contribute 90 percent of the maximum cancer risk or maximum 

hazard index at the highest exposure location, as well as a summary of the results of our 

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

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

risk assessment results is available in Appendix 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. 
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66

Worst-case acute HQs were calculated for every HAP that has an acute benchmark. For cases 

where the screening acute HQ was greater than 1, we further refined the estimates by

determining the highest HQ value that is outside facility boundaries. Analysis of potential 

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

exceed the acute ERPG-1 value for ethyl acrylate. Table 8.2-2 provides more information on 

the acute risk estimates for HAP that had an acute HQ greater than 1 for any benchmark. 

After these refinements, the highest worst-case acute HQ value is 9 (based on the ethyl 

acrylate ERPG-1). This worst-case exposure estimate corresponds to an HQ of 0.01 based on 

the 1-hour AEGL-1 value. For ethyl acrylate, the ERPG-1 value is indicative of the odor 

recognition threshold, while the AEGL-1 value is indicative of a level which 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 emissions at all other facilities indicated no potential to cause acute impacts of 

concern. While these estimated worst-case exceedances indicate that there is some potential 

for such acute exposures to occur, we note that exceeding the modeled ERPG-1 or AEGL-1

values does not necessarily indicate that adverse effects will occur, only that they cannot be 

ruled out. Further, in characterizing the potential for acute noncancer impacts of concern, it is 

important to remember the upward bias of these worst-case exposure estimates and to 

consider the results along with the rather large 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 that 

this assumption further biases the HQ values high, but to an unknown extent, given that we do 

not know the actual size of the processing areas at each of these facilities. Taking all of this 

into consideration, these acute impact screening results indicate only the potential for acute 

impacts of concern, while the uncertainties 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. 
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Table 8.2-1 Summary of Source Category Level Risks for Methyl MethacrylateButadiene-Styrene Production

Result HAP “Drivers”

Facilities in Source Category

Number of Facilities Estimated to be in Source 

Category 2 n/a

Number of Facilities Identified in NEI and 

Modeled in Preliminary Risk Assessment 2 n/a

Cancer Risks

Maximum Individual Lifetime Cancer Risk (in 

1 million) 0.4 1,3-butadiene

Number of Facilities with Maximum Individual Lifetime Cancer Risk:

Greater than or equal to 100 in 1 

million 0 n/a

Greater than or equal to 10 in 1 

million 0 n/a

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

Chronic Noncancer Risks

Maximum Reproductive Hazard Index 0.007 1,3-butadiene

Number of Facilities with Maximum Reproductive Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Refined Screening Results

Maximum Acute Hazard Quotient 9

0.01

ethyl acrylate (ERPG-1)

ethyl acrylate (AEGL-1)

Number of Facilities With Potential for Acute 

Effects 1 ethyl acrylate

Population Exposure

Number of People Living Within 50 

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

Number of People Exposed to Cancer Risk:

Greater than or equal to 100 in 1 

million 0 n/a

Greater than or equal to 10 in 1 

million 0 n/a

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

Number of People Exposed to Noncancer Reproductive Hazard Index:

Greater than 1 0 n/a

Estimated Cancer Incidence (excess cancer 

cases per year) 0.00003 n/a

Contribution of HAP to Cancer Incidence

1,3-butadiene 100% n/a
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Table 8.2-2 Summary of Acute Refined Screening Results for Methyl Methacrylate-ButadieneStyrene 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/m3)

AEGL-1 

(1-hr) 

(mg/m3)

ERPG-1 

(mg/m3)

AEGL-2

(1-hr)

(mg/m3)

ERPG-2 

(mg/m3)

HAP Max. 1-hr. 

Air Conc. 

(mg/m3)

Ethyl acrylate 0.37 0.01/9 0.002/0.003 34 0.041 150 120

Notes on Refined Process:

1) The screening was performed for all emitted HAP with available acute dose-response values. Only those pollutants whose

screening HQs were greater than 1 for at least one acute threshold value are shown in the table.

2) HAP with available acute dose-response values which are not in the table do not carry any potential for posing acute health risks, 

based on an analysis of currently available emissions data.

Notes on Acute Dose-Response Values:

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

AEGL – Acute exposure guideline levels represent emergency exposure (1-hour) limits for the general public.

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

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

AEGL-2 is the exposure level above which it is predicted that the general population, including susceptible individuals, could 

experience irreversible or other serious, long-lasting adverse health effects of an impaired ability to escape.

EPRG – Emergency Removal Program guidelines represent emergency exposure (1-hour) limits for the general public.

ERPG-1 is the maximum level below which it is believed that nearly all individuals could be exposed for up to 1 hour without 

experiencing other than mild, transient adverse health effects.

ERPG-2 is the maximum exposure below which it is believed that nearly all individuals could be exposed for up to 1 hour without 

experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual’s ability to 

take protective action.

The facility-wide 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 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. The 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 facility-wide cancer risk is driven 

almost exclusively by emissions of 1,3-butadiene from equipment leaks from the MBS 

process. The maximum facility-wide TOSHI for the source category is less than 1. 

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

Methacrylate-Butadiene-Styrene Production

Methyl Methacrylate-ButadieneStyrene ProductionNumber of Facilities Binned by Facility-Wide 

MIR (in 1 million)

Source Category MIR Contribution 

to Facility-Wide MIR

<1 1≤ 

MIR<10

10≤ 

MIR<100

> 100 Total

> 90% 1 0 0 0 1
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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-butadiene-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 

polymerization, 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, suspending 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, toys, mobile homes, and margarine tubs. 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 acrylonitrilebutadiene-styrene 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 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 facilities) 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-butadiene, cumene, 

methyl methacrylate, and xylenes (mixed). These six HAP account for over 90 percent of the 

total emissions by mass. No PB-HAP

50 are reported in the data set for the acrylonitrilebutadiene-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. 
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Table 9.1-1 Summary of Emissions from the Acrylonitrile-Butadiene-Styrene Production Source 

Category and Availability of Dose-Response Values

HAPa Emissions

(tpy)

Number of 

Facilities 

Reporting HAP

(5 facilities in 

data set)

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

Unit Risk PB-HAP?

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 Methyl Ether 0.5 1 

Acetaldehyde 0.5 1   

o-Xylene 0.3 1  

Vinyl Acetate 0.2 1  

2,4-Dichlorophenoxy Acetic Acid 0.03 1

Chloroacetic Acid 0.02 1 

Glycol Ethers 0.02 1  

Ethyl Acrylate 0.01 1 

2,4,6-Trichlorophenol 0.007 1 

N,N-Dimethylformamide 0.004 1  

Phosgene 0.003 1  

Hydroquinone 0.002 1

Naphthalene 0.002 1  

Ethylene Oxide 0 1   

a Notes for how HAP were speciated for risk assessment:

 For emissions reported generically as “Glycol Ethers” or specific glycol ethers not found on EPA’s Technology 

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

b

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

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

This section presents the results of the risk assessment for the acrylonitrile-butadiene-styrene 

production source category. The basic chronic inhalation risk estimates presented here are the 

maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer 

incidence. We also present results from our acute inhalation impact screening in the form of 

maximum hazard quotients. Also presented are the HAP “drivers,” which are the HAP that 

collectively contribute 90 percent of 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 or risks associated with the maximum allowed emissions under 

the current MACT standards. A detailed summary of the facility-specific risk assessment 

results is available in Appendix 4. 

Tables 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 from 

emissions of 1,3-butadiene, indicating no significant potential for chronic noncancer impacts. 

Worst-case acute HQs were calculated for every HAP that has an acute benchmark, and the 

highest acute HQ value of 2 (based on the acetaldehyde REL) is shown in Table 9.2-1. For 

cases where the screening acute HQ was greater than 1, we further refined the estimates by

determining the highest HQ value that is outside facility boundaries. Table 9.2-1 provides 

more information on the acute risk estimates for HAP that had an acute HQ greater than 1 for 

any benchmark. The highest refined worst-case acute HQ value remains 2 based on the 

acetaldehyde REL, with only one facility showing the potential to exceed the REL. This

estimated worst-case acute impact corresponds to an acute HQ of 0.04 based on the 

acetaldehyde ERPG-1. Refer to Table 9.2-2 for further information on the refined acute risk 

estimate.

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

concern. While these estimated worst-case exceedances indicate that there is some potential 

for such acute exposures to occur, we note that exceeding the modeled REL or ERPG-1 

values does not necessarily indicate that adverse effects will occur, 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 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. 
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Table 9.2-1 Summary of Source Category Level Risks for Acrylonitrile-ButadieneStyrene Production

Result HAP “Drivers”

Facilities in Source Category

Number of Facilities Estimated to be in Source 

Category 5 n/a

Number of Facilities Identified in NEI and 

Modeled in Preliminary Risk Assessment 5 n/a

Cancer Risks

Maximum Individual Lifetime Cancer Risk (in 

1 million) 30 acrylonitrile, 1,3-butadiene

Number of Facilities with Maximum Individual Lifetime Cancer Risk:

Greater than or equal to 100 in 1 

million 0 n/a

Greater than or equal to 10 in 1 

million 3 acrylonitrile, 1,3-butadiene

Greater than or equal to 1 in 1 million 4

acrylonitrile, 1,3-butadiene, ethyl 

benzene

Chronic Noncancer Risks

Maximum Reproductive Hazard Index 0.2 1,3-butadiene

Number of Facilities with Maximum Reproductive Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Screening Results

Maximum Acute Hazard Quotient 2

0.04

acetaldehyde (REL)

acetaldehyde (ERPG-1)

Number of Facilities With Potential for Acute 

Effects 1 acetaldehyde

Population Exposure

Number of People Living Within 50 

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

Number of People Exposed to Cancer Risk:

Greater than or equal to 100 in 1 

million 0 n/a

Greater than or equal to 10 in 1 

million 530 n/a

Greater than or equal to 1 in 1 million 32,000 n/a

Number of People Exposed to Noncancer Reproductive Hazard Index:

Greater than 1 0 n/a

Estimated Cancer Incidence (excess cancer 

cases per year) 0.003 n/a

Contribution of HAP to Cancer Incidence

acrylonitrile 66% n/a

1,3-butadiene 32% n/a
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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/m3)

AEGL-1 

(1-hr) 

(mg/m3)

ERPG-1 

(mg/m3)

AEG

L-2

(1-hr)

(mg/

m

3

)

ERP

G-2 

(mg/

m

3 HAP Max. 1-hr. )

Air Conc. 

(mg/m3)

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

Notes on Screening Process:

1) The screening was performed for all emitted HAP with available acute dose-response values. Only those pollutants 

whose screening HQs were greater than 1 for at least one acute threshold value are shown in the table.

2) HAP with available acute dose-response values which are not in the table do not carry any potential for posing 

acute health risks, based on an analysis of currently available emissions data.

Notes on Acute Dose-Response Values:

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

exposures.

AEGL – Acute exposure guideline levels represent emergency exposure (1-hour) limits for the general public.

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

individuals, could 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 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 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 and 1,3-butadiene from process vents. The 

maximum facility-wide TOSHI for the source category is less than 1. 
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Table 9.2-3 Source Category Contribution to Facility-Wide Cancer Risks – 

Acrylonitrile-Butadiene-Styrene Production

Acrylonitrile-Butadiene-Styrene 

Production

Number of Facilities Binned by Facility-Wide 

MIR (in 1 million)

Source Category MIR Contribution 

to Facility-Wide MIR

<1 1≤ MIR<10 10≤ MIR<100 > 100 Total

> 90% 0 0 3 0 3

50-90% 0 0 1 0 1

10-50% 1 0 0 0 1

< 10% 0 0 0 0 0

Total 1 0 4 0 5

10. General Discussion of Uncertainties and How They Have Been 

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 

modeling estimates. The chronic exposure modeling uncertainties are considered relatively 

small in comparison, since we are using EPA’s refined local dispersion model with sitespecific 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 derived at census block centroid locations rather than actual 

residences. This uncertainty is known to create potential underestimates and overestimates of 

the actual MIR values for individual facilities, but, overall, it is not thought to have a 

significant impact on the estimated MIR for a source category. Finally, we did not factor in 

the possibility of a source closure occurring during the 70-year chronic exposure period, 

leading to a potential upward bias in both the MIR and population risk estimates; nor did we 

factor in the possibility of population growth during the 70-year chronic exposure period, 

leading to a potential downward bias in both the MIR and population risk estimates.

A sensitivity analysis performed for the 1999 NATA found that the selection of the 

meteorology dataset location could result in a range of chronic ambient concentrations which 

varied from as much as 17% below the estimated value to as much as 84% higher 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.
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We have purposely biased the acute screening results high, considering that they depend upon 

the joint occurrence of independent factors, such as hourly emissions rates, meteorology and 

human activity patterns. Furthermore, in cases where multiple acute threshold values are 

considered scientifically acceptable we have chosen the most conservative of these 

assessments, erring on the side of overestimating potential health risks from acute exposures. 

In the cases where these results indicated the potential for exceeding short-term health 

thresholds, we have refined our assessment by developing a better understanding of the 

geography of the facility relative to potential exposure locations and the true variability of 

short-term emission rates. 

10.2 Uncertainties in the Dose-Response Relationships

In the sections that follow, separate discussions are provided on uncertainty associated with 

cancer potency factors and noncancer reference values. Cancer potency values are derived for 

chronic (lifetime) exposures. Noncancer reference values are generally derived for chronic 

exposures (up to a lifetime), but may also be derived for acute (<24 hours), short-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 with the 

emissions included in an assessment, we rely on both chronic (cancer and noncancer) and 

acute (noncancer) benchmarks, which are described in more detail below.

Although every effort is made to identify peer-reviewed dose-response values for all HAPs

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

potency values or reference values for chronic non-cancer or acute effects (inhalation or 

ingestion). Since exposures to these pollutants cannot be included in a quantitative risk 

estimate, an understatement of risk for these pollutants at environmental exposure levels is 

possible.

Additionally, chronic dose-response values for certain compounds included in the assessment 

may be under EPA IRIS review, and revised assessments may determine that these pollutants 

are more or less potent than currently thought. We will re-evaluate risks if, as a result of these 

reviews, a dose-response metric changes enough to indicate that the risk assessment may

significantly mischaracterize human health risk

Cancer assessment

The discussion of dose-response uncertainties in the estimation of cancer risk below focuses 

on the uncertainties associated with the specific approach currently used by the EPA to 

develop cancer potency factors. In general, these same uncertainties attend the development 

of cancer potency factors by CalEPA, the source of peer-reviewed cancer potency factors 

used where EPA-developed values are not yet available. To place this discussion in context, 

we provide a quote from the EPA’s Guidelines for Carcinogen Risk Assessment [30] (herein 

referred to as Cancer Guidelines). “The primary goal of EPA actions is protection of human 

health; accordingly, as an Agency policy, risk assessment procedures, including default 

options that are used in the absence of scientific data to the contrary, should be health 
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protective.” The approach adopted in this document is consistent with this approach as 

described in the Cancer Guidelines.

For cancer endpoints EPA usually derives an oral slope factor for ingestion and a unit risk 

value for inhalation exposures. These values allow estimation of a lifetime probability of 

developing cancer given long-term exposures to the pollutant. Depending on the pollutant 

being evaluated, EPA relies on both animal bioassay and epidemiological studies to 

characterize cancer risk. As a science policy approach, consistent with the Cancer 

Guidelines, EPA uses animal cancer bioassays as indicators of potential human health risk 

when other human cancer risk data are unavailable. 

Extrapolation of study data to estimate potential risks to human populations is based upon 

EPA’s assessment of the scientific database for a pollutant using EPA’s guidance documents 

and other peer-reviewed methodologies. The EPA Cancer Guidelines describes the Agency’s 

recommendations for methodologies for cancer risk assessment. EPA believes that cancer 

risk estimates developed following the procedures described in the Cancer Guidelines and 

outlined below generally provide an upper bound estimate of risk. That is, EPA’s upper 

bound estimates represent a “plausible upper limit to the true value of a quantity” (although 

this is usually not a true statistical confidence limit).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 risk 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 limitations for some uses (e.g. priority setting, expected 

benefits analysis).

Such health risk assessments have associated uncertainties, some which may be considered 

quantitatively, and others which generally are expressed qualitatively. Uncertainties may vary 

substantially among cancer risk assessments associated with exposures to different pollutants, 

since the assessments employ different databases with different strengths and limitations and 

the procedures employed may differ in how well they represent actual biological processes for 

the assessed substance. EPA’s Risk Characterization Handbook also 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 chemicals is not underestimated (although defaults are not intended to overtly 

overestimate risk). See EPA 2004 An Examination of EPA Risk Assessment Principles and Practices, 

EPA/100/B-04/001 available at: http://www.epa.gov/osa/pdfs/ratf-final.pdf.
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choices, data, models and assumptions [31]. Some of the major sources of uncertainty and 

variability in deriving cancer risk values are described more fully below. 

(1) The qualitative similarities or differences between tumor responses observed in 

experimental animal bioassays and those which would occur in humans are a source of 

uncertainty in cancer risk assessment. In general, EPA does not assume that tumor sites 

observed in an experimental animal bioassay are necessarily predictive of the sites at which 

tumors would occur in humans.54 However, unless scientific support is available to show 

otherwise, EPA assumes that tumors in animals are relevant in humans, regardless of target 

organ concordance. For a specific pollutant, qualitative differences in species responses can 

lead to either under-estimation or over-estimation of human cancer risks. 

(2) 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 blood 

concentration of the pollutant or the quantity of agent metabolized in the body). Quantitative 

uncertainties result when the appropriate choice of a dose metric is uncertain or when dose 

metric estimates are themselves uncertain (e.g., as can occur when alternative 

pharmacokinetic models are available for a compound). Uncertainty in dose estimates may

lead to 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 species size and empirical comparisons of toxicity between experimental animals and 

humans. For a particular pollutant, the quantitative difference in cancer potency between 

experimental animals and humans may be either greater than or less than that estimated by

baseline scientific scaling predictions due to 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 generally developed using a benchmark dose (BMD) analysis to estimate a dose at which 

there is a specified excess risk of cancer, which is used as the point of departure (or POD) for 

the remainder of the calculation. Statistical uncertainty in developing a POD using a 

benchmark dose (BMD) approach is generally addressed though use of the 95% lower 

confidence limit on the 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 the EPA Cancer Guidelines: “The default option is that positive effects in animal cancer studies indicate 

that the agent under study can have carcinogenic potential in humans.” and “Target organ concordance is not a 

prerequisite for evaluating the implications of animal study results for humans.”
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(5) Extrapolation from high to low doses is an important, and potentially large, source of 

uncertainty in cancer risk assessment. EPA uses different approaches to low dose risk 

assessment (i.e., developing estimates of risk for exposures to environmental doses of an 

agent from observations in experimental or epidemiological studies at higher dose) depending 

on the available data and understanding of a pollutant’s mode of action (i.e., the manner in 

which a pollutant causes cancer). EPA’s Cancer Guidelines express a preference for the use 

of reliable, compound-specific, biologically-based risk models when feasible; however, such 

models are rarely available. The mode of action for a pollutant (i.e., the manner in which a 

pollutant causes cancer) is a key consideration in determining how risks should be estimated 

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

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

(straight line from POD) approach is used when available mode of action data support a linear 

(e.g., nonthreshold response) or as the most common default approach when a compound’s 

mode of action is unknown. 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 pollutants that interact with DNA and 

induce mutations. Pollutants whose effects are additive to background biological processes in 

cancer development can also be predicted to have low-dose linear responses, although the 

slope of this relationship may not be the same as the slope estimated by the straight line 

approach. 

EPA most frequently utilizes a linear low-dose extrapolation approach as a baseline sciencepolicy 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 thresholds are likely to lead to sigmoidal-shaped 

dose-response functions for a population. This report notes sources of variability in the 

human population: “One might expect these individual tolerances to vary extensively in 

humans depending on genetics, coincident exposures, nutritional status, and various other 

susceptibility factors...” Thus, if a distribution of thresholds approach is 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 line 
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risk estimates can be quantified by comparing risk estimates using the BMDL value to central 

estimate BMD values, although these differences are generally not a large contributor to 

uncertainty in risk assessment (Subramaniam et. al., 2006) [33]. It is important to note that 

earlier EPA assessments, including the majority of those for which risk values exist today, 

were generally developed using the multistage model to extrapolate down to environmental 

dose levels and did 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 another source of uncertainty in 

assessments. In the diverse human population, some individuals are likely to be more 

sensitive to the action of a carcinogen than the typical individual, although compound-specific 

data to evaluate this variability are generally not available. There may also be important life 

stage differences in the quantitative potency of carcinogens and, with the exception of the 

recommendations in EPA’s Supplemental Cancer Guidance for carcinogens with a mutagenic 

mode of action, risk assessments do not generally quantitatively address life stage differences. 

However, one approach used commonly in EPA assessments that may help address variability

in response is to extrapolate human response from results observed in the most sensitive 

species and sex tested, resulting 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 noncancer reference values represent chronic exposure levels that are intended to be 

health-protective. That is, EPA and other organizations which develop noncancer reference 

values (e.g., the Agency for Toxic Substances and Disease Registry – ATSDR) utilize an 

approach that is intended not to underestimate risk in the 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 against appreciable risk of 

deleterious effects. Uncertainty factors are commonly default values55 e.g., factors of 10 or 3, 

used in the absence of compound-specific data; where data are available, uncertainty factors 

may also be developed using compound-specific information. When data are limited, more 

 

55

 According to the NRC report Science and Judgment in Risk Assessment (NRC, 1994) “[Default] options are 

generic approaches, based on general scientific knowledge and policy judgment, that are applied to various 

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 chemicals is not underestimated (although defaults are not intended to overtly 

overestimate risk). See EPA 2004 An examination of EPA Risk Assessment Principles and Practices,

EPA/100/B-04/001 available at: http://www.epa.gov/osa/pdfs/ratf-final.pdf. 
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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 ingestion 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 

population (including sensitive subgroups) that is likely to be without an appreciable risk of 

deleterious effects during a lifetime.56 To derive values that are intended to be “without 

appreciable risk,” EPA’s methodology relies upon an uncertainty factor (UF) approach

[34],[35] which includes consideration of both uncertainty and variability.

 

EPA begins by evaluating all of the available peer-reviewed literature to determine noncancer endpoints of concern, evaluating the quality, strengths and limitations of the available 

studies. EPA typically chooses the relevant endpoint that occurs at the lowest dose, often 

using statistical modeling of the available data, and then determines the appropriate point of 

departure (POD) for derivation of the reference value. A POD is determined by (in order of 

preference): (1) a statistical estimation using the benchmark dose (BMD) approach; (2) use of 

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

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

level (LOAEL).

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

the reference value [36]. While collectively termed “UFs”, these factors account for a 

number of different quantitative considerations when utilizing observed animal (usually

rodent) or human toxicity data in a risk assessment. The UFs are intended to account for: (1) 

variation in susceptibility among the members of the human population (i.e., inter-individual 

variability); (2) uncertainty in extrapolating from experimental animal data to humans (i.e., 

interspecies differences); (3) uncertainty in extrapolating from data obtained in a study with 

less-than-lifetime exposure (i.e., extrapolating from subchronic to chronic exposure); (4) 

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-reviewed assessment-specific data are not available, default 

adjustment values are selected for the individual UFs. For each type of uncertainty (when 

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

UF value leading to a downward adjustment of 10-3000 fold from the selected POD. An UF 

of 3 is used when the data do not support the use of a 10-fold factor. If an extrapolation step 

or adjustment is not relevant to an assessment (e.g., if applying human toxicity data and an 

interspecies extrapolation is not required) the associated UF is not used. The major 

adjustment steps are described more fully below.

1) Heterogeneity among humans is a key source of variability as well as uncertainty. 

Uncertainty related to human variation is considered in extrapolating doses from a subset or 

 

56 See IRIS glossary
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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 

pollutant-specific data on human variation, a 10-fold UF is used to account for uncertainty

associated with human variation. Human variation may be larger or smaller; however, data to 

examine the potential magnitude of human variability are often unavailable. In some 

situations, a smaller UF of 3 may be applied to reflect a known lack of significant variability

among humans.

2) Extrapolation from results of studies in experimental animals to humans is a 

necessary step for the majority of chemical risk assessments. When interpreting animal data, 

the concentration at the POD (e.g. NOAEL, BMDL) in an animal model (e.g. rodents) is 

extrapolated to estimate the human response. While there is long-standing scientific support 

for the use of animal studies as indicators of potential toxicity to humans, there are 

uncertainties in such extrapolations. In the absence of data to the contrary, the typical 

approach is to use the most relevant endpoint from the most sensitive species and the most 

sensitive sex in assessing risks to the average human. Typically, compound specific data to 

evaluate relative sensitivity in humans versus rodents 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 specific 

chemical, differences in species responses may be greater or less than this value.

Pharmacokinetic models are useful to examine species differences in pharmacokinetic 

processing and associated 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 uncertainty in extrapolating from 

laboratory animals to humans in the derivation of a reference value. If information on one or 

the other of these components is available and accounted for in the cross-species 

extrapolation, a UF of 3 may be used for the remaining component.

3) In the case of reference values for chronic exposures where only data from shorter 

durations are available (e.g., 90-day subchronic studies in rodents) or when such data are 

judged more appropriate for development of an RfC, an additional UF of 3 or 10-fold is 

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

4) 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 is 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. 
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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 characterization of the 

chemical’s toxicity. In the absence of studies for a known or suspected endpoint of concern, a 

UF of 10 or 3-fold is typically applied.

Acute noncancer assessment

Many of the UFs used to account for variability and uncertainty in the development of acute 

reference values are quite similar to those developed for chronic durations, but more often 

using individual UF values that may be less than 10. UFs are applied based on chemicalspecific or health effect-specific information (e.g., simple irritation effects do not vary

appreciably between human individuals, hence a value of 3 is typically used), or based on the 

purpose for the reference value (see the following paragraph). The UFs applied in acute 

reference value derivation include: 1) heterogeneity among humans; 2) uncertainty in 

extrapolating from animals to humans; 3) uncertainty in LOAEL to NOAEL adjustments; and 

4) uncertainty in accounting for an incomplete database on toxic effects of potential concern. 

Additional adjustments are often applied to account for uncertainty in extrapolation from 

observations at one exposure duration (e.g., 4 hours) to arrive at a POD for derivation of an 

acute reference value at another exposure duration (e.g., 1 hour). 

Not all acute reference values are developed for the same purpose and care must be taken 

when interpreting the results of an acute assessment of human health effects relative to the 

reference value or values being exceeded. Where relevant to the estimated exposures, the 

lack of threshold values at different levels of severity should be factored into the risk 

characterization as potential uncertainties. 
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