Residual Risk Assessment for 7 Source Categories: 

Printing and Publishing 

Marine Tank Vessel Loading Operations 

Pharmaceuticals Production 

Epichlorohydrin Elastomers 

Polybutadiene Rubber 

Styrene Butadiene 

Nitrile Butadiene 

by 

EPA’s Office of Air Quality Planning and Standards 

Office of Air and Radiation 

January 2011 
2

Table of Contents 

1 Introduction ............................................................................................................................. 5

2 Methods................................................................................................................................... 6

2.1 Emissions and source data ................................................................................................ 6

2.2 Dispersion modeling for inhalation exposure assessment ................................................ 6

2.3 Estimating human inhalation exposure ............................................................................ 9

2.4 Acute risk screening and refined assessments ................................................................ 10

2.5 Multipathway and environmental risk screening ........................................................... 11

2.6 Dose-response assessment.............................................................................................. 12

2.6.1 Sources of chronic dose-response information ....................................................... 12

2.6.2 Sources of acute dose-response information ........................................................... 21

2.7 Risk characterization ...................................................................................................... 26

2.7.1 General .................................................................................................................... 26

2.7.2 Mixtures .................................................................................................................. 27

2.7.3 Facility-wide risks ................................................................................................... 28

3 Results summaries and risk characterizations for the 7 source categories ........................... 28

3.1 Printing and publishing .................................................................................................. 29

3.1.1 Source category description and results .................................................................. 29

3.1.2 Risk characterization ............................................................................................... 35

3.2 Marine tank vessel loading ............................................................................................. 37

3.2.1 Source category description and results .................................................................. 37

3.2.2 Risk characterization ............................................................................................... 42

3.3 Pharmaceuticals production ........................................................................................... 43

3.3.1 Source category description and results .................................................................. 43

3.3.1 Risk characterization ............................................................................................... 47

3.4 Epichlorohydrin elastomers production ......................................................................... 51

3.4.1 Source category description and results .................................................................. 51

3.4.2 Risk characterization ............................................................................................... 52

3.5 Polybutadiene rubber production ................................................................................... 55

3.5.1 Source category description and results .................................................................. 55

3.5.2 Risk characterization ............................................................................................... 56

3.6 Styrene butadiene rubber and latex production .............................................................. 59

3.6.1 Source category description and results .................................................................. 59

3.6.2 Risk characterization ............................................................................................... 61

3.7 Nitrile butadiene rubber production ............................................................................... 63

3.7.1 Source category description and results .................................................................. 63

3.7.2 Risk characterization ............................................................................................... 64

4 General discussion of uncertainties and how they have been addressed .............................. 66

4.1 Exposure modeling uncertainties ................................................................................... 66

4.2 Uncertainties in the dose-response relationships ........................................................... 67

5 References ............................................................................................................................. 75
3

Index of Tables 

Table 2.2-1 AERMOD version 09292 model options for RTR II modeling ................................. 7

Table 2.6-1.A Dose-Response Values for Chronic Inhalation Exposure to Carcinogens ........... 17

Table 2.6-2.A Dose-Response Values for Chronic Inhalation Exposure to Noncarcinogens ..... 19

Table 2.6-2.B Dose-Response Values for Chronic Oral Exposure to Noncarcinogens ............... 21

Table 3.1-1 Summary of Emissions and Availability of Dose-Response Values for the Printing 

and Publishing Source Category ................................................................................................... 31

Table 3.1-2 Summary of Source Category Level Risks for Printing and Publishing .................. 33

Table 3.1-3 Summary of Acute Refined Results for Printing and Publishing ............................. 34

Table 3.1-4 Source Category Contribution to Facility-Wide Cancer Risks – Printing and 

Publishing ..................................................................................................................................... 36

Table 3.2-1 Summary of Emissions and Availability of Dose-Response Values for the Marine 

Tank Vessel Loading Operations Source Category ...................................................................... 39

Table 3.2-2 Summary of Source Category Level Risks for Marine Tank Vessel Loading 

Operations ..................................................................................................................................... 41

Table 3.2-3 Source Category Contribution to Facility-Wide Cancer Risks – Marine Tank Vessel

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

Table 3.3-1 Summary of Emissions and Availability of Dose-Response Values for the 

Pharmaceuticals Production Source Category .............................................................................. 45

Table 3.3-2 Summary of Source Category Level Risks for Pharmaceuticals .............................. 48

Table 3.3-3 Summary of Acute Refined Results for Pharmaceuticals Production ...................... 50

Table 3.3-4 Summary Category Contribution to Facility-Wide Cancer Risks - Pharmaceuticals

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

Table 3.4-1 Summary of Emissions and Availability of Dose-Response Values for the 

Epichlorohydrin Elastomers Production Source Category ........................................................... 52

Table 3.4-2 Summary of Source Category Level Risks for Epichlorohydrin Elastomers 

Production ..................................................................................................................................... 54

Table 3.4-3 Source Category Contribution to Facility-Wide Cancer Risks - Epichlorohydrin ... 55

Table 3.5-1 Summary of Emissions and Availability of Dose-Response Values for the 

Polybutadiene Rubber Source Category ....................................................................................... 56

Table 3.5-2 Summary of Source Category Level Risks for Polybutadiene Rubber Production .. 58

Table 3.5-2 Source Category Contribution to Facility-Wide Cancer Risks - Polybutadiene ...... 59

Table 3.6-1 Summary of Emissions and Availability of Dose-Response Values for Styrene 

Butadiene Rubber and Latex Production ...................................................................................... 60

Table 3.6-2 Summary of Source Category Level Risks for Styrene Butadiene – Rubber and 

Latex Production ........................................................................................................................... 62

Table 3.6-2 Source Category Contribution to Facility-Wide Cancer Risks - Styrene ................. 63

Table 3.7-1 Summary of Emissions and Availability of Dose-Response Values for Nitrile 

Butadiene Rubber Production ....................................................................................................... 64

Table 3.7-2 Summary of Source Category Level Risks for Nitrile Butadiene Rubber Production

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

Table 3.7-2 Source Category Contribution to Facility-Wide Cancer Risks – Nitrile Butadiene . 66
4

Appendices 

Appendix 1 Emissions Inventory Support Memorandums 

Appendix 2 Technical Support Document for HEM-AERMOD Modeling 

Appendix 3 Meteorological Data for HEM-AERMOD Modeling 

Appendix 4 Analysis of data on short-term emission rates relative to long-term emission rates 

Appendix 5 TRIM-Based Multipathway Screening Scenario 

Appendix 6 Detailed Risk Modeling Results 

Appendix 7 Acute Impacts Refined Analysis Figures 

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 

MOA Mode of action 

NATA National Air Toxics Assessment 

NEI National Emissions Inventory 

POM Polycyclic organic matter 

REL Reference exposure level 

RfC Reference concentration 

RfD Reference dose 

TOSHI Target-organ-specific hazard index 

URE Unit risk estimate
5

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)(2) requires the Environmental Protection Agency (EPA, or the Agency) to 

develop technology-based standards for categories of industrial 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 a memo entitled “EPA’s Actions in Response to Key Recommendations of 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 standard) performed for 7 source categories. The 7 

source categories are: 

 

Printing and Publishing 

Marine Tank Vessel Loading 

Pharmaceuticals Production 

Epichlorohydrin Elastomers 

Polybutadiene Rubber 

Styrene Butadiene 

Nitrile Butadiene
6

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

of chronic inhalation exposures and human health risks for both cancer and noncancer endpoints, 

as well as descriptions of the methods used to screen for acute health risks, chronic noninhalation health risks, and adverse environmental effects. Since none of the screening 

assessments indicated any significant 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. Screening assessments indicated a concern for 

acute health effects for all 5 of the source categories. Thus, a more refined analysis for acute 

exposure impacts for 5 source categories was performed. 

2 Methods 

2.1 Emissions and source data 

Data from the 2005 National Emissions Inventory (NEI) which were used and published as part 

of the 2005 National-Scale Air Toxics Assessment (NATA) served as the starting point for this 

assessment. The 2005 NEI contains information on actual emissions during the entire 2005 base 

year. Using the process MACT code1

, we developed a subset of this inventory that contains 

emissions and facility data for each of the 3 source categories addressed. 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 7 source categories, and/or who have extensive 

knowledge of the characteristics of these industries. NEI data was updated with industry 

supplied data as available. The goal of the engineering review was to identify readily-apparent 

limitations and issues with the emissions data (particularly those that would greatly influence 

risk estimates) and to make changes to the data set where possible to address these issues and 

decrease the uncertainties associated with the assessment. 

Details on the development of the emissions and source data for these source categories are 

discussed in Section 3. The emissions data and modifications made to the NEI data are 

discussed in the Appendix 1, entitled “Emissions Inventory Support Memorandums.” 

2.2 Dispersion modeling for inhalation exposure assessment 

Both long- and short-term inhalation exposure concentrations and associated health risk from 

each facility in each of the source categories of interest were estimated using the Human 

Exposure Model in combination with the American Meteorological Society/EPA Regulatory 

Model dispersion modeling system (HEM-AERMOD). The approach used in applying this 

modeling system is outlined below, and further details are provided in Appendix 2. HEMAERMOD 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

 The tagging of 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. MACT codes may be assigned either at the process level or at the site level in the point source data (e.g., the 

MACT code for municipal waste combustors (MWCs) is assigned at the site level whereas the MACT code for 

petroleum refinery catalytic cracking is assigned at the process level). 
7

The dispersion model in the HEM-AERMOD system, AERMOD version 09292, is a state-ofthe-science Gaussian plume dispersion model that is preferred by EPA for modeling point, area, 

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

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

average ambient concentration 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 HEM-AERMOD modeling system is to predict ambient 

concentrations at locations of interest. The AERMOD model options employed are summarized 

in Table 2.2-1 and are discussed further below. 

Table 2.2-1 AERMOD version 09292 model options for RTR II 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 at 16 radials) 

Discrete (census block centroids) 

Terrain characterization Actual from USGS 1-degree DEM data 

Building downwash Not Included 

Plume deposition/depletion Not Included 

Urban source option No 

Meteorology 1 year representative NWS from nearest site (158 stations) 

 In HEM-AERMOD, meteorological data are ordinarily selected from a list of 158 National 

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

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

of the conditions at the subject facility. Ideally, when considering off-site meteorological data 

most site specific dispersion modeling efforts will employ up to five years of data to capture 

variability in weather patterns from year to year. However, because we had 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-prediction of long-term ambient levels at some locations, likewise it may result in overprediction 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 3 (Meteorological Data Processing Using AERMET for HEM-AERMOD) 

provides a complete listing of stations and assumptions along with further details used in 

processing the data through AERMET. The sensitivity of model results to the selection of the 
8

nearest weather station and the use of one year of meteorological data is discussed in “Risk and 

Technology Review (RTR) Risk Assessment Methodologies” [2]. 

The HEM-AERMOD system estimates ambient concentrations at the geographic centroids of 

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

the user. The model accounts for 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. 

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 applied the general assumption to all source categories that the 

maximum one-hour emission rate from any source was ten times the average annual hourly 

emission rate for that source. 

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. This choice of a factor of ten for screening was originally 

based on engineering judgment. To develop a more robust peak-to-mean emissions factor, and 

in response to one of the key messages from the SAB consultation on our RTR Assessment Plan, 

we performed an analysis using a short-term emissions dataset from a number of sources located 

in Texas (originally reported on by Allen et al. 2004)[7]. In that report, the Texas Environmental 

Research Consortium Project compared hourly and annual emissions data for volatile organic 

compounds for all facilities in a heavily-industrialized 4-county area (Harris, Galveston, 

Chambers, and Brazoria Counties, TX) over an eleven-month time period in 2001. We obtained 

the dataset and performed our own analysis, focusing that analysis on sources which reported 

emitting high quantities of HAP over short periods of time (see Appendix 4, “Analysis of data on 

short-term emission rates relative to long-term emission rates”). Most peak emission events 

were less than twice the annual average, 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 the factor of ten for all initial screening; it is intended to 

cover routinely-variable emissions as well as startup, shutdown, and malfunction (SSM) 

emissions. While there are some documented emission excursions above this level, our analysis 

of the data from the Texas Environmental Research Consortium suggests that this factor should 

cover more than 99% of the short-term peak gaseous or volatile HAP emissions from typical 

industrial sources. 
9

 

Census block elevations for HEM-AERMOD modeling were determined nationally from the US 

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

resolution of about 90 meters. Elevations of polar grid points used in estimating short- and longterm 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 to the elevation to that of the nearest block. If the 

elevation is not provided for the emission source, the model takes the average elevation of all 

sectors of the nearest 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 2. 

2.3 Estimating human inhalation exposure 

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

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

reside in the census block. That is, this 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 

1996, 1999, 2002, and 2005 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 will 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 highlyexposed residents by modeling their short-term behavior could add a systematic low bias to these 

results. 

We did not address long-term migration nor population growth or decrease over 70 years, instead 

basing the assessment on the assumption that each person’s predicted exposure is constant over 

the course of their lifetime which is assumed to be 70 years. In assessing cancer risk, we 

generally estimated three metrics; the maximum individual risk (MIR) which is defined as the 

risk associated with a lifetime of exposure at the highest concentration, the population risk 

distribution, and the cancer incidence. This assumption of not considering short or long-term 

population mobility does not bias the estimate of the theoretical MIR nor does it affect the 

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

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

shifting it toward higher estimated individual risks at the upper end and reducing the number of 

people estimated to be at lower risks, thereby biasing the risk estimates high. 
10

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 

began with a screening assessment, which relies on readily available data and uses conservative 

assumptions that in combination approximate a worst-case exposure. The result of this screening 

process is that either the facility being assessed poses no 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 sitespecific data could be used to determine that acute exposures are not a concern, and significant 

additional data collection would not be 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: 

• 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. 
11

As mentioned above, when we identify acute impacts which exceed their relevant benchmarks, 

we pursue refining our acute screening estimates. In some cases, this includes use of a refined 

emissions multiplier to estimate the peak hourly emission rates from the average rates. For the 

source categories in the 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 7 for the 

detailed results for these sites. 

2.5 Multipathway and environmental risk screening 

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

(i.e., multipathway exposures) or adverse environmental impacts were screened by first 

determining whether any sources emitted any hazardous air pollutants known to be persistent and 

bioaccumulative in the environment (PB-HAP). The PB-HAP compounds or compound classes 

are identified for the screening from the EPA’s Air Toxics Risk Assessment Library [8]. 

Examples of PB-HAP are cadmium compounds, chlordane, chlorinated dibenzodioxins and 

furans, DDE, heptachlor, hexachlorobenzene, hexachlorocyclohexane, lead compounds, mercury 

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

toxaphene, and trifluralin. Emissions of POM, lead, cadmium, and mercury were identified in 

the emissions inventory for the source categories included in this document. 

These 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.FaTE2

 model. This screening scenario uses environmental media outputs from the peerreviewed 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.3 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 de 

minimis emission rates developed for screening potentially significant multi-pathway impacts. 

For the purpose of developing de minimis emission rates for our multi-pathway screening, we 

derived emission levels for each PB HAP 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 de minimis emission rate, we compared maximum estimated chronic (3-month 

average) 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 of any significance. 

 

2

 EPA’s Total Risk Integrated Methodology (General Information) http://epa.gov/ttn/fera/trim_gen.html 3

 EPA’s Human Health Risk Assessment Protocol (HHRAP) for Hazardous Waste Combustion Facilities; 

http://www.epa.gov/epaoswer/hazwaste/combust/riskvol.htm#volume1 
12

In all instances, modeling of emissions of cadmium, mercury, and POM associated with the 7 

source categories using our screening scenario indicated that human exposures via noninhalation pathways were well below levels of concern for cancer risk or noncancer hazard. For 

the purposes of this screening assessment, the levels of concern below which risks were 

considered insignificant were 1 in a million for lifetime cancer risk and a hazard quotient of 1.0 

for noncancer impacts. In evaluating emissions of lead compounds, since an ingestion reference 

dose has not been established for chronic noncancer effects, we compared maximum chronic 

atmospheric concentrations with the current National Ambient Air Quality Standard (NAAQS) 

for lead (0.15 ug/m3) and noted that all impacts are well below this value, allowing us to 

conclude that potential multipathway risks from lead compounds are insignificant. 

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 assured 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 HAPs, 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. 

2.6 Dose-response assessment 

2.6.1 Sources of chronic dose-response information 

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

(either by inhalation or ingestion) for the HAPs reported in the emissions inventory were based 

on the EPA Office of Air Quality Planning and Standards’ existing recommendations for HAPs 

[9], also used for NATA 1999, 2002, and 2005 [10]. This information has been obtained from 

various sources and prioritized according to (1) conceptual consistency with EPA risk 

assessment guidelines and (2) level of peer review received. The prioritization process was 

aimed at incorporating into our assessments the best available science with respect to doseresponse 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 risk assessment. 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 
13

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/m3

 in air.” The SF is “an upper 

bound, approximating a 95% confidence limit, on the increased cancer risk from a lifetime 

exposure to an agent. This estimate, [is] usually expressed in units of proportion (of a 

population) affected per 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 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 
14

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

Technical Support Document for developing their chronic assessments4: “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 adverse 

health effects are anticipated in the general human population.” CalEPA's quantitative doseresponse information on carcinogenicity by inhalation exposure is expressed in terms of the 

URE [16], defined similarly to EPA's URE. 

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

professional judgment, as follows: 

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

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

compounds in the group for which dose-response values were 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 

from further assessment. 

2) Where possible for emissions of unspecified mixtures of HAP categories such as metal 

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

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

3) In 2004, EPA determined that the CIIT dose-response value for formaldehyde (5.5 x 10-9 per 

μg/m3

) was based on better science than the IRIS dose-response value (1.3 x 10-5 per μg/m3), 

and we switched from using the IRIS value to the CIIT value in risk assessments supporting 

regulatory actions. This determination was based on a substantial body of research on the 

inhalation dosimetry for formaldehyde in rodents and primates by the CIIT Centers for 

Health Research (formerly the CIIT), with a focus on use of rodent data for refinement of the 

quantitative cancer dose-response assessment [17, 18, 19]. The CIIT’s risk assessment of 

formaldehyde incorporated mechanistic and dosimetric information on formaldehyde. 

However, recent research published by EPA indicates that, when the CIIT’s two-stage 

modeling assumptions are varied, resulting dose-response estimates can vary by several 

orders of magnitude [18, 19, 20, 20]. These findings are not supportive of interpreting the 

CIIT model results as providing a conservative (health-protective) estimate of human risk 

[21]. The recent EPA research also examined the contribution of the two-stage modeling for 

formaldehyde towards characterizing the relative weights of key events in the mode-of-action 

of a carcinogen. For example, in the EPA research, the model-based inference in the 

published CIIT study that formaldehyde’s direct mutagenic action is not relevant to the 

compound’s tumorigenicity was found not to hold under variations of modeling assumptions 

[22]. Additionally, in 2007, the California Environmental Protection Agency considered a 

 

4

 Air Toxics Hot Spots Program, Risk Assessment Guidelines, Part III - Technical Support Document 

for the Determination of Noncancer 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) 
15

petition to use the CIIT URE value rather than its 1992 cancer risk value of 6 X 10-6 per 

ug/m3

. After consideration and consultation with their Scientific Review Panel of Toxic Air 

Contaminants, they decided not to change from their 1992 value [23, 24]. As a result of 

these findings, EPA no longer considers the CIIT URE value to be health protective, and we 

are again using the Agency’s current value on IRIS, which was last revised in 1991, and 

which is more than 2000 times greater than the CIIT value. We note that a new IRIS reassessment has been drafted and sent to the NAS for review. The NAS review is expected to 

be completed by March of 2011. 

4) The IRIS URE for nickel inhalation was derived from evidence of the carcinogenic effects of 

insoluble nickel compounds in crystalline form. Soluble nickel species, and insoluble species 

in amorphous form, do not appear to produce genotoxic effects by the same toxic mode of 

action as insoluble crystalline nickel. Nickel speciation information for some of the largest 

nickel-emitting sources (including oil combustion, coal combustion, and others) suggests that 

at least 35% of total nickel emissions may be soluble compounds. The remaining insoluble 

nickel emissions are not well-characterized. Consistent with this limited information, this 

assessment will conservatively assume that 65% of emitted nickel is insoluble and that all 

insoluble nickel is crystalline. The nickel URE (based on nickel subsulfide, and 

representative of pure insoluble crystalline nickel) was adjusted to reflect an assumption that 

65% of the total mass of nickel may be carcinogenic. The noncancer dose-response values 

were not adjusted because noncancer effects of nickel are not thought to be limited to the 

crystalline, insoluble form. 

5) A substantial proportion of POM reported to EPA’s national emission inventory (NEI) were 

not speciated into individual compounds. As a result, it was necessary to apply the same 

simplifying assumptions to this assessment that were used for the 1999 NATA study [25]. 

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

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

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

6) For 2 carcinogenic substances, (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 m3

/d inhalation rate, as follows:

Where: URE = Unit risk estimate for inhalation (risk per μg/m3

) 

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

per kg body mass per day) 

( ) ⎟

⎟

⎠

⎞

⎜

⎜

⎝

⎛

×⎟

⎟

⎠

⎞

⎜

⎜

⎝

⎛

× × ⎟

⎟

⎠

⎞

⎜

⎜

⎝

⎛

⋅ ⎟ = ⎠

⎞ ⎜

⎝

⎛ − −

g

mg

d

m

kg d kg

mg CPS

m

g URE

μ

μ

1000

1 20

70

1 3 1 1

3
16

 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 inventories for the 7 source categories include emissions of 85 HAP. Of these, 34 

are classified as known, probable, or possible carcinogens, with quantitative cancer doseresponse values available. These 34 HAP, their quantitative inhalation chronic cancer doseresponse values, and the source of each value are listed in Table 2.6-1.A. The POM compounds 

with chronic oral cancer dose-response values available (for which multipathway screening 

assessments were performed) are listed in Table 2.6-1.B. 

The emissions inventories for the 7 source categories include emissions of 75 HAP with 

quantitative inhalation chronic noncancer threshold values available; two of these HAP 

(cadmium and mercury), for which multipathway assessments were performed, also have 

quantitative oral chronic noncancer threshold values available. These 75 HAP, their threshold 

values, and the source of the value are listed in Table 2.6-2.A and Table 2.6-2.B. 
17

Table 2.6-1.A Dose-Response Values for Chronic Inhalation Exposure to Carcinogens 

URE (unit risk estimate for cancer) = cancer risk per μg/m3 of average lifetime exposure. Sources: IRIS 

= EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Health 

Hazard Assessment, EPA/OAQPS = interim value recommended by the EPA Office of Air Quality 

Planning and Standards, Conv. Oral = Converted from an oral dose-response assessment. 

Pollutant 

CAS 

Number5

URE 

(1/μg/m3) Source 

1,3-Butadiene 106990 3.0E-05 IRIS

1,4-Dioxane 123911 7.7E-06 CAL

2-Nitropropane 79469 5.6E-06 EPA OAQPS

2,4-Toluene diisocyanate 584849 1.1E-05 CAL

Acetaldehyde 75070 2.2E-06 IRIS

Acetamide 60355 2.0E-05 CAL

Acrylonitrile 107131 6.8E-05 IRIS

Allyl chloride 107051 6.0E-06 CAL

Aniline 62533 1.6E-06 CAL

Arsenic compounds 7440382 4.3E-03 IRIS

Benzene 6 71432 7.8E-06 IRIS

Beryllium compounds 7440417 2.4E-03 IRIS

Bis(2-ethylhexyl)phthalate 117817 2.4E-06 CAL

Cadmium compounds 7440439 1.8E-03 IRIS

Carbon tetrachloride 56235 6.0E-6 IRIS

Chromium (VI) compounds 18540299 1.2E-02 IRIS

Epichlorohydrin 106898 1.2E-06 IRIS

Ethyl benzene 100414 2.5E-06 CAL

Ethylene dichloride 107062 2.6E-05 IRIS

Ethylene oxide 75218 8.8E-05 CAL

Formaldehyde 50000 1.3E-05 IRIS

Hydrazine 302012 4.9E-03 IRIS

Isophorone 78591 2.7E-07 Conv. Oral 7

Methyl tert-butyl ether 1634044 2.6E-07 CAL

Methylene chloride 75092 4.7E-07 IRIS

Naphthalene 91203 3.4E-05 CAL

Nickel compounds 7440020 1.6E-04 EPA OAQPS8

p-Dichlorobenzene 106467 1.1E-05 CAL

Polycyclic organic matter (POM) 246 11 EPA OAQPS11

 - Benzo(a)anthracene 56553 1.0E-04 EPA OAQPS9

 

5

 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. 6

 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 μg/m3

. The low end of the range is 2.2E-06 per μg/m3. 7

 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. 8

 65% of the IRIS URE for nickel refinery dust, as explained above. 
18

Table 2.6-1.A Dose-Response Values for Chronic Inhalation Exposure to Carcinogens 

URE (unit risk estimate for cancer) = cancer risk per μg/m3 of average lifetime exposure. Sources: IRIS 

= EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Health 

Hazard Assessment, EPA/OAQPS = interim value recommended by the EPA Office of Air Quality 

Planning and Standards, Conv. Oral = Converted from an oral dose-response assessment. 

Pollutant 

CAS 

Number5

URE 

(1/μg/m3) Source 

 - Benzo(a)pyrene 50328 1.0E-03 EPA OAQPS11

 - Benzo(b)fluoranthene 205992 1.0E-04 EPA OAQPS11

 - Benzo(k)fluoranthene 207089 1.0E-04 EPA OAQPS11

 - Chrysene 218019 1.0E-05 EPA OAQPS11

 - Dibenz(a,h)anthracene 53703 1.0E-03 EPA OAQPS11

 - Indeno(1,2,3-cd)pyrene 193395 1.0E-04 EPA OAQPS11

Propylene dichloride 78875 1.9E-05 Conv. Oral 10

Propylene oxide 75569 3.7E-06 IRIS

Tetrachloroethylene 127184 5.9E-06 CAL

Trichloroethylene 79016 2.0E-06 CAL

Vinyl chloride 75014 8.8E-06 IRIS

Table 2.6-1.B Dose-Response Values for Chronic Oral Exposure to Carcinogens 

SF (oral slope factor for cancer) = cancer risk per mg/kg/d of average lifetime exposure. Sources: IRIS 

= EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Health 

Hazard Assessment, EPA/OAQPS = interim value recommended by the EPA Office of Air Quality 

Planning and Standards. 

Pollutant 

CAS 

Number11

SF 

(1/mg/kg/d) Source 

Polycyclic organic matter (POM)12 246 0.5 EPA OAQPS

- Benzo(a)anthracene 56553 1 EPA OAQPS

- Benzo(a)pyrene 50328 10 EPA OAQPS

- Benzo(b)fluoranthene 205992 1 EPA OAQPS

- Benzo(k)fluoranthene 207089 1 EPA OAQPS

- Chrysene 218019 0.1 EPA OAQPS

- Dibenz(a,h)anthracene 53703 10 EPA OAQPS

- Indeno(1,2,3-cd)pyrene 193395 1 EPA OAQPS

 9

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

also used in the 1999 National Air Toxics Assessment, are available at 

http://www.epa.gov/ttn/atw/nata1999/99pdfs/pomapproachjan.pdf 10 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. 11 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. 12 Includes other unspeciated POM emissions (e.g., total PAH). 
19

Table 2.6-2.A 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 and Disease Registry. 

Pollutant 

CAS 

Number 

RfC 

(mg/m3) Source 13

1,1,1-Trichloroethane 71556 5 IRIS 

1,2-Epoxybutane 106887 0.02 IRIS -- M 

1,2,4-Trichlorobenzene 120821 0.2 HEAST 

1,3-Butadiene 106990 0.002 IRIS -- M 

1,4-Dioxane 123911 3.6 ATSDR 

2-Nitropropane 79469 0.02 IRIS 

2,4-Toluene diisocyanate 584849 0.00007 IRIS -- M 

Acetaldehyde 75070 0.009 IRIS -- L 

Acetonitrile 75058 0.06 IRIS -- M 

Acrolein 107028 0.00002 IRIS -- M 

Acrylic acid 79107 0.001 IRIS -- M 

Acrylonitrile 107131 0.002 IRIS -- M 

Allyl chloride 107051 0.001 IRIS -- L 

Aniline 62533 0.001 IRIS 

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 disulfide 75150 0.7 IRIS -- M 

Carbon tetrachloride 56235 0.1 IRIS 

Chlorine 7782505 0.00015 ATSDR 

Chlorobenzene 108907 1 CAL 

Chloroform 67663 0.098 ATSDR 

Chromium compounds14 7440473 0.0001 

 - Chromium (VI) compounds 18540299 0.0001 IRIS -- M 

Cobalt compounds 7440484 0.0001 ATSDR 

Cresols (mixed) 1319773 0.6 CAL 

Cumene 98828 0.4 IRIS -- M 

Cyanide compounds15 57125 0.003 IRIS -- L 

Diethanolamine 111422 0.003 CAL 

Dimethyl formamide 68122 0.03 IRIS -- M 

 

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

level of confidence in the RfC value, as reported in the IRIS file. 14 Chromium compounds are converted to Chromium (VI) compounds by source category specific ratio. 

15 The value for hydrogen cyanide used as a surrogate. 
20

Table 2.6-2.A 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 and Disease Registry. 

Pollutant 

CAS 

Number 

RfC 

(mg/m3) Source 13

Epichlorohydrin 106898 0.001 IRIS -- M 

Ethyl benzene 100414 1 IRIS -- L 

Ethylene dichloride 107062 2.4 ATSDR 

Ethylene glycol 107211 0.4 CAL 

Ethylene oxide 75218 0.03 CAL 

Formaldehyde 50000 0.0098 ATSDR 

Glycol ethers18 171 0.02 IRIS -- M 

 - 2-Butoxyethyl acetate16 112072 0.02 IRIS -- M 

 - Ethylene glycol ethyl ether 110805 0.2 IRIS -- M 

 - Ethylene glycol methyl ether 109864 0.02 IRIS -- M 

 - Diethylene glycol monobutyl ether18 112345 0.02 IRIS -- M 

 - n-Hexyl carbitol18 112594 0.02 IRIS -- M 

Hydrazine 302012 0.0002 CAL 

Hydrochloric acid 7647010 0.02 IRIS -- L 

Hydrofluoric acid 7664393 0.014 CAL 

Hydrogen cyanide 74908 0.003 IRIS -- L 

Isophorone 78591 2 CAL 

Lead compounds 7439921 0.00015 EPA OAQPS 

Manganese compounds 7439965 0.00005 IRIS -- M 

Mercury (elemental) 7439976 0.0003 IRIS -- M 

Methanol 67561 4 CAL 

Methyl chloride 74873 0.09 IRIS -- M 

Methyl isobutyl ketone 108101 3 IRIS -- L/M 

Methyl methacrylate 80626 0.7 IRIS -- M/H 

Methyl tert-butyl ether 1634044 3 IRIS -- M 

Methylene chloride 75092 1 ATSDR 

Methylene diphenyl diisocyanate 101688 0.0006 IRIS -- M 

Naphthalene 91203 0.003 IRIS -- M 

n-Hexane 110543 0.7 IRIS -- M 

Nickel compounds 7440020 0.00009 ATSDR 

p-Dichlorobenzene 106467 0.8 IRIS -- M 

Phenol 108952 0.2 CAL 

Phosgene 75445 0.0003 IRIS -- M 

Phthalic anhydride 85449 0.02 CAL 

Propylene dichloride 78875 0.004 IRIS -- M 

Propylene oxide 75569 0.03 IRIS -- M 

 

16 The value for ethylene glycol methyl ether was used as a surrogate. 
21

Table 2.6-2.A 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 and Disease Registry. 

Pollutant 

CAS 

Number 

RfC 

(mg/m3) Source 13

Selenium compounds 7782492 0.02 CAL 

Styrene 100425 1 IRIS -- M 

Tetrachloroethene 127184 0.27 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 

Vinylidene chloride 75354 0.2 IRIS -- M 

Xylenes (mixed)19 1330207 0.1 IRIS -- M 

 - m-Xylene17 108383 0.1 IRIS -- M 

 - o-Xylene19 95476 0.1 IRIS -- M 

 - p-Xylene19 106423 0.1 IRIS -- M 

Table 2.6-3.B Dose-Response Values for Chronic Oral Exposure to Noncarcinogens 

RfD (reference dose) = an estimate (with uncertainty spanning perhaps an order of 

magnitude) of a continuous oral 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 and Disease Registry. 

Pollutant CAS Number 

RfD 

(mg/kg/d) Source 18

Cadmium compounds 7440439 0.0005 IRIS – H 

Mercuric chloride19 7439976 0.0003 IRIS – H 

 - Methyl mercury21 22967926 0.0001 IRIS – H 

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 [26]. 

Depending on availability, the results from screening acute assessments are compared to both 

 

17 The RfC for mixed xylenes was used as a surrogate. 

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

level of confidence in the RfC value, as reported in the IRIS file. 19 The multipathway exposure assessment for mercury included fate and transport analysis, that included separate 

oral exposure estimates for divalent mercury and methylmercury. 
22

“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 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 (Reference: U.S. EPA. 

Graphical Arrays of Chemical-Specific Health Effect Reference Values for Inhalation Exposures 

[Final Report]. (U.S. Environmental Protection Agency, Washington, D.C., EPA/600/R-09/061, 

2009. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003.) 

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 [27]. 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 that, “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: 
23

“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. 

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) [28] 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 (ERPG2), 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 
24

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 emissions inventories for the 7 source categories include emissions of 59 HAP with relevant 

and available quantitative acute dose-response threshold values. These HAPs, their acute 

threshold values, and the source of the value are listed below in Table 2.6-3. 

Table 2.6- Dose-Response Values for Acute Exposure 

Pollutant 

CAS 

Number 

AEGL-1 

(1-hr) 

(mg/m3) 

AEGL-2 

(1-hr) 

(mg/m3) 

ERPG-1 

(mg/m3) 

ERPG-2

(mg/m3) 

REL 

(mg/m3) 

1,1,1-Trichloroethane 71556 1300 3300 1300 3300 68

1,3-Butadiene 106990 1500 12000 1500 12000 

1,4-Dioxane 123911 61 1200 3

2,4-Toluene diisocyanate 584849 0.14 0.59 0.14 1.1 

Acetaldehyde 75070 81 490 81 490 0.47 

Acetonitrile 75058 22 540 

Acrolein 107028 0.069 0.23 0.069 0.23 0.0025

Acrylic acid 79107 4.4 140 4.4 140 6

Acrylonitrile 107131 10 130 22 77

Allyl chloride 107051 8.8 170 9.4 130 

Arsenic compounds 7440382 0.0002

Benzene 71432 170 2600 170 2600 1.3

Beryllium compounds 7440417 0.025 

Biphenyl 92524 61 

Carbon disulfide 75150 40 500 40 500 6.2

Carbon tetrachloride 56235 280 1200 280 1200 1.9

Chlorine 7782505 1.5 5.8 1.5 5.8 0.21

Chloroacetic acid 79118 26 

Chlorobenzene 108907 46 690 

Chloroform 67663 310 310 0.15

Cumene 98828 250 1500 

Cyanide compounds20 57125 2.2 7.8 7.8 0.34 

Dimethyl formamide 68122 270 6 270 

Dimethyl sulfate 77781 0.12 0.62 

Epichlorohydrin 106898 22 91 22 91 1.3

Ethyl acrylate 140885 34 150 34 150 

Ethylene dichloride 107062 200 810 

Ethylene glycol 

Ethylene oxide 75218 81 81 

Formaldehyde 50000 1.1 17 1.1 17 0.055

Glycol ethers21 171 0.093 

 

20 Acute values for hydrogen cyanide were used as surrogates. 

21 The value for ethylene glycol methyl ether (0.093) was used as a surrogate for glycol ether compounds without an 

REL value and for unspeciated glycol ethers. 
25

Table 2.6- Dose-Response Values for Acute Exposure 

Pollutant 

CAS 

Number 

AEGL-1 

(1-hr) 

(mg/m3) 

AEGL-2 

(1-hr) 

(mg/m3) 

ERPG-1 

(mg/m3) 

ERPG-2

(mg/m3) 

REL 

(mg/m3) 

 - 2-Butoxyethyl acetate 112072 0.093 

 - Diethylene glycol monobutyl ether 112345 0.093

 - Diethylene glycol monoethyl ether 111900 0.093

 - Ethylene glycol ethyl ether 110805 0.37

 - Ethylene glycol ethyl ether acetate 111159 0.14

 - Ethylene glycol methyl ether21 109864 0.093

 - n-Hexyl carbitol 112594 0.093 

 - Phenyl cellosolve 122996 0.093 

 - Propyl cellosolve 2807309 0.093 

Hydrazine 302012 0.13 17 0.13 17 

Hydrochloric acid 7647010 2.7 33 2.7 33 2.1

Hydrofluoric acid 7664393 0.82 20 0.82 20 0.24

Hydrogen cyanide 74908 2.2 7.8 7.8 0.34

Mercury (elemental) 7439976 1.7 2 0.0006

Methanol 67561 690 2700 690 2700 28

Methyl chloride 74873 1900 1900

Methyl iodide 74884 150 290 

Methyl methacrylate 80626 70 490 

Methyl tert-butyl ether 1634044 180 2100 

Methylene chloride 75092 690 1900 690 1900 14

Methylene diphenyl diisocyanate 101688 0.2 2 

n-Hexane 110543 12000 

Nickel compounds 7440020 0.006

Phenol 108952 58 89 58 89 5.8

Phosgene 75445 1.2 1.2 0.004

Propylene oxide 75569 170 690 170 690 3.1

Styrene 100425 85 550 85 550 21

Tetrachloroethene 127184 240 1600 240 1600 20

Toluene 108883 750 4500 750 1900 37

Trichloroethylene 79016 700 2400 700 2400 

Triethylamine 121448 2.8

Vinyl acetate 108054 24 630 18 260 

Vinyl chloride 75014 640 3100 640 3100 180

Xylenes (mixed) 1330207 560 4000 22

 - m-Xylene 108383 560 4000 22

 - p-Xylene 106423 560 4000 22

 - o-Xylene 95476 560 4000 22
26

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 [29] 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 [30], in 2002 

by the Agency’s information quality guidelines [31], and in the OMB/OSTP September 2007 

Memorandum on Updated Principles for Risk Analysis22, 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 for each 

source category (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 this 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-year period (i.e., the assumed human 

lifespan) at that exposure. Because UREs for most HAPs are upper-bound estimates, actual risks 

at a given exposure level may be lower than predicted, and could be zero. 

For EPA’s list of carcinogenic HAPs that act by a mutagenic mode-of-action [32], we applied 

EPA’s Supplemental Guidance for Assessing Susceptibility from Early-Life Exposure to 

Carcinogens [33]. 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 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 

 

22Memorandum 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) 
27

on evidence that carcinogenic POM have the same mutagenic mechanism of action as does 

benzo[a]pyrene. For this reason, EPA implementation policy [34] 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 

assessment 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 equallyplausible 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 predicted to be above the RfC, the risk 

characterization includes the degree of confidence ascribed to the RfC values for the 

compound(s) of concern (i.e., high, medium, or low confidence) and discusses the impact of this 

on possible health interpretations. 

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

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

incorporate generally conservative uncertainty factors in the face of uncertain extrapolations, 

such that an HQ greater than one does not necessarily suggest the onset of adverse 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 truly a potential for significant acute risks. 

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. 
28

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

[35,36] default assumption of additivity of effects, and combined 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 HAPs that act by similar toxic modes of 

action, or (where this information is absent) that affect the same target organ. This process 

creates, for each target organ, a target-organ-specific hazard index (TOSHI), defined as the sum 

of hazard quotients for individual HAPs that affect the same organ or organ 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. 

2.7.3 Facility-wide risks 

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

using emissions data from the 2005 NEI. For the facilities in these source categories, we 

extracted from the results, based on facility ID, estimates of all HAP emissions sources at the 

facility, including emissions sources that are not part of the source categories but that are located 

within a contiguous area and are under common control. We then analyzed risks due to the 

inhalation of the HAP for the populations residing within 50 kilometers of each facility. The 

results of these facility-wide assessments are summarized below in the individual source 

category Risk Characterization sections of this document. The complete results of the facilitywide assessments are provided in Table 2 (associated with the source category of interest) of 

Appendix 6. 

3 Results summaries and risk characterizations for the 7 source 

categories 

In this section, the results of the risk assessments for each of the 7 source categories are 

presented separately. Each subsection includes the following information for each source 

category: 
29

1) A narrative description of the source category, including a discussion of the processes 

involved and the number of facilities EPA knows or expects are affected by the MACT 

standard; 

2) A table of emissions for the entire category showing HAP emitted, total source category 

emission rates for each HAP, and numbers of facilities reporting emissions of each HAP; 

3) A table summarizing the chronic inhalation risk results showing the number of facilities 

modeled, the number of people within 50 km, the MIR for the entire source category, the 

number of facilities for which the facility-specific MIR exceeds specific cancer and 

noncancer benchmarks, the number of people for whom the risks exceed the same 

benchmarks, the estimated total cancer incidence, and identifying the specific HAPs 

contributing the most to those risks (HAPs identified as “drivers” include those contributing 

the most to the risk metric, up to 90% of its value). In addition, this table indicates the 

maximum HQ from the acute inhalation screening and an indication of how many facilities 

showed HQ values above 1; 

4) In those cases where the acute inhalation screening showed an HQ value greater than 1 for 

any combination of source and pollutant, a table summarizing the acute screening results 

showing available acute dose-response values for each affected pollutant, for three effect 

levels (REL, AEGL-1/ERPG-1, and AEGL-2/ERPG-2), if available, the maximum acute 

screening exposure estimated, and the associated HQ values; 

5) A narrative summarizing the risk characterization for that category. 

Detailed accounting of the changes made to the inventory for each source category as a result of 

the engineering reviews and comments received can be found in Appendix 1. Detailed source 

category facility-level results for both chronic and acute inhalation risk assessments and facilitywide results of the chronic inhalation risk assessments for each of the 7 source categories can be 

found in Appendix 6. 

3.1 Printing and publishing 

3.1.1 Source category description and results 

The printing and publishing source category includes facilities that use rotogravure, flexography, 

and other methods, such as lithography, letterpress, and screen printing, to print a variety of 

substrates, including paper, plastic film, metal foil, and vinyl. The MACT standards focused on 

those facilities that perform publication rotogravure printing, product and package rotogravure 

printing, and wide-web flexographic printing. Publication rotogravure printing refers to printing 

using a rotogravure press of various paper products, including catalogs, magazines, direct mail 

advertisements, display advertisements, miscellaneous brochures and other advertisements, 

newspaper sections and inserts, periodicals, and telephone directories. Product and packaging 

rotogravure printing entails the production, on a rotogravure press, of any printed substrate not 
30

otherwise defined as publication rotogravure printing. This includes (but is not limited to) 

folding cartons, flexible packaging, labels and wrappers, gift wraps, wall and floor coverings, 

upholstery, decorative laminates, and tissue products. Wide-web flexographic printing is a 

technique for printing substrates of 18 inches or wider in which the applied pattern is raised 

above the printing plate and the image carrier is made of rubber or other elastomeric materials. 

The wide-web flexographic presses are used to print flexible and rigid packaging; newspapers, 

magazines, and directories; paper towels, tissues, and similar products; and printed vinyl shower 

curtains and wallpaper. Research and laboratory facilities are not subject to the provisions of the 

MACT standards unless they are co-located with production lines. 

The MACT rule applies to HAP present in the inks, ink extenders, solvents, coatings, varnishes, 

primers, adhesives, and other materials applied with rotogravure and wide-web flexographic 

presses. HAP emissions from printing and publishing facilities in this source category can vary 

depending on the type of HAP present in the inks, solvents, etc., mentioned above. HAP 

emissions can also vary depending on the operating hours of the facility. Some sources operate 

twenty-four hours a day, seven days a week, while other sources operate less frequently. 

In rotogravure printing, a gravure plate or cylinder is used to allow fluid inks to flow from the 

cells to the substrate at high press speeds. In addition to inks, other materials such as adhesives, 

primers, coatings, and varnishes may be applied with rotogravure presses. These materials dry 

by evaporation as the substrate passes through hot air dryers. For publication rotogravure 

printers, facilities use toluene/xylene based ink systems and operate solvent recovery systems 

based on carbon adsorption with steam regeneration. Emission sources at publication 

rotogravure printing facilities include evaporation of HAP (solvents) from inks and coatings, 

solvents used for press cleaning, and storage of inks, coatings, and solvents. 

Product and packaging rotogravure differs from publication rotogravure with respect to the 

materials used (i.e., product and packaging rotogravure uses a wider variety of ink systems, color 

sets, and materials applied) and applicable control devices. Consequently, the control of HAP 

emissions, which originate from the inks and other applied materials (e.g., adhesives and 

coatings), varies across facilities. Some facilities use a variety of thermal and catalytic oxidizers 

as well as activated carbon based solvent recovery systems, while others comply without using 

control devices by using low HAP content materials. Emission sources at product and packaging 

rotogravure facilities include evaporation of HAP (solvents) from inks, coatings and adhesives, 

solvents used for press cleaning, and storage of inks, coatings, adhesives, and solvents. 

Flexographic inks include both waterborne and solvent-based systems that are used to achieve 

sufficient ink fluidity. Waterborne inks contain a relatively low proportion of HAP, principally 

ethylene glycol and glycol ethers. Waterborne inks that contain no HAP are available for some 

applications. Most solvent-based flexographic inks contain few or no HAP. Emission sources at 

wide-web flexographic printing facilities include evaporation of HAP (solvents) from inks, 

coatings and adhesives, solvents used for press cleaning, and storage of inks, coatings, adhesives, 

and solvents. 

At the time of MACT promulgation in 1995, EPA estimated that there were approximately 200 

publication rotogravure, product and packaging rotogravure, and wide-web flexographic printing 
31

facilities nationwide that would be subject to these MACT regulations. After further review by 

EPA to remove area source facilities from the data set, we now believe the Printing and 

Publishing source category to be comprised of 172 facilities emitting a reported combined total 

of 7,460 tons/year of HAP into the atmosphere. Refer to Appendix 1 for details on how the 

emissions inventory was developed. 

Table 3.1-1 summarizes the emissions for the Printing and Publishing Industry source category. 

Based on the data set, the HAP emitted in largest quantities from these sources are toluene, 

glycol ethers, methanol, xylenes, methyl isobutyl ketone, hexane, ethyl benzene, methyl 

chloroform, and ethylene glycol. Total emissions from these nine HAP account for 99 percent of 

the mass emitted across all 172 facilities. On an individual HAP basis, toluene is reported as 

emitted from 97 facilities (56 percent). Persistent and bioaccumulative HAP (PB HAP) reported 

in the data set for this source category include emissions of cadmium, lead, and mercury at very 

low levels. 

 

Tables 3.1-2 and 3.1-3 provide information summarizing health risks for this source category. 

Table 3.1-1 Summary of Emissions and Availability of Dose-Response Values for the Printing and 

Publishing Source Category 

HAPa Emissions 

(tpy) 

Number of 

Facilities 

Reporting HAP 

(172 facilities in 

data set) 

Prioritized Inhalation Dose-Response Value Identified 

by OAQPSb

PBHAP? Unit Risk 

Estimate for 

Cancer? 

Reference 

Concentration 

for Noncancer? 

Health Benchmark 

Values for Acute 

Noncancer? 

Toluene 6,605 97 Υ Υ

Glycol Ethers 172 44 Υ Υ

Xylenes (Mixture of o, m, and 

p Isomers) 145 55 Υ Υ

Methyl Isobutyl Ketone 140 32 Υ 

Methanol 114 56 Υ Υ

Hexane 84 25 Υ Υ

Ethyl Benzene 57 22 Υ Υ 

Methyl Chloroform 54 9 Υ Υ

Ethylene Glycol 41 28 Υ Υ

Diethylene Glycol Monobutyl 

Ether 15 6 Υ Υ

Diethylene Glycol Monoethyl 

Ether 11 7 Υ Υ

Vinyl Acetate 9 12 Υ Υ

Ethylene Glycol Methyl Ether 3 9 Υ Υ

N,N-Dimethylformamide 2 2 Υ Υ

Methylene Chloride 2 6 Υ Υ Υ

Diethanolamine 1 6 Υ 

Hydrochloric Acid 0.8 1 Υ Υ

Formaldehyde 0.7 16 Υ Υ Υ

Bis(2-Ethylhexyl)Phthalate 0.6 2 Υ Υ 

Hydroquinone 0.6 4 

Cumene 0.4 8 Υ Υ
32

Table 3.1-1 Summary of Emissions and Availability of Dose-Response Values for the Printing and 

Publishing Source Category 

HAPa Emissions 

(tpy) 

Number of 

Facilities 

Reporting HAP 

(172 facilities in 

data set) 

Prioritized Inhalation Dose-Response Value Identified 

by OAQPSb

PBHAP? Unit Risk 

Estimate for 

Cancer? 

Reference 

Concentration 

for Noncancer? 

Health Benchmark 

Values for Acute 

Noncancer? 

m-Xylene 0.4 1 Υ

N-Hexyl Carbitol 0.3 1 Υ 

Isophorone 0.2 2 Υ Υ 

4,4'-Methylenediphenyl 

Diisocyanate 0.1 1 Υ Υ

Triethylamine 0.1 3 Υ Υ

Dimethyl Phthalate 0.06 2 

Methyl Methacrylate 0.05 1 Υ Υ

Benzene6 0.03 6 Υ Υ Υ

Naphthalene 0.03 4 Υ Υ 

Cellosolve Acetate 0.02 1 Υ Υ

Dibutyl Phthalate 0.02 1 

Phenyl Cellosolve 0.02 3 Υ Υ

Phenol 0.01 1 Υ Υ

Carbon Tetrachloride 0.01 1 Υ Υ Υ

Chlorobenzene 0.008 1 Υ Υ

Acrylic Acid 0.002 3 Υ Υ

2,4-Toluene Diisocyanate 0.001 3 Υ Υ Υ

Ethyl Acrylate 0.0004 1 Υ

Chromium (VI) Compounds 0.00004 2 Υ Υ 

Nickel & Compounds 0.00002 2 Υ Υ

Cadmium & Compounds 0.00001 2 Υ Υ Υ

1,4-Dichlorobenzene 0.00001 2 Υ Υ 

Lead Compounds (Inorganic) 0.000005 2 Υ Υ

Styrene 0.000004 1 Υ Υ

Manganese & Compounds 0.000004 2 Υ 

Mercury & Compounds 0.000003 2 Υ Υ Υ

Arsenic & Compounds 

(Inorganic Including Arsine) 0.000002 2 Υ Υ Υ

POM72002 0.0000003 2 Υ Υ

a

 Notes for how HAP were speciated for risk assessment: 

• For emissions of any chemicals or chemical groups classified as polycyclic organic matter (POM), emissions were 

grouped into POM subgroups as found on EPA’s Technology Transfer Network website for the 2002 National-Scale 

Air Toxics Assessment at http://www.epa.gov/nata2002/methods.html#pom. (Approach to Modeling POM). 

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

Transfer network website 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 . 
33

Table 3.1-2 Summary of Source Category Level Risks for Printing and Publishing 

Result HAP “Drivers” 

Facilities in Source Category 

Number of Major Source Facilities Estimated to 

be in Source Category 172 n/a 

Number of Facilities Identified in NEI and 

Modeled 172 n/a 

Cancer Risks 

Maximum Individual Lifetime Cancer Risk (in 1 

million) 4 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 1 ethyl benzene 

Chronic Noncancer Risks 

Maximum Respiratory Hazard Index 0.08 ethylene glycol 

Number of Facilities with Maximum Respiratory Hazard Index: 

 Greater than 1 0 n/a 

Acute Noncancer Screening Results

Maximum Acute Hazard Quotient 

20 

1 

1 

toluene (REL) 

toluene (AEGL-1) 

toluene (ERPG-1) 

Number of Facilities With Potential for Acute 

Effects 7 toluene 

Acute Noncancer Refined Results

Maximum Acute Hazard Quotient 

10 

0.5 

0.5 

toluene (REL) 

toluene (AEGL-1) 

toluene (ERPG-1) 

Number of Facilities With Potential for Acute 

Effects 6 toluene 

Population Exposure 

Number of People Living Within 50 Kilometers 

of Facilities Modeled 118,000,000 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 300 n/a 

Number of People Exposed to Respiratory Hazard Index: 

 Greater than 1 0 n/a 

Estimated Cancer Incidence (excess cancer cases 

per year) 0.0006 n/a 

Contribution of HAP to Cancer Incidence 

 ethyl benzene 70% n/a 

 formaldehyde 28% 
Table 3.1-3 Summary of Acute Refined Results for Printing and Publishing

Refined Results MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE-RESPONSE V

HAP 

Max. 1-

hr. Air 

Conc. 

(mg/m3) 

Based on REL 

Based on 

AEGL1/ERPG-1 

Based on 

AEGL2/ERPG-2 REL (mg/m3) AEGL-1 (1-hr) (mg/m3) ERPG-1 (mg/m3) A

(

toluene 384 10 0.5/0.5 0.2/0.3 37 750 750 

Notes on Process: 

1) Acute screening was performed for all emitted HAP with available acute dose-response values. Where acute screening HQ values exceeded 

performed. Only those pollutants whose refined HQs were equal to or greater than 1 for at least one acute threshold value are shown in the t

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 a

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 eff

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 irr

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 

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 experienc

irreversible or other serious health effects or symptoms which could impair an individual’s ability to take protective action. 
35

3.1.2 Risk characterization 

There were 172 facilities identified as being a part of this source category, and they were all 

included in the assessment. The results of the risk assessment showed the highest individual 

cancer risk to be 4-in-1 million, with this cancer risk being led by emissions of ethyl benzene. 

Based on information obtained during the comment period, we believe the risk for this facility 

is now below 1-in-a million. All other facilities in this source category are below 1-in-a 

million. Cancer incidence associated with the inhalation of emissions from facilities in this 

source category is 0.0006 cases per year. 

Chronic noncancer risks were not identified as significant. The maximum estimated chronic 

noncancer hazard index was 0.08, and its magnitude was dominated by the contribution from 

ethylene glycol emissions. This value is well below 1, an exposure level generally considered 

to be without appreciable health risks. 

The MACT-allowable emissions from this source category could be up to five times greater 

than the actual emissions. Applying this scaling factor, results in a potential MIR of 20 and 

HI of 0.4. 

The screening assessment for acute impacts suggests that short-term toluene concentrations at 

seven of the publication rotogravure facilities modeled could exceed acute thresholds, 

assuming worst-case meteorological conditions are present, using our default assumption that 

the maximum hourly emissions of toluene exceed the average hourly emission rate by a factor 

of ten, and using a default source to receptor distance of 100 m. Emissions of toluene showed 

the potential to create maximum hourly concentrations which could exceed the acute REL by 

a factor of 20 (HQREL = 20) and potentially reach the level of the AEGL-1 (HQAEGL-1 = 1). 

For the publication rotogravure facilities that exceeded acute toluene thresholds in the 

screening assessment, we refined the assessment by plotting receptors on facility aerial 

photographs and determining maximum offsite concentrations. Once we performed these 

refinements, estimated maximum offsite concentrations were seen to exceed the acute REL at 

six publication rotogravure facilities. The highest offsite concentration exceeds the REL by a 

factor of 10 and is about half of the AEGL-1 value (HQREL = 10, HQAEGL-1 = 0.5). This 

occurs near a public road north of a facility. At this facility, meteorological conditions 

leading to offsite exceedances of the REL could occur as frequently as 90 hours per year, or 

about 1 percent of the time. At the facility where we estimate the REL to be most frequently 

exceeded, the maximum REL exceedance is by a factor of 4, and meteorological conditions 

leading to offsite exceedances of the REL could occur as frequently as 138 hours per year, or 

about 2 percent of the time. Further, experts on this source category suggest that the factor of 

10 multiplier (used in the acute risk screening) is most likely high for publication rotogravure 

printing. They suggest that a more appropriate multiplier would be in the range of 5 or less. 

Using a multiplier of 5 (or less) would reduce the estimated acute impacts by half (or more) 

from the values presented. Details on the refined acute assessment can be found in Appendix 

7.
36

While our assessment did identify some emissions of PB-HAP from this source category, 

none of these emissions are anticipated to pose any potential multipathway risks based on our 

application of the PB-HAP screening scenario developed using the TRIM.FaTE model 

(Appendix 5). Thus, our assessment did not identify any potential for this source category to 

pose significant chronic non-inhalation risks, nor did we identify any potential for adverse 

environmental impacts. 

Based on our technical knowledge of this source category and the lack of comments on our 

understanding of the source category proposed in the NPRM, we have a high degree of 

confidence that our assessment covers the majority of the source category (at least 90% of the 

total facilities) and that we have accurately characterized the emissions. As such, we believe 

that the exposure portion of our assessment accurately represents maximum chronic inhalation 

exposures and total population exposures for the purpose of estimating cancer incidence. 

Since we did not refine our population exposure assessment to account for residential moves 

over the course of 70 years or the possibility of facility closures, our estimates of the 

magnitudes of individual risks in the exposed population are likely overestimates, and our 

estimates of the total number of people exposed are likely underestimates. 

The facility-wide MIR and HI available in Appendix 6 are based on emissions, as identified in 

the NEI database, from all emissions sources at the identified facilities. The maximum 

facility-wide risks are estimated to be a cancer MIR of 20 in a million and a hazard index (HI) 

of 20, which occur at different facilities. The source category contribution to the facility-wide 

risk at both facilities is less than 1% for MIR and HI. Subsequently after the risk modeling 

was complete, we received data that identified an error in emissions that caused the highest 

facility-wide HI value (20). After reviewing the updated emissions and assessing the risk, the 

HI dropped significantly. The next highest facility-wide HI is 2 associated with another 

facility. The source category contribution to the HI risk at this facility is less than 1%. 

Table 3.1-4 Source Category Contribution to Facility-Wide Cancer Risks – Printing and 

Publishing 

Printing and Publishing 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% 29 1 0 0 30 

50-90% 3 0 0 0 3 

10-50% 6 0 0 0 6 

< 10% 123 9 1 0 133 

Total 161 10 1 0 172 
37

3.2 Marine tank vessel loading 

3.2.1 Source category description and results 

Marine tank vessel loading operations are facilities that load and unload liquid commodities in 

bulk, such as crude oil, gasoline and other fuels, and some chemicals and solvent mixtures. 

The cargo is pumped from the terminal's large, above-ground storage tanks through a network 

of pipes and into a storage compartment (tank) on the vessel. Most marine tank vessel 

loading operations are associated with petroleum refineries or synthetic organic chemical 

manufacturers, or are independent terminals. Marine vessel loading operations located at 

petroleum refineries are not included in this source category; their emissions are regulated by 

the MACT standard for the petroleum refinery source category. Using Army Corps of 

Engineers information, we estimated that there were around 800 marine tank vessel loading 

and unloading operations in the year 2000; however, many of these facilities are not subject to 

the Marine Vessels MACT regulation because they are not at major sources of HAP, do not 

load or unload any HAPs, or because they only load liquids in containers such as drums, 

which are not subject to this MACT. We estimate there are about 300 major source facilities 

with MTVLO.23 

During marine tank vessel loading operations, HAP emissions can occur as the liquid that is 

being loaded into the vessel displaces vapors from the vessel's tank. The major HAP emission 

points for marine tank vessel loading operations include open tank hatches and overhead vent 

systems. Vent systems collect vapors displaced during loading and route them to a vertical 

pipe or stack. The vapors are released well above the height of the deck with an upward 

velocity to help isolate the vapors from the deck. Other possible emission points are hatch 

covers or domes, pressure-vacuum relief valves, seals, and vents. Emissions may also occur 

during ballasting (i.e., the process of drawing ballast as water into a cargo hold). 

In reviewing Version 1.0 of the 2002 NEI (February 2006), we developed the initial marine 

vessel data set by identifying facilities with a marine tank vessel operation MACT code. EPA 

engineers subsequently reviewed the data set and identified several marine tank vessel loading 

operations that were located at petroleum refineries and thus should not be included in the 

data set for the marine tank vessel loading source category. 

The data set contains information for 152 facilities with a total of 411 tons/year of HAP 

emissions. While the 152 facilities included in our assessment represent about half of the 

approximately 300 major source facilities with MTVLO expected to be in the category, we 

believe the sample of 152 facilities to be representative of the 300 facilities. Thus we used the 

site-specific assessment of the 152 (which includes, on average, the higher (by more than 

twice) MTVLO emissions from all facilities with) to obtain our best estimate of the maximum 

individual risk for the entire category and then develop an estimate of the total cancer 

incidence associated with the category by multiplying the incidence for the 152 facilities by a 

factor of 2 (or roughly 300 divided by 152). For further information on how our analysis of 

 

23 See emission memo for estimates of facilities. August 12, 2010, “Update Emissions Data Used in Residual 

Risk Modeling for the Marine Tank Vessel Loading Operations Source Category,” Karen Schaffner, RTI 

International, to Stephen Shedd and Mary Tom Kissell, EPA. Docket item. 
38

the emissions inventory supports this determination of representativeness and how the 

emissions inventory changed, see the Emissions Inventory Support Memoranda in Appendix 

1. 

Table 3.2-1 summarizes the emissions for the marine tank vessel loading operations source 

category. Based on these data, the HAP emitted in largest quantities in total from these 

sources are hexane, methyl tert-butyl ether, toluene, methanol, benzene, xylene compounds, 

butadiene, styrene, cumene, ethylene dichloride, naphthalene, ethyl benzene, 

trichloroethylene, acrylonitrile tetrachloroethylene, propylene oxide, vinyl acetate, 

acetaldehyde, and chloroform. The total emissions for these 19 HAP account for 99 percent 

of the mass emitted across the source category. Hexane, toluene, xylene compounds, and 

benzene are reported as emissions from at least 102 of the 152 representative facilities in the 

data set (67 percent). Persistent and bioaccumulative HAP (PB HAP) emissions reported in 

the data set for the marine tank vessel loading operation source category are POM, cadmium, 

mercury compounds, and lead. 

Table 3.2-2 provides information summarizing health risks for this source category. 
39

Table 3.2-1 Summary of Emissions and Availability of Dose-Response Values for the 

Marine Tank Vessel Loading Operations Source Category 

HAPa Emissions 

(tpy) 

Number of 

Facilities 

Reporting HAP 

(152 facilities in 

data set) 

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

PBHAP? Unit Risk 

Estimate for 

Cancer? 

Reference 

Concentration 

for Chronic 

Noncancer? 

Health 

Benchmark 

Values for Acute 

Noncancer? 

Hexane 87 104 Υ Υ 

Methyl Tert-Butyl Ether 62 12 Υ Υ Υ 

Toluene 46 111 Υ Υ 

Methanol 48 25 Υ Υ 

Benzene 42 105 Υ Υ Υ 

Xylenes (Mixture of o, m, 

and p Isomers) 31 102 Υ Υ 

1,3-Butadiene 27 5 Υ Υ Υ

Styrene 23 27 Υ Υ 

Cumene 10 28 Υ Υ 

Ethylene Dichloride 6 8 Υ Υ Υ 

Naphthalene 8 20 Υ Υ

Ethyl Benzene 5 47 Υ Υ 

Trichloroethylene 3 4 Υ Υ Υ 

Acrylonitrile 2 7 Υ Υ Υ 

Tetrachloroethylene 2 8 Υ Υ Υ 

Propylene Oxide 2 3 Υ Υ Υ

Vinyl Acetate 2 7 Υ Υ

Acetaldehyde 1 2 Υ Υ Υ

Chloroform 1 2 Υ Υ

Glycol Ethers 0.5 3 Υ Υ

2,2,4-Trimethylpentane 0.4 12 

Methylene Chloride 0.4 1 Υ Υ Υ

Methyl Methacrylate 0.3 3 Υ Υ

Biphenyl 0.2 12 Υ

m-Xylene 0.2 2 Υ Υ

Phenol 0.2 16 Υ Υ

Aniline 0.2 2 Υ Υ Υ

Methyl Isobutyl Ketone 0.2 2 Υ

Ethylene Glycol 0.1 21 Υ

o-Xylene 0.09 2 Υ Υ

Ethyl Acrylate 0.08 2 Υ

2-Nitropropane 0.08 2 Υ Υ

Acrylic Acid 0.06 3 Υ Υ

Vinyl Chloride 0.04 1 Υ Υ Υ

1-Chloro-2,3-

Epoxypropane 0.02 1 Υ Υ Υ

1,2-Epoxybutane 0.02 1 Υ

Carbon Tetrachloride 0.02 1 Υ Υ Υ
40

HAPa Emissions 

(tpy) 

Number of 

Facilities 

Reporting HAP 

(152 facilities in 

data set) 

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

PBHAP? Unit Risk 

Estimate for 

Cancer? 

Reference 

Concentration 

for Chronic 

Noncancer? 

Health 

Benchmark 

Values for Acute 

Noncancer? 

Cellosolve Solvent 0.01 1 Υ Υ

Ethylene Glycol 

Monoethyl Ether 0.007 1 Υ Υ

Cresols (mixed) 0.005 12 Υ

Dimethyl Formamide 0.006 1 Υ Υ

Formaldehyde 0.003 1 Υ Υ Υ

Chlorobenzene 0.002 1 Υ Υ

Hydrochloric Acid 0.001 1 Υ Υ

Diethanolamine 0.001 1 Υ

Methylene Diphenyl 

Diisocyanate 0.001 1 Υ Υ

Propylene Dichloride 0.0006 1 Υ Υ

1,2,4-Trichlorobenzene 0.0006 1 Υ

Chlorine 0.0005 1 Υ Υ

Diethylene Glycol 

Monoethyl Ether 0.0005 1 Υ

o-Cresol 0.0005 1 Υ

POM 71002 0.0002 2 Υ

p-Xylene 0.0001 1 Υ Υ

Manganese & Compounds 0.00006 1 Υ

Lead & Compounds 0.00002 1 Υ Υ

Chromium 0.00001 1 Υ

Nickel 0.000009 1 Υ Υ

Arsenic 0.000006 1 Υ Υ

Cadmium Compounds 0.000003 1 Υ Υ

Mercury Compounds 0.000003 1 Υ Υ

Selenium Compounds 0.000002 1 Υ

Beryllium Compounds 0.000001 1 Υ Υ Υ

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”). 

• For emissions reported generically as “chromium” or “chromium & compounds,” emissions are speciated for this 

category as 75 percent “chromium (III) compounds” and 25 percent “chromium (VI) compounds.” Chromium 

speciation profiles can be found on the EPA’s Technology Transfer Network website for emissions inventories at 

http://www.epa.gov/ttn/chief/net/2002inventory.html. 

• For emissions of any chemicals or chemical groups classified as polycyclic organic matter (POM), emissions were 

grouped into POM subgroups as found on EPA’s Technology Transfer Network website for the 2002 National-Scale Air 

Toxics Assessment at http://www.epa.gov/nata2002/methods.html#pom. (Approach to Modeling POM). 

• 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 in section 2.6. 
41

Table 3.2-2 Summary of Source Category Level Risks for Marine Tank Vessel Loading 

Operations 

Result HAP “Drivers” 

Facilities in Source Category 

Number of Facilities Estimated to be Subject to 

MACT in Source Category 300 n/a 

Number of Facilities Identified in NEI and 

Modeled in NPRM Risk Assessment 152 n/a 

Cancer Risks 

Maximum Individual Lifetime Cancer Risk (in 1 

million) from any Facility in the Category 5024 benzene, 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 1 benzene, 1,3-butadiene 

 Greater than or equal to 1 in 1 million 2 benzene, 1,3-butadiene 

Chronic Noncancer Risks 

Maximum Reproductive Hazard Index 0.8 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 19 benzene (REL) 

Number of Facilities With Potential for Acute 

Effects 2 glycol ethers, benzene 

Acute Noncancer Refined Results

Maximum Acute Hazard Quotient 1 benzene (REL) 

Number of Facilities With Potential for Acute 

Effect 0 n/a 

Population Exposure 

Number of People Living Within 50 Kilometers 

of Facilities Modeled 61,000,000 n/a 

Number of People Exposed to Cancer Risk: 25

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

 Greater than or equal to 10 in 1 million 9,000 n/a 

 Greater than or equal to 1 in 1 million 513,000 n/a 

Number of People Exposed to Noncancer Immunological Hazard Index: 

 Greater than 1 0 n/a 

Estimated Cancer Incidence (excess cancer 

cases per year) 0.04 n/a 

Contribution of HAP to Cancer Incidence

 1,3-butadiene 59% n/a 

 benzene 21% n/a 

 naphthalene 14% n/a 

 acrylonitrile 4% n/a 

 ethylene dichloride 2% n/a 

 

24 These results are based on 2005 data. As a result of data obtained during the proposal comment period, we 

believe today’s MIR is below 1-in-1 million for all facilities in the source category. 25 Risk was scaled up to represent the universe of potential facilities from the 152 facilities in the data base to 

300 facilities or a factor of 2 (300/152). 
42

3.2.2 Risk characterization 

The maximum individual cancer risk estimated for the Marine Vessel Loading source 

category is about 50 in a million. One facility had a maximum individual risk greater than 1 

in a million, and this was primarily due to emissions of benzene and 1,3-butadiene. For the 

facility, we estimated that there are approximately 513,000 people with individual cancer risk 

levels at or above 1 in a million. We also estimated that the total cancer incidence associated 

with the inhalation of HAP emissions from this source category is 0.04 cases per year or about 

1 case every 5 years. These results are based on 2005 data. As a result of data obtained 

during the proposal comment period, we believe today’s MIR is below 1-in-1 million for all 

facilities in the source category. 

Chronic noncancer risks were determined to be insignificant, with a maximum chronic 

noncancer hazard index of 0.8, dominated by the contribution from 1,3-butadiene emissions. 

Additionally, our acute screening assessment identified two facilities with the potential for 

acute risks above 1. One facility had an acute screening value of 5 at the REL level due to 

glycol ether emissions, and the other facility had an acute screening value of 19 at the REL 

level due to benzene emissions. After the refined analyses were performed the facility with 

an acute value of 5 for glycol ethers reduced to an acute value below 1, and the facility with 

an acute value of 19 for benzene reduced to 1.49 (rounded to 1). Refer to Appendix 7 for 

details on the refined assessment. 

While our assessment did identify some emissions of PB-HAP from this source category, 

none of these emissions were anticipated to pose any potential multipathway risks based on 

our application of the PB-HAP screening scenario developed using the TRIM.FaTE model 

(Appendix 5). Thus, our assessment did not identify any potential for this source category to 

pose significant chronic non-inhalation risks, nor did we identify any potential for adverse 

environmental impacts. 

 The results of the facility-wide assessments are summarized in Table 3.2-3. The results 

indicate that 35 facilities containing Marine Tank Vessel Loading Operations have a facilitywide cancer MIR greater than 1 in a million. The maximum facility-wide cancer MIR is 90 in 

a million, with the source category contributing less than 1 percent. There are also 6 facilities 

with a facility-wide TOSHI value greater than 1. The maximum facility-wide TOSHI value 

of 4 (reproductive system), has a source category contribution of less than 1%. In general, the 

contribution of the source category to elevated facility-wide cancer or noncancer risks is low 

throughout the facilities in this source category. 

Table 3.2-3 Source Category Contribution to Facility-Wide Cancer Risks – Marine Tank 

Vessel 

Marine Tank Vessel Number of Facilities Binned by Facility-Wide MIR 

(in 1 million) 

Source Category MIR 

Contribution to Facility-Wide 

<1 1≤MIR<10 10≤MIR<100 > 100 Total 
43

MIR 

> 90% 68 0 1 0 69 

50-90% 3 0 1 0 4 

10-50% 5 2 0 0 7 

< 10% 39 20 13 0 72 

Total 115 22 15 0 152 

Analysis of potential differences between actual emission levels and the maximum emissions 

allowable under the MACT standards indicated that MACT allowable emission levels may be 

up to 3 times greater than actual emission levels. Considering this difference, the risk results 

from the inhalation risk assessment indicate that the maximum excess lifetime individual 

cancer risk could be up to 150 in a million, and that the maximum chronic noncancer TOSHI 

value could be as high as 2 at the MACT-allowable emissions level. In reality for the facility 

with the source category risk of 50, we believe the actual and allowable emissions to be the 

same. 

3.3 Pharmaceuticals production 

3.3.1 Source category description and results 

The pharmaceutical manufacturing process consists of chemical production operations that 

produce drugs and medication. These operations include chemical synthesis (deriving a 

drug’s active ingredient) and chemical formulation (producing a drug in its final form). 

During pharmaceutical manufacturing operations, HAP emissions can occur from breathing 

and withdrawal losses from chemical storage tanks, venting of process vessels, leaks from 

piping and equipment used to transfer HAP compounds (equipment leaks), and volatilization 

of HAP from wastewater streams. HAP emitted from the pharmaceutical manufacturing 

process include hydrochloric acid, and a range of volatile organic compounds, such as 

methylene chloride, methanol, N,N-dimethylformamide, and toluene, among others. 

Pharmaceutical operations are typically batch processes and highly plant-specific. We believe 

that there are 27 pharmaceutical manufacturing facilities subject to the MACT regulations. 

The data set for Pharmaceuticals Production contains emissions and facility data for the 27 

facilities thought to be currently in operation and subject to the MACT standard. Only the 

emissions from these 27 facilities, totaling about 1,056 tons/year, were included in our 

assessment. Refer to Appendix 1 for details on how the emissions inventory was developed. 

Table 3.3-1 summarizes the emissions for the Pharmaceuticals Production data set. Based on 

the modeled data set, the HAP emitted in largest quantities in total from these sources are 

methylene chloride, methanol, acetonitrile, toluene, hexane, ethylene glycol, methyl tert-butyl 

ether, hydrochloric acid, N,N-dimethylformamide, ethylene dichloride, xylenes, hydrogen 

fluoride, methyl chloride, triethylamine, methyl isobutyl ketone, and chloroform. These 16 

HAP account for 99 percent of the mass of HAP emissions in the data set for the 

Pharmaceuticals Production source category. Methanol is reported as emissions from 23 of 

the 27 facilities (85 percent) in the data set. Methylene chloride, acetonitrile, and toluene are 

reported as emitted by at least 15 facilities (56 percent) each. Persistent and bioaccumulative 
44

HAP (PB HAP)26 emissions in the data set for the pharmaceutical manufacturing source 

category include lead, mercury, and cadmium compounds as well as a range of polynuclear 

aromatic hydrocarbons (PAH). 

Tables 3.3-2 and 3.3-3 provide information summarizing the health risks results for this 

source category.

 

26 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. 
45

Table 3.3-1 Summary of Emissions and Availability of Dose-Response Values for the Pharmaceuticals 

Production Source Category 

HAPa Emissions (tpy) 

Number of 

Facilities 

Reporting 

HAP (27 

facilities in 

data set) 

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

PBHAP

? 

Unit Risk 

Estimate for 

Cancer? 

Reference 

Concentration 

for Noncancer? 

Health 

Benchmark 

Values for Acute 

Noncancer? 

Methylene Chloride 388 19 Υ Υ Υ

Methanol 322 23 Υ Υ 

Acetonitrile 91 15 Υ Υ 

Toluene 90 18 Υ Υ 

Hexane 44 12 Υ 

Ethylene Glycol 36 2 Υ 

Methyl Tert-Butyl Ether 31 8 Υ Υ Υ 

Hydrochloric Acid 11 11 Υ Υ 

N,N-Dimethylformamide 11 9 Υ Υ 

Ethylene Dichloride 7 3 Υ Υ Υ 

Xylenes (Mixture of o, m, 

and p Isomers) 5 8 Υ Υ 

Hydrogen Fluoride 5 2 Υ Υ 

Triethylamine 3 7 Υ Υ 

Methyl Chloride 3 3 Υ Υ 

Methyl Isobutyl Ketone 2 3 Υ 

Chloroform 2 5 Υ Υ 

Ethyl Benzene 1 6 Υ 

Glycol Ethers 1 4 Υ Υ 

Cyanide & Compounds 0.6 5 Υ 

Formaldehyde 0.6 7 Υ Υ Υ 

Hydrogen Cyanide 0.5 1 Υ Υ

Acetaldehyde 0.3 2 Υ Υ Υ 

Allyl Chloride 0.2 1 Υ Υ Υ 

Benzene 0.2 5 Υ Υ Υ 

Chloroacetic Acid 0.1 1 Υ 

Lead & Compounds 0.1 3 Υ Υ

Manganese & Compounds 0.1 3 Υ 

Chlorobenzene 0.09 3 Υ Υ 

Phosgene 0.08 1 Υ Υ 

Cumene 0.06 1 Υ Υ 

1-Chloro-2,3-Epoxypropane 0.05 2 Υ Υ Υ 

Phenol 0.03 3 Υ Υ 

Acetophenone 0.02 2 

Lead 0.01 2 Υ Υ

p-Dioxane 0.01 1 Υ Υ Υ 

Hydrazine 0.009 1 Υ Υ Υ 

Methyl Iodide 0.008 1 Υ 

Quinoline 0.008 1 

Phthalic Anhydride 0.004 1 Υ Υ 
46

Table 3.3-1 Summary of Emissions and Availability of Dose-Response Values for the Pharmaceuticals 

Production Source Category 

HAPa Emissions (tpy) 

Number of 

Facilities 

Reporting 

HAP (27 

facilities in 

data set) 

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSb

PBHAP

? 

Unit Risk 

Estimate for 

Cancer? 

Reference 

Concentration 

for Noncancer? 

Health 

Benchmark 

Values for Acute 

Noncancer? 

PAH, total 0.004 2 Υ Υ

Dimethyl Sulfate 0.002 1 Υ 

Benzo[g,h,i]Perylene 0.0009 3 Υ Υ

Cadmium & Compounds 0.0006 2 Υ Υ Υ

Ethylene Glycol Methyl 

Ether 0.0004 1 Υ Υ 

Mercury & Compounds 0.00003 1 Υ Υ Υ

Acetamide 0.000002 1 Υ

Acrolein 0.0000006 1 Υ Υ 

Naphthalene 0.00000004 1 Υ Υ 

Chromium (VI) 0.00000002 1 Υ Υ 

Phenanthrene 0.000000001 1 Υ Υ

Nickel & Compounds 0.0000000003 1 Υ Υ Υ 

Pyrene 0.0000000003 1 Υ Υ

Fluoranthene 0.0000000002 1 Υ Υ

Fluorene 0.0000000002 1 Υ Υ

Chromium & Compounds 0.0000000002 1 Υ Υ 

Arsenic & Compounds 

(Inorganic Including 

Arsine) 0.00000000003 1 Υ Υ

Υ

 

Anthracene 0.00000000002 1 Υ Υ

Cobalt & Compounds 0.00000000001 1 Υ 

Acenaphthene 0.00000000001 1 Υ Υ

Acenaphthylene 0.00000000001 1 Υ Υ

Benz[a]Anthracene 0.00000000001 1 Υ Υ

Benzo[b]Fluoranthene 0.00000000001 1 Υ Υ

Benzo[k]Fluoranthene 0.00000000001 1 Υ Υ

Chrysene 0.00000000001 1 Υ Υ

Indeno[1,2,3-c,d]Pyrene 0.00000000001 1 Υ Υ

Benzo[a]Pyrene 0.000000000008 1 Υ Υ

Dibenzo[a,h]Anthracene 0.000000000008 1 Υ Υ

Selenium & Compounds 0.0000000000004 1 Υ 

Beryllium & Compounds 0.0000000000002 1 Υ Υ Υ 

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.” 

b

 Specific dose-response values for each chemical are identified in Section 2.6.
47

3.3.1 Risk characterization 

This section presents the results of the risk assessment for the Pharmaceuticals 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 assessments in the form of maximum 

hazard quotients, as well as the results of our screen for potential non-inhalation risks from 

PB HAP. Also presented are the HAP “drivers,” which are the HAP that collectively 

contribute 90 percent of the maximum cancer risk or maximum hazard 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 6. 

Tables 3.3-1 and 3.3-2 summarize the preliminary chronic and acute inhalation risk results for 

this source category. The maximum individual cancer risk estimated for the 27 facilities in 

the Pharmaceutical Production source category is about 3 in a million. Four facilities 

showed a maximum individual cancer risk above 1 in a million. The major pollutants 

contributing to these risks were ethylene dichloride, methylene chloride, and hydrazine. For 

these facilities, we estimated that there are approximately 0 people with individual cancer risk 

levels at or above 10 in a million and 2,000 people with individual cancer risk levels at or 

above 1 in a million. We also estimated that the total cancer incidence associated with the 

inhalation of HAP emissions from the Pharmaceuticals Production source category is 0.0008 

cases per year or about 8 cases every 10,000 years. The emission source associated with the 

highest incidence for this source category is process vents, accounting for about 60% of the 

total cancer incidence. 

Chronic noncancer risks were determined to be insignificant, with a maximum chronic 

noncancer hazard index of 0.2, dominated by the contribution from manganese emissions. 

Our acute screening assessment identified 1 facility with potential acute impact concerns 

associated with acetonitrile emissions, indicating that this facility had the potential to exceed 

the AEGL-1 level by a factor of 2. The acute screening also identified 4 facilities with a 

potential to exceed the REL level for 5 pollutants – methylene chloride, methanol, 

acetonitrile, glycol ether, and chloroform. 
48

Table 3.3-2 Summary of Source Category Level Risks for Pharmaceuticals 

Result HAP “Drivers” 

Facilities in Source Category 

Number of Facilities Estimated to be Subject to 

MACT in Source Category 27 n/a 

Number of Facilities Identified in NEI and 

Modeled in Risk Assessment 2727 n/a 

Cancer Risks 

Maximum Individual Lifetime Cancer Risk (in 1 

million) 3 ethylene dichloride 

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 4 ethylene dichloride, methylene 

chloride, hydrazine 

Chronic Noncancer Risks 

Maximum Neurological Hazard Index 0.2 manganese compounds 

Number of Facilities with Maximum Neurological Hazard Index: 

 Greater than 1 0 n/a 

Acute Noncancer Screening Results

Maximum Acute Hazard Quotient 

4 

2 

0.06 

methylene chloride (REL) 

acetonitrile (AEGL-1) 

acetonitrile (AEGL-2) 

Number of Facilities With Potential for Acute 

Effects 4 methylene chloride, methanol, , chloroform, glycol ethers, acetonitrile 

Acute Noncancer Refined Results

Maximum Acute Hazard Quotient 2 

0.5 

chloroform (REL) 

acetonitrile (AEGL-1) 

Number of Facilities With Potential for Acute 

Effects 2 glycol ethers, chloroform 

Population Exposure 

Number of People Living Within 50 Kilometers 

of Facilities Modeled 36,000,000 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 2,000 n/a 

Number of People Exposed to Neurological Hazard Index: 

 Greater than 1 0 n/a 

Estimated Cancer Incidence (excess cancer cases 

per year) 0.0008 n/a 

Contribution of HAP to Cancer Incidence 

 

27 After the risk assessment was completed, it was learned that the Bristol Myers Squibb facility in Barceloneta, 

PR closed in 2009. Because the facility was operating at the time of the assessment, it remains in the data set at 

this time. It does not have the highest maximum individual lifetime cancer risk estimate, the highest hazard 

index estimate, or the highest acute hazard quotient estimate. 
49

Result HAP “Drivers” 

 methylene chloride 58% n/a 

 Hydrazine 20% n/a 

 ethylene dichloride 14% n/a 

For the facilities that exceeded acute thresholds in the screening assessment, we refined the 

assessment by plotting receptors on facility aerial photographs and determining maximum 

offsite concentrations. Once we performed these refinements, the estimated maximum offsite 

HQ value for methanol dropped to 0.9 (based on the REL), for acetonitrile the value dropped 

to 0.5 (AEGL-1), and for methylene chloride the HQ value dropped to 1 (based on the REL). 

Only the estimated maximum offsite concentrations of chloroform and glycol ether were seen 

to potentially exceed acute REL values at two facilities (maximum HQREL = 2), and there 

were no exceedances of the next highest threshold value for chloroform, the AEGL-2 

(HQAEGL-2 = 0.001) or glycol ether. Meteorological conditions leading to offsite exceedances 

of the REL could occur as frequently as 13 hours per year, or about 0.1 percent of the time. 

Details on the refined acute assessment can be found in Appendix 7.

Our assessment did identify some emissions of PB-HAP from this source category. Lead 

emissions at one facility were close to, but below, our screening range level of 350 lb/yr. 

Since our screening level is based on the lowest end of the proposed range for a possible 

revised lead NAAQS, we believe lead emissions at this facility do not pose any significant 

potential for multipathway risks. None of the other emissions were seen to pose any potential 

for multipathway risks based on the application of the PB-HAP screening scenario developed 

using the TRIM.FaTE model (see Appendix 5 for details). Thus, our assessment did not 

identify any potential for this source category to pose significant chronic non-inhalation risks, 

nor did we identify any potential for adverse environmental impacts. 

Based on our direct interaction with the facilities in this source category and on the lack of 

comments to the contrary to our NPRM, we have a high degree of confidence that our 

assessment covers the entire source category and that we have accurately characterized the 

emissions. As such, we believe that the exposure portion of our assessment reasonably 

represents maximum chronic inhalation exposures and total population exposures for the 

purpose of estimating cancer incidence. 
Table 3.3-3 Summary of Acute Refined Results for Pharmaceuticals Production 

Refined Results MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE-RESPONSE VA

HAP 

Max. 1-hr. 

Air Conc. 

(mg/m3) 

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

(1-h

(mg/

acetonitrile 10 n/a 0.5 0.02 22 54chloroform 0.3 2 n/a 0.001 0.15 31glycol ethers 0.2 2 n/a n/a 0.093 methanol 25 1 0.1 0.001 28 690 690 270methylene chloride 18 1 0.08 0.001 14 690 690 190

Notes on Process: 

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

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 a

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 eff

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 irr

long-lasting adverse health effects of 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 

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 experienc

irreversible or other serious health effects or symptoms which could impair an individual’s ability to take protective action.
51

The facility-wide MIR and HI available in Appendix 6 are based on emissions, as identified in 

the NEI database, from all emissions sources at the identified facilities. The results of the 

facility-wide MIR are summarized in Table 3.3-4. The maximum facility-wide risks are 

estimated to be a cancer MIR of 40 in a million and a HI of 0.8, both of which occur at the 

same facility. The source category contribution to the facility-wide risk at this facility is 

minimal; the cancer MIR is 0.005 in a million and the maximum noncancer HI is zero for 

respiratory/neurological and 0.00001 for liver. In contrast, there are other facilities where the 

source category impacts dominate the facility-wide risk. For example, one of the facilities 

with the highest cancer source category MIR (3 in a million) contributes 75% to its facilitywide cancer MIR of 4 in a million. 

Table 3.3-4 Summary Category Contribution to Facility-Wide Cancer Risks - 

Pharmaceuticals

Pharmaceuticals 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% 6 1 0 0 7 

50-90% 7 4 0 0 11 

10-50% 0 1 0 0 1 

< 10% 5 2 1 0 8 

Total 18 8 1 0 27 

Analysis of potential differences between actual emission levels and the maximum emissions 

allowable under the MACT standards indicated that MACT allowable emission levels may be 

up to 25% greater than actual emission levels. Considering this difference, the risk results 

from the inhalation risk assessment indicate that the maximum excess lifetime individual 

cancer risk could be up to 4 in a million, and that the maximum chronic noncancer TOSHI 

value could be as high as 0.3 at the MACT-allowable emissions level. 

3.4 Epichlorohydrin elastomers production 

3.4.1 Source category description and results 

 Epichlorohydrin elastomers are widely used in the automotive industry. The main 

epichlorohydrin elastomers are polyepichlorohydrin, epi-ethylene oxide (EO) copolymer, epiallyl glycidyl ether (AGE) copolymer, and epi-EO-AGE terpolymer. The primary HAP 

emitted during production are epichlorohydrin and toluene. Sources of HAP emissions for the 

epichlorohydrin elastomer source category include raw material storage vessels, front-end 
52

process vents, back-end process operations, wastewater operations, and equipment leaks. The 

majority of the emissions come from equipment leaks. The process "front-end" includes prepolymerization, reaction, stripping, and material recovery operations; and the process "backend" includes all operations after stripping (predominately drying and finishing). When EPA 

developed the proposed MACT rule in 1995, only one facility was identified for the 

epichlorohydrin elastomer production source category. 

From information gathered during the MACT development and in more recent contacts with 

the industry, the number of operating major source facilities with processes belonging in the 

Epichlorohydrin Elastomers Production source category is one. EPA identified this one 

facility in Version 1.0 of the 2002 NEI (February 2006). Based on existing NEI data of 

MACT codes, SCC codes, and pollutants emitted, EPA then identified the processes at each 

facility believed to be in the Epichlorohydrin Elastomers Production source category, and 

replaced the information in the NEI for these processes with data collected directly from the 

industry in 2004 as part of preliminary residual risk efforts. The data for this one facility 

comprised the data set for this source category with a total of 106 tons/year HAP emitted into 

the atmosphere. We believe that this one facility represents the complete source category, 

with a total of 106 tons/year HAP emitted into the atmosphere. This facility was the only one 

included in the assessment. Refer to Appendix 1 for details on how the emissions inventory 

changed. 

Table 3.4-1 summarizes the emissions for the Epichlorohydrin Elastomers Production source 

category. Emissions of toluene, the primary solvent in the process, account for over 99 

percent of the total emissions. Epichlorohydrin represents a much smaller percent of the total 

emissions, as most of this monomer reacts in the process to form the final product and is not 

available to be emitted to the atmosphere. No persistent and bioaccumulative HAP (PB HAP) 

emissions were reported for this facility. 

Table 3.4-2 provides information summarizing health risks results for this source category. 

Table 3.4-1 Summary of Emissions and Availability of Dose-Response Values for the 

Epichlorohydrin Elastomers Production Source Category 

HAP Emissions 

(tpy) 

Number 

of 

Facilities 

Reporting 

HAP (1 

facility in 

data set) 

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSa

PBHAP? 

Unit Risk 

Estimate 

for 

Cancer? 

Reference 

Concentration 

for Noncancer? 

Health Benchmark 

Value for Acute 

Noncancer? 

Toluene 44 1 Υ Υ 

Epichlorohydrin 0.4 1 Υ Υ Υ 

Ethylene Oxide 0.09 1 Υ Υ Υ 

3.4.2 Risk characterization 
53

This section presents the results of the risk assessment for the Epichlorohydrin Elastomers 

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 assessments in the form 

of maximum hazard quotients, as well as the results of our screen for potential non-inhalation 

risks from PB HAP. Also presented are the HAP “drivers,” which are the HAP that 

collectively contribute 90 percent of the maximum cancer risk or maximum hazard 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 6. 

Table 3.4-1 summarizes the preliminary chronic and acute inhalation risk results for this 

source category. The maximum individual cancer risk estimated for the 1 facility in the 

Epichlorohydrin Elastomers Production source category is about 10 in a million. The 

major pollutants contributing to these risks were ethylene oxide and epichlorohydrin. For 

the facility, we estimated that there are approximately 90 people with individual cancer 

risk levels at or above 10 in a million and 800 people with individual cancer risk levels at 

or above 1 in a million. We also estimated that the total cancer incidence associated with 

the inhalation of HAP emissions from the Epichlorohydrin Elastomers Production source 

category is 0.0001 cases per year or about 1 case every 10,000 years. The emission 

source associated with the highest incidence for this source category is equipment leaks, 

accounting for about 75% of the total cancer incidence. 

Chronic noncancer risks were determined to be insignificant, with a maximum chronic 

noncancer hazard index of 0.1, dominated by the contribution from epichlorohydrin 

emissions. Our assessment did not identify any potential for this source category to pose 

significant acute inhalation risks, chronic non-inhalation risks, or adverse environmental 

impacts. 
54

Table 3.4-2 Summary of Source Category Level Risks for Epichlorohydrin Elastomers 

Production 

Result HAP “Drivers” 

Facilities in Source Category 

Number of Major Source Facilities Estimated to 

be in Source Category 1 n/a 

Number of Facilities Identified in NEI and 

Modeled in Risk Assessment 1 n/a 

Cancer Risks 

Maximum Individual Lifetime Cancer Risk (in 1 

million) 10a

 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 1 ethylene oxide 

 Greater than or equal to 1 in 1 million 1 ethylene oxide 

Chronic Noncancer Risks 

Maximum Respiratory Hazard Index 0.1 epichlorohydrin 

Number of Facilities with Maximum Respiratory Hazard Index: 

 Greater than 1 0 n/a 

Acute Noncancer Screening Results

Maximum Acute Hazard Quotient 

0.2 

0.01 

0.003 

epichlorohydrin (REL) 

epichlorohydrin (AEGL-1) 

ethylene oxide (ERPG-2) 

Number of Facilities With Potential for Acute 

Effects 0 n/a 

Population Exposure 

Number of People Living Within 50 Kilometers 

of Facilities Modeled 218,000 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 90 n/a 

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

Number of People Exposed to Respiratory Hazard Index: 

 Greater than 1 0 n/a 

Estimated Cancer Incidence (excess cancer cases 

per year) 0.0001 n/a 

Contribution of HAP to Cancer Incidence 

 ethylene oxide 98% n/a 

 epichlorohydrin 2% n/a 

Notes: 

a

 The highest maximum individual lifetime cancer risk for any epichlorohydrin elastomers facility was estimated as 30 in 1 million. However, the 

coordinates given for southwest corner of the area source (i.e., the fugitive emissions) are believed to be incorrect, so the results using those 

coordinates are not reported. The maximum risks presented in the table are those estimated using the best estimate of the emission point’s actual 

location. 

The facility-wide MIR and HI available in Appendix 6 are based on emissions, as identified in 

the NEI database, from all emissions sources at the identified facility. The results of the 

facility-wide MIR are summarized in Table 3.4-3. The maximum facility-wide risks at the one 
55

facility with an operating epichlorohydrin elastomers process are estimated to be a cancer 

MIR of 10 in a million and a noncancer HI of 0.5. The source category contribution to the 

facility-wide risk at this facility is 100% for the MIR and 20% for the HI. 

Table 3.4-3 Source Category Contribution to Facility-Wide Cancer Risks - Epichlorohydrin

Epichlorohydrin Elastomers 

Production 

Number of Facilities Binned by Facility-Wide MIR 

(in 1 million) 

Source Category MIR 

Contribution to Facility-Wide 

MIR 

<1 1≤MIR<10 10≤MIR<100 > 100 Total 

> 90% 1 1 

50-90% 

10-50% 

< 10% 

Total 1 1 

The MACT-allowable emissions from this source category are estimated to be approximately 

the same as the modeled actual emissions; therefore, the risk results are equal. 

3.5 Polybutadiene rubber production 

3.5.1 Source category description and results 

Polybutadiene rubber (PBR) is a homopolymer of 1,3-butadiene (i.e., 1,3-butadiene is the 

only monomer used in the production of this polymer), and the PBR production source 

category includes any facility that polymerizes 1,3-butadiene. Both the solution and 

emulsion polymerization processes are used to produce PBR, and the process can be 

conducted as either a batch or continuous process. If the solution process is employed, 

the reaction is conducted in an organic solvent (hexane or toluene), which helps to 

dissipate heat generated by the reaction and control the reaction rate. The primary HAP 

emitted during production include hexane, 1,3-butadiene, styrene, and toluene. Sources 

of HAP emissions include raw material storage vessels, front-end process vents, back-end 

process operations, wastewater operations, and equipment leaks. The majority of the 

emissions come from back-end process operations. The process "front-end" includes prepolymerization, reaction, stripping, and material recovery operations; and the process 

"back-end" includes all operations after stripping (predominately drying and finishing). 

Most of the PBR manufactured in the U.S. is used in the production of tires in the 

construction of the tread and sidewalls. PBR is also used as a modifier in the production 

of other polymers and resins (e.g., polystyrene). When EPA developed the MACT rule, 

five facilities were identified for the PBR source category. 

From information gathered during the MACT development and from more recent 

contacts with the industry, we estimated that there are five major source facilities with 
56

processes belonging in the Polybutadiene Rubber Production source category. Refer to 

Appendix 1 for details on how the emissions inventory was developed. 

Table 3.5-1 summarizes the emissions for the Polybutadiene Rubber Production source 

category data set. Of the five facilities, three utilize hexane as the solvent in their 

solution process, one facility uses toluene as its solvent, and the fifth uses a non-HAP 

organic solvent. Based on the data, the total HAP emissions by mass from these facilities 

are dominated by hexane and toluene that account for 70 and 23 percent of the total 

emissions, respectively. Styrene and 1,3-butadiene are reported as emissions from all 

five facilities and collectively account for about four percent of the total emissions. No 

persistent and bioaccumulative HAP (PB HAP) were reported for the facilities. 

Table 3.5-2 provides information summarizing health risks for this source category. 

Table 3.5-1 Summary of Emissions and Availability of Dose-Response Values for the 

Polybutadiene Rubber Source Category 

HAPa Emissions 

(tpy) 

Number 

of 

Facilities 

Reporting 

HAP (5 

facilities 

in data 

set) 

Prioritized Inhalation Dose-Response Value Identified 

by OAQPS 

PBHAP? Unit Risk 

Estimate for 

Cancer? 

Reference 

Concentration for 

Noncancer? 

Health Benchmark 

Values for Acute 

Noncancer? 

Hexane 1,584 4 Υ Υ 

Toluene 510 2 Υ Υ

1,3-Butadiene 74 5 Υ Υ Υ

Styrene 68 5 Υ Υ

Ethyl Benzene 23 1 Υ

Chlorobenzene 2 1 Υ Υ

Methanol 0.07 1 Υ Υ

Nickel 0.0007 1 Υ Υ Υ

3.5.2 Risk characterization 

The maximum individual cancer risk estimated for the 5 facilities in the Polybutadiene 

Rubber Production source category is about 30 in a million, with this cancer risk being 

dominated by emissions of 1,3-butadiene. For these facilities, we estimated that there are 

approximately 20 people with individual cancer risk levels at or above 10 in a million, and 

24,000 people with individual cancer risk levels at or above 1 in a million. We also estimated 

that the total cancer incidence associated with the inhalation of these emissions is 0.003 cases 

per year, or about 3 cases every 1,000 years. Even though “back-end” processes are the 

highest source of emissions, the emission source associated with the highest incidence for this 

source category is “front end” process vents, accounting for about 50% of the total cancer 

incidence. 
57

Chronic noncancer risks were determined to be insignificant, with a maximum chronic 

noncancer hazard index of 0.3, dominated by the contribution from 1,3-butadiene emissions. 

Our acute screening assessment identified 1 facility with potential acute impacts of concern 

based on its toluene emissions, which indicated the potential to exceed the acute REL by a 

factor of 12 (HQREL = 10). Since the acute screening analysis showed an acute value over 1 

for this facility, a refined analysis was performed. The results of this refinement showed the 

acute for this one facility would be at an REL of 1. Therefore, it is unlikely that offsite 

concentrations near these facilities would result in a significant acute exposure. Details on the 

refined acute assessment can be found in Appendix 7. Our assessment did not identify any 

potential for this source category to pose significant chronic non-inhalation risks or adverse 

environmental impacts. 
58

Table 3.5-2 Summary of Source Category Level Risks for Polybutadiene Rubber 

Production 

Result HAP “Drivers” 

Facilities in Source Category 

Number of Major Source Facilities Estimated to 

be in Source Category 5 n/a 

Number of Facilities Identified in NEI and 

Modeled in Risk Assessment 5 n/a 

Cancer Risks 

Maximum Individual Lifetime Cancer Risk (in 1 

million) 3028 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 2 1,3-butadiene 

 Greater than or equal to 1 in 1 million 4 1,3-butadiene 

Chronic Noncancer Risks 

Maximum Reproductive Hazard Index 0.3 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 

12 

0.6 

0.2 

toluene (REL) 

toluene (AEGL-1) 

toluene (ERPG-2) 

Number of Facilities With Potential for Acute 

Effects 1 toluene 

Acute Noncancer Refined Results

Maximum Acute Hazard Quotient 1 toluene (REL) 

Number of Facilities With Potential for Acute 

Effects 0 n/a 

Population Exposure 

Number of People Living Within 50 Kilometers 

of Facilities Modeled 1,700,000 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 20 n/a 

 Greater than or equal to 1 in 1 million 24,000 n/a 

Number of People Exposed to 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 

 1,3-butadiene 98% n/a 

 ethyl benzene 2% n/a 

 

28 The individual source category risk is 20 in a million; however because of the close proximity of 2 facilities in 

the source category the highest predicted MIR for the source category is 30 in a million. 
59

The facility-wide MIR and HI available in Appendix 6 are based on emissions, as identified in 

the NEI database, from all emissions sources at the identified facility. The results of the 

facility-wide MIR are summarized in Table 3.5-3. The maximum individual risk (MIR) and 

hazard index (HI) presented in the spreadsheet are based on emissions, as identified in the 

database, from all emissions sources at the identified facility. The maximum facility-wide 

risks at the one facility with an operating styrene butadiene process are estimated to be a 

cancer MIR of 30 in a million and an HI of 0.3. The source category contribution to the 

facility-wide risk at this facility is 90% for both the MIR and the HI. 

Table 3.5-3 Source Category Contribution to Facility-Wide Cancer Risks - Polybutadiene

Polybutadiene Rubber Production Number of Facilities Binned by Facility-Wide 

MIR (in 1 million) 

Source Category MIR Contribution 

to Facility-Wide MIR 

<1 1≤ MIR<10 10≤ MIR<100 > 100 Total 

> 90% 2 2 4 

50-90% 

10-50% 1 1 

< 10% 

Total 3 2 5 

The MACT-allowable emissions from this source category are estimated to be approximately 

the same as the modeled actual emissions; therefore, the risk results are equal. 

3.6 Styrene butadiene rubber and latex production 

3.6.1 Source category description and results 

The styrene butadiene rubber and latex production source category includes any facility that 

manufactures copolymers consisting of styrene and butadiene monomer units. This source 

category is divided into three subcategories due to technical process and HAP emission 

differences: (1) the production of styrene-butadiene rubber by emulsion, (2) the production of 

styrene-butadiene rubber by solution, and (3) the production of latex. Styrene-butadiene 

rubber is coagulated and dried, while latex is not. For both styrene-butadiene rubber 

processes, the monomers used are styrene and 1,3-butadiene; either process can be conducted 

as a batch or a continuous process. 

The production of styrene butadiene rubber by emulsion is conducted in water containing 

monomers (styrene and 1,3-butadiene) and polymerization agents. Sources of HAP emissions 

for the emulsion subcategory include raw material storage vessels, front-end process vents, 

back-end process operations, wastewater operations, and equipment leaks. Most of the 

emissions come from back-end process operations. The process "front-end" includes prepolymerization, reaction, stripping, and material recovery operations; and the process "backend" includes all operations after stripping (predominately drying and finishing). The primary 

HAP emitted by emulsion styrene butadiene rubber production are styrene and 1, 3-butadiene. 
60

Emulsion styrene butadiene rubber is used in the production of tires and other automobile 

parts, adhesives, floor tiles, gaskets, belts, hoses, and other products. 

The production of styrene butadiene rubber is conducted in a solution composed of 

hydrocarbon solvents, monomers, and polymerization agents. These facilities use hexane or 

toluene as a solvent. Sources of HAP emissions for the solution subcategory include raw 

material storage vessels, front-end process vents, back-end process operations, wastewater 

operations, and equipment leaks. Most of the emissions come from back-end process 

operations (70 percent of total emissions at the time of MACT promulgation). The primary 

HAP emitted by production of solution styrene butadiene rubber are hexane, 1, 3-butadiene, 

styrene, and toluene. These products are used in footwear, conveyor belts, tires, hoses, 

flooring and adhesives. 

Styrene butadiene latex is produced by the emulsion process (i.e., in water containing 

monomers and polymerization agents) in a process similar to that used to make styrene 

butadiene by emulsion; however, at styrene butadiene latex facilities, the final product is a 

latex and not a dried solid. The primary HAP emitted by styrene butadiene latex production 

are styrene and 1,3-butadiene. Sources of HAP emissions include raw material storage 

vessels, front-end process vents, wastewater operations, and equipment leaks. 

We continue to believe that there are six facilities nationwide in this source category with a 

combined total of 303 tons/year of HAP emitted to the atmosphere. Refer to Appendix 1 for 

details on how the emissions inventory was developed. 

Table 3.6-1 summarizes the emissions for the Styrene Butadiene Rubber and Latex 

Production source category data set. Styrene, 1,3-butadiene, ethyl benzene, xylenes, and 

carbon disulfide account for 99 percent of the emissions by mass. Styrene is the largest 

fraction of the total emissions by mass (90 percent) and is emitted by all 6 facilities. 

1,3-butadiene is also reported as an emission by all 9 facilities and accounts for most of the 

remaining mass emitted (about 5 percent). No persistent and bioaccumulative HAP (PB 

HAP) were reported by the facilities. 

Table 3.6-2 provides information summarizing the health risks results for this source 

category. 

Table 3.6-1 Summary of Emissions and Availability of Dose-Response Values for 

Styrene Butadiene Rubber and Latex Production 

HAP Emissions (tpy) 

Number of 

Facilities 

Reporting HAP 

(6 facilities in 

data set) 

Prioritized Inhalation Dose-Response Value 

Identified by OAQPSa

PBHAP? Unit Risk 

Estimate for 

Cancer? 

Reference 

Concentration 

for Noncancer? 

Health 

Benchmark 

Values for Acute 

Noncancer? 

Styrene 275 6 Υ Υ

1,3-Butadiene 14 6 Υ Υ Υ

Ethyl Benzene 4 4 Υ 

Xylenes (Mixture of o, 4 2 Υ Υ
61

m, and p Isomers) 

Carbon Disulfide 3 1 Υ Υ

Acrylic Acid 0.8 3 Υ Υ

Toluene 0.7 2 Υ Υ

Benzene 0.7 1 Υ Υ Υ

Methanol 0.6 1 Υ Υ

Acrylonitrile 0.1 1 Υ Υ Υ

Vinylidene Chloride 0.05 1 Υ 

Hydrochloric Acid 0.04 1 Υ Υ

Ethyl Acrylate 0.04 1 Υ

Methyl Methacrylate 0 1 Υ Υ

3.6.2 Risk characterization 

The maximum individual cancer risk estimated for the 6 facilities in the Styrene Butadiene 

Rubber and Latex Production source category is about 10 in a million, with this cancer risk 

being dominated by emissions of 1,3-butadiene. For these facilities, we estimated that there 

are approximately 3 people with individual cancer risk levels at or above 10 in a million, and 

25,000 people with individual cancer risk levels at or above 1 in a million. We also estimated 

that the total cancer incidence associated with the inhalation of these emissions is 0.004 cases 

per year, or about 2 cases every 500 years. Even though “back-end” processes are the highest 

source of emissions, the emission source associated with the highest incidence for this source 

category is “front end” process vents, accounting for about 50% of the total cancer incidence. 

Chronic noncancer risks were determined to be insignificant, with a maximum chronic 

noncancer hazard index of 0.2, dominated by the contribution from 1,3-butadiene emissions. 

Our acute screening assessment identified 1 facility with potential acute impacts of concern 

based on its styrene emissions, which indicated the potential to exceed the acute REL by a 

factor of 2 (HQREL = 2). Since the acute screening analysis showed an acute value over 1 for 

this facility, a refined analysis was performed. The results of this refinement showed the 

acute for this one facility would to be below 1 (HQREL = 0.4). Details on the refined acute 

assessment can be found in Appendix 7. Our assessment did not identify any potential for this 

source category to pose significant chronic non-inhalation risks or adverse environmental 

impacts. 
62

Table 3.6-2 Summary of Source Category Level Risks for Styrene Butadiene – Rubber 

and Latex Production 

Result HAP “Drivers” 

Facilities in Source Category 

Number of Major Source Facilities Estimated to 

be in Source Category 6 n/a 

Number of Facilities Identified in NEI and 

Modeled in Risk Assessment 6 n/a 

Cancer Risks 

Maximum Individual Lifetime Cancer Risk (in 1 

million) 10 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 1 1,3-butadiene 

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

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 

0.6 

0.09 

styrene (REL) 

styrene (AEGL-1) 

styrene (AEGL-2) 

Number of Facilities With Potential for Acute 

Effects 1 styrene 

Acute Noncancer Refined Results

Maximum Acute Hazard Quotient 0.4 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 6,700,000 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 3 n/a 

 Greater than or equal to 1 in 1 million 25,000 n/a 

Number of People Exposed to Reproductive Hazard Index: 

 Greater than 1 0 n/a 

Estimated Cancer Incidence (excess cancer cases 

per year) 0.004 n/a 

Contribution of HAP to Cancer Incidence 

 1,3-butadiene 98% n/a 

 ethyl benzene 1% n/a 

The facility-wide MIR and HI available in Appendix 6 are based on emissions, as identified in 

the NEI database, from all emissions sources at the identified facilities. The facility with the 

maximum facility-wide risks is estimated to have a cancer MIR of 70 in a million and an HI 
63

of 1. The source category contribution to the facility-wide risk at this facility is about 5% for 

the MIR and 10% for the HI. The facility with the next highest MIR is 40 in a million with an 

HI of 1. The source category contribution to the facility wide MIR is 5% and 10% for the HI. 

Table 3.6-3 Source Category Contribution to Facility-Wide Cancer Risks - Styrene

Styrene Butadiene Rubber and 

Latex Production 

Number of Facilities Binned by Facility-Wide 

MIR (in 1 million) 

Source Category MIR 

Contribution to Facility-Wide MIR 

<1 1≤ MIR<10 10≤ MIR<100 > 100 Total 

> 90% 1 1 

50-90% 2 2 

10-50% 1 1 

< 10% 2 2 

Total 1 2 3 6 

The MACT-allowable emissions from this source category are estimated to be approximately 

the same as the modeled actual emissions; therefore, the risk results are equal. 

3.7 Nitrile butadiene rubber production 

3.7.1 Source category description and results 

Nitrile butadiene rubber (NBR) is a copolymer of 1,3-butadiene and acrylonitrile, and the 

NBR production source category includes any facility that polymerizes 1,3-butadiene and 

acrylonitrile. The emulsion, bulk, or solvent processes can be used to produce NBR. Either a 

continuous or a batch process can be used in production of NBR. In the manufacturing of 

NBR, the initial polymerization and stripping steps are similar to those used in the production 

of latex, except that polymerization of latex is typically a higher conversion reaction. The 

major difference between these two production processes is that in the production of nitrile 

butadiene rubber, the polymer is coagulated and dried, while in the production of latex, the 

stripped latex is simply blended with other specialty ingredients to produce the final nitrile 

butadiene latex product. The drying and finishing steps that make up the back-end processes 

for nitrile butadiene rubber are significant sources of HAP emissions. Other sources of HAP 

emissions include raw material storage vessels, front-end process vents, wastewater 

operations, and equipment leaks. The process "front-end" includes pre-polymerization, 

reaction, stripping, and material recovery operations; and the process "back-end" includes all 

operations after stripping (predominately drying and finishing). Depending on its specific 

composition, NBR can be resistant to oil and chemicals, a property that facilitates its use in 

disposable gloves, hoses, seals, and a variety of automotive applications. In 1995, four active 

facilities were identified that produced nitrile butadiene rubber. At one facility, the NBR 

equipment was also used to produce styrene-butadiene by the emulsion process (SBRE), as 

well as styrene-butadiene latex (SBL). When EPA developed the MACT rule, four facilities 

were identified for the nitrile butadiene rubber production source category. From more recent 

contacts with the industry, it is estimated that there is only one major source facility with 

processes belonging in the Nitrile Butadiene Rubber Production source category. 
64

The total emissions in the data set were 1.8 tons/year of HAP emitted to the atmosphere from 

the one remaining facility. Refer to Appendix 1 for details on how the emissions inventory 

was developed. 

Table 3.7-1 summarizes the emissions for the Nitrile Butadiene Rubber Production source 

category data set. 1,3-butadiene and acrylonitrile account for over 99 percent of the total 

HAP emissions. No persistent and bioaccumulative HAP (PB HAP) were emitted by the 

facilities in this source category. 

Table 3.7-2 provides information summarizing the health risks results for this source 

category. 

Table 3.7-1 Summary of Emissions and Availability of Dose-Response Values for Nitrile 

Butadiene Rubber Production 

HAP Emissions 

(tpy) 

Number of 

Facilities 

Reporting HAP 

(1 facility in 

data set) 

Prioritized Inhalation Dose-Response Value 

Identified by OAQPS 

PBHAP? Unit Risk 

Estimate for 

Cancer? 

Reference 

Concentration 

for 

Noncancer? 

Health 

Benchmark 

Values for Acute 

Noncancer? 

1,3-Butadiene 0.9 1 Υ Υ Υ

Acrylonitrile 0.9 1 Υ Υ Υ

3.7.2 Risk characterization 

The maximum individual cancer risk estimated for the one facility in the Nitrile Butadiene 

Rubber Production source category is about 2 in a million, with this cancer risk being 

dominated by emissions of acrylonitrile. For this facility, we estimated that there are no 

people with individual cancer risk levels at or above 10 in a million, and 70 people with 

individual cancer risk levels at or above 1 in a million. We also estimated that the total cancer 

incidence associated with the inhalation of these emissions is 0.0004 cases per year, or less 

than 1 case every 1,000 years. 

Chronic noncancer risks were determined to be insignificant, with a maximum chronic 

noncancer hazard index of 0.009, dominated by the contribution from 1,3-butadiene 

emissions. Our acute screening assessment resulted in no potential acute risk above 1. 
65

Table 3.7-2 Summary of Source Category Level Risks for Nitrile Butadiene Rubber 

Production 

Result HAP “Drivers” 

Facilities in Source Category 

Number of Major Source Facilities Estimated to 

be in Source Category 1 n/a 

Number of Facilities Identified in NEI and 

Modeled in Risk Assessment 1 n/a 

Cancer Risks 

Maximum Individual Lifetime Cancer Risk (in 1 

million) 2 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 0 n/a 

 Greater than or equal to 1 in 1 million 1 acrylonitrile, 1,3-butadiene 

Chronic Noncancer Risks 

Maximum Reproductive Hazard Index 0.009 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 0.001 

0.00009 

acrylonitrile (AEGL-1) 

acrylonitrile (ERPG-2) 

Number of Facilities With Potential for Acute 

Effects 0 n/a 

Population Exposure 

Number of People Living Within 50 Kilometers 

of Facilities Modeled 1,000,000 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 70 n/a 

Number of People Exposed to Reproductive Hazard Index: 

 Greater than 1 0 n/a 

Estimated Cancer Incidence (excess cancer cases 

per year) 0.0004 n/a 

Contribution of HAP to Cancer Incidence 

 acrylonitrile 72% n/a 

 1,3-butadiene 28% n/a 

The facility-wide MIR and HI available in Appendix 6 are based on emissions, as identified in 

the NEI database, from all emissions sources at the identified facility. The maximum facilitywide risks at the one facility with an operating nitrile butadiene process are estimated to be a 

cancer MIR of 5 in a million and an HI of 0.03. The source category contribution to the 

facility-wide risk at this facility is about 30% for both the MIR and HI. 
66

Table 3.7-3 Source Category Contribution to Facility-Wide Cancer Risks – Nitrile Butadiene

Nitrile Butadiene Rubber 

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% 

50-90% 

10-50% 1 1 

< 10% 

Total 1 1 

The MACT-allowable emissions from this source category are estimated to be approximately 

the same as the modeled actual emissions; therefore, the risk results are equal. 

4 General discussion of uncertainties and how they have been 

addressed 

While each of the source-category-specific sections presented earlier in this document discuss 

specific uncertainties unique to each category, the following general discussion of 

uncertainties applies to all of them. 

4.1 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 

reasonably representative meteorology. It is possible that population exposure estimates are 

also biased slightly higher 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 
67

varied from as much as 17% below the predicted value to as much as 84% higher than the 

predicted value. This variability translates directly to the predicted exposures and risks in our 

assessment, indicating that the actual risks could vary from 17% lower to 84% higher than the 

predicted values. 

We have purposely biased the acute screening results high, considering that they depend upon 

the joint occurrence of independent factors, such as hourly emissions rates, meteorology and 

human activity patterns. 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. In each of these cases, we have determined that this refined 

information reduced the likelihood of acute health concerns. 

4.2 Uncertainties in the dose-response relationships 

In the sections that follow, separate discussions are provided on uncertainty associated with 

cancer potency factors and for noncancer reference values. Cancer potency values are derived 

for chronic (lifetime) exposures. Noncancer reference values are generally derived for 

chronic exposures (up to a lifetime), 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 this 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 this 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 this 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 
68

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.[37] (herein 

referred to as Cancer Guidelines). “The primary goal of EPA actions is protection of human 

health; accordingly, as an Agency policy, risk assessment procedures, including default 

options that are used in the absence of scientific data to the contrary, should be health 

protective.” The approach adopted in this 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).29 In some circumstances, the true risk 

could be as low as zero; however, in other circumstances the risk could also be greater.30 

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.31 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). 

 

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

30 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. 

31According 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. 
69

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 

choices, data, models and assumptions [38]. 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 is 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.32 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 predictions. 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 

 

32 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.” 
70

(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). 

(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. A recent National Research Council report (NRC, 2006)33 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 

 

33 NRC (National Research Council) 2006. Assessing the Human Health Risks of Trichloroethylene. National 

Academies Press, Washington DC 
71

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 

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) [39]. 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 values34 e.g., factors of 10 or 3, 

 

34 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 
72

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 

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 daily oral exposure (RfD) or of 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.35 To derive values that are intended to be “without 

appreciable risk,” EPA’s methodology relies upon an uncertainty factor (UF) approach 

[40],[41] 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 [42]. 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 

 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. 

35 See IRIS glossary 
73

UF value leading to a downward adjustment of 10-3000 fold from the selected POD. An UF 

of 3 is used when the data do not support the use of a 10-fold factor. If an extrapolation step 

or adjustment is not relevant to an assessment (e.g., if applying human toxicity data and an 

interspecies extrapolation is not required) the associated UF is not used. The major 

adjustment steps are described more fully below. 

 1) Heterogeneity among humans is a key source of variability as well as uncertainty. 

Uncertainty related to human variation is considered in extrapolating doses from a subset or 

smaller-sized population, often of one sex or of a narrow range of life stages (typical of 

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. 
74

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. 

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. 

 
75

5 References 

 

1. US EPA, 2006. Emission Standards for Hazardous Air Pollutants. 

http://www.epa.gov/ttn/atw/mactfnlalph.html. 

2 US EPA, 2009. Risk and Technology Review (RTR) Risk Assessment Methodologies: For 

Review by the EPA’s Science Advisory Board with Case Studies – MACT I Petroleum Refining 

Sources and Portland Cement Manufacturing. EPA-452/R-09-006. 

http://www.epa.gov/ttn/atw/rrisk/rtrpg.html. 

3. US EPA, 2010. SAB’s Response to EPA’s RTR Risk Assessment Methodologies. 

http://yosemite.epa.gov/sab/sabproduct.nsf/4AB3966E263D943A8525771F00668381/$File/EP

A-SAB-10-007-unsigned.pdf 

4. US EPA, 2010. Memorandum from Dave Guinnup to the RTR Wood Furniture Docket 

(Docket ID Number EPA-HQ-OAR-2010-0786), entitled, “EPA’s Actions in Response to Key 

Recommendations of the SAB Review of RTR Risk Assessment Methodologies”. 

5. US EPA, 2005. Revision to the Guideline on Air Quality Models: Adoption of a Preferred 

General Purpose (Flat and Complex Terrain) Dispersion Model and Other Revisions; Final 

Rule. 40 CFR Part 51. http://www.epa.gov/EPA-AIR/2005/November/Day-09/a21627.htm

6. US EPA, 2004. Users’ guide for the AMS/EPA regulatory model – AERMOD. EPA-454/B03-001. http://www.epa.gov/scram001/7thconf/aermod/aermodugb.pdf. 

7. Allen, D., C. Murphy, Y. Kimura, W. Vizuete, T. Edgar, H. Jeffries, B.-U. Kim, M. Webster, 

and M. Symons, 2004. Variable industrial VOC emissions and their impact on ozone 

formation in the Houston Galveston Area. Final Report: Texas Environmental Research 

Consortium Project H-13. 

http://files.harc.edu/Projects/AirQuality/Projects/H013.2003/H13FinalReport.pdf

8. US EPA, 2004. Air Toxics Risk Assessment Reference Library, Volume 1. EPA-453-K-04- 

001A. http://www.epa.gov/ttn/fera/risk_atra_vol1.html. 

9. US EPA, 2005. Table 1. Prioritized Chronic Dose-Response Values (2/28/05). Office of 

Air Quality Planning and Standards. http://www.epa.gov/ttn/atw/toxsource/table1.pdf

10. US EPA, 2005. 1999 National Air Toxics Risk Assessment. 

http://www.epa.gov/ttn/atw/nata1999

11. US EPA, 2008. Integrated Risk Information System. http://www.epa.gov/iris/index.html. 

12. US Agency for Toxic Substances and Disease Registry. 2006. Minimum Risk Levels (MRLs) 

for Hazardous Substances. http://www.atsdr.cdc.gov/mrls.html. 

13. US EPA, 1994. US Environmental Protection Agency. Methods for Derivation of 

Inhalation Reference Concentrations and Application of Inhalation Dosimetry. 

EPA/600/8-90/066F. Office of Research and Development. Washington, DC: U.S.EPA.
76

 

14. NRC, 1994. National Research Council. Science and Judgment in Risk Assessment. 

Washington, DC: National Academy Press. 

15. CA Office of Environmental Health Hazard Assessment, 2005. Chronic Reference 

Exposure Levels Adopted by OEHHA as of February 2005. 

http://www.oehha.ca.gov/air/chronic_rels/AllChrels.html. 

16. CA Office of Environmental Health Hazard Assessment, 2005. Technical Support Document 

for Describing Available Cancer Potency Factors, May 2005. 

http://www.oehha.ca.gov/air/hot_spots/may2005tsd.html. 

17 Conolly, RB, Kimbell, JS, Janszen, D, Schlosser, PM, Kalisak, D, Preston, J, and Miller, FJ. 

2003. Biologically Motivated Computational Modeling of Formaldehyde Carcinogencity in 

the F344 Rat. Tox Sci 75: 432-447. 

18 Conolly, RB, Kimbell, JS, Janszen, D, Schlosser, PM, Kalisak, D, Preston, J, and Miller, FJ. 

2004. Human Respiratory Tract Cancer Risks of Inhaled Formaldehyde: Dose-Response 

Predictions Derived from Biologically-Motivated Computational Modeling of a Combined 

Rodent and Human Dataset. Tox Sci 82: 279-296. 

19 Chemical Industry Institute of Toxicology (CIIT). 1999. Formaldehyde: Hazard 

Characterization and Dose-Response Assessment for Carcinogenicity by the Route of 

Inhalation. CIIT, September 28, 1999. Research Triangle Park, NC. 

20 Subramaniam, R; Chen, C; Crump, K; et al. (2008). Uncertainties in Biologically-Based 

Modeling of Formaldehyde-Induced Cancer Risk: Identification of Key Issues. Risk Anal 28 

(4):907-923. 

21 Crump, K; Chen, C; Fox, J; et al. (2008). Sensitivity Analysis of Biologically Motivated 

Model for Formaldehyde-Induced Respiratory Cancer in Humans. Ann Occup Hyg 52:481-

495. 

22 Subramaniam RP; Crump KS; Van Landingham C; White P; Chen C; Schlosser PM (2007). 

Uncertainties in the CIIT model for formaldehyde-induced carcinogenicity in the rat: A limited 

sensitivity analysis–I. Risk Anal, 27: 1237–1254. 

23 CalEPA. (2005). Letter from JR Froines, Chair of Scientific Review Panel to B Jordan, Interim 

Chairperson, Air Resources Board, California Environmental Protection Agency. 

24 CalEPA. (2007). Final Statement of Reeasons for Rulemaking Including Summary of 

Comments and Agency Responses. Public hearing to consider adoption of the proposed 

airborne toxic control measure to reduce formaldehyde emissions from composite wood 

products. Public Hearing Date: April 26, 2007. 

25. US EPA, 2006. Approach for modeling POM. Technical support information for the 1999 

National Air Toxics Assessment. 

http://www.epa.gov/ttn/atw/nata1999/99pdfs/pomapproachjan.pdf. 
77

 

26. US EPA, 2005. Table 2. Acute Dose-Response Values for Screening Risk Assessments 

(6/02/2005). Office of Air Quality Planning and Standards. 

http://www.epa.gov/ttn/atw/toxsource/table2.pdf

27. CA Office of Environmental Health Hazard assessment, 2000. All Acute Reference Exposure 

Levels developed by OEHHA as of May 2000. 

http://www.oehha.ca.gov/air/acute_rels/allAcRELs.html

28. American Industrial Hygiene Association , 2009. Current AIHA ERPG Values. 

http://www.aiha.org/insideaiha/volunteergroups/Documents/ERP-erpglevels.pdf. 

29. US EPA, 1995. Guidance for Risk Characterization. Science Policy Council. 

http://www.epa.gov/OSA/spc/pdfs/rcguide.pdf. 

30. US EPA, 2000. Risk Characterization Handbook. EPA 100-B-00-002. 

31. US EPA, 2002. EPA’s Guidelines for Ensuring and Maximizing the Quality, Objectivity, 

Utility, and Integrity of Information Disseminated by the Environmental Protection Agency. 

EPA Office of Environmental Information. EPA/260R-02-008. 

http://www.epa.gov/quality/informationguidelines/documents/EPA_InfoQualityGuidelines.pdf

32. US EPA, 2006. Performing risk assessments that include carcinogens described in the 

Supplemental Guidance as having a mutagenic mode of action. Science Policy Council Cancer 

Guidelines Implementation Workgroup Communication II: Memo from W.H. Farland dated 

14 June 2006. http://www.epa.gov/osa/spc/pdfs/CGIWGCommunication_II.pdf

33. US EPA, 2005. Supplemental guidance for assessing early-life exposure to carcinogens. 

EPA/630/R-03003F. http://www.epa.gov/ttn/atw/childrens_supplement_final.pdf. 

34. US EPA, 2005. Science Policy Council Cancer Guidelines Implementation Workgroup 

Communication I: Memo from W.H. Farland dated 4 October 2005 to Science Policy 

Council. http://www.epa.gov/osa/spc/pdfs/canguid1.pdf 

35. US EPA, 1986. Guidelines for the Health Risk Assessment of Chemical Mixtures. 

EPA/630/R-98/002. http://www.epa.gov/NCEA/raf/pdfs/chem_mix/chemmix_1986.pdf

36. US EPA, 2000. Supplementary Guidance for Conducting Health Risk Assessment of Chemical 

Mixtures. EPA/630/R-00/002. 

http://www.epa.gov/ncea/raf/pdfs/chem_mix/chem_mix_08_2001.pdf

37. US EPA, 2005. Guidelines for Carcinogen Risk Assessment (2005). U.S. Environmental 

Protection Agency, Washington, DC, EPA/630/P-03/001F, 2005. 

http://cfpub.epa.gov/ncea/raf/recordisplay.cfm?deid=116283 

38. US EPA, 2000. Risk Characterization Handbook. EPA 100-B-00-002. 

39. R.P. Subramaniam, P. White and V.J. Cogliano. 2006. Comparison of cancer slope factors 

using different statistical approaches, Risk Anal. Vol 26, p. 825–830. 

40. US EPA. 1993. Reference Dose (RfD): Description and Use in Health Risk Assessments. 
78

 

http://www.epa.gov/iris/rfd.htm. 

41. US EPA. 1994. Methods for Derivation of Inhalation Reference Concentrations and 

Application of Inhalation Dosimetry. 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=71993. 

42. US EPA. 2002. A Review of the Reference Dose and Reference Concentration Processes. 

http://www.epa.gov/ncea/iris/RFD_FINAL1.pdf.