## 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 Qualit y Planning and Standards
Office of Air and Radiation January 2011

### Table of Contents

1 Introduction .................................................................................................................. ........... 5
2 Methods ....................................................................................................................... ............ 6
2.1 Emissions and source data ................................................................................................ 6
2.2 Dispersion modeling for inhala tion exposure assessment ................................................ 6
2.3 Estimating human inhalation exposure ............................................................................ 9
2.4 Acute risk screening and refined assessments ................................................................ 10
2.5 Multipathway and environmen tal 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 ...................................................... Error! Bookmark not defined.
2.7.1 General .................................................................... Error! Bookmark not defined.
2.7.2 Mixtures .................................................................. Error! Bookmark not defined.
2.7.3 Facility-wide risks ................................................... Error! Bookmark not defined.
3 Results summaries and risk character izations for the 7 source categories Error! Bookmark not defined.
3.1 Printing and publishing................................................... Error! Bookmark not defined.
3.1.1 Source category descri ption and results .................. Error! Bookmark not defined.
3.1.2 Risk characterization ............................................... Error! Bookmark not defined.
3.2 Marine tank vessel loading ............................................. Error! Bookmark not defined.
3.2.1 Source category descri ption and results .................. Error! Bookmark not defined.
3.2.2 Risk characterization ............................................... Error! Bookmark not defined.
3.3 Pharmaceuticals production ........................................... Error! Bookmark not defined.
3.3.1 Source category descri ption and results .................. Error! Bookmark not defined.
3.3.1 Risk characterization ............................................... Error! Bookmark not defined.
3.4 Epichlorohydrin elastomers production ......................... Error! Bookmark not defined.
3.4.1 Source category descri ption and results .................. Error! Bookmark not defined.
3.4.2 Risk characterization ............................................... Error! Bookmark not defined.
3.5 Polybutadiene rubber production ................................... Error! Bookmark not defined.
3.5.1 Source category descri ption and results .................. Error! Bookmark not defined.
3.5.2 Risk characterization ............................................... Error! Bookmark not defined.
3.6 Styrene butadiene rubber and latex production .............. Error! Bookmark not defined.
3.6.1 Source category descri ption and results .................. Error! Bookmark not defined.
3.6.2 Risk characterization ............................................... Error! Bookmark not defined.
3.7 Nitrile butadiene r ubber production ............................... Error! Bookmark not defined.
3.7.1 Source category descri ption and results .................. Error! Bookmark not defined.
3.7.2 Risk characterization ............................................... Error! Bookmark not defined.
4 General discussion of uncertainties and how they have been addressed Error! Bookmark not defined.
4.1 Exposure modeling uncertainties ................................... Error! Bookmark not defined.
4.2 Uncertainties in the dose -response relationships ............ Error! Bookmark not defined.
5 References ............................................................................. Error! Bookmark not defined.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 Chr onic Inhalation Exposure to Carcinogens ........... 17 Table 2.6-2.A Dose-Response Values for Chroni c Inhalation Exposure to Noncarcinogens ..... 19 Table 2.6-2.B Dose-Response Values for Chr onic Oral Exposure to Noncarcinogens ............... 21 Table 3.1-1 Summary of Emi ssions and Availability of Dose-Response Values for the Printing and Publishing Source Category ..................................... Error! Bookmark not defined. Table 3.1-2 Summary of S ource Category Level Risks for Printing and Publishing Error! Bookmark not de f Table 3.1-3 Summary of Acute Refined Results for Printing and Publishing Error! Bookmark not defined. Table 3.1-4 Source Category Contribution to Facility-Wide Cancer Risks – Printing and Publishing ...................................................................................... Error! Bookmark not defined. Table 3.2-1 Summary of Emissions and Availability of Dose-Response Values for the Marine Tank Vessel Loading Operations Source Category ...................... Error! Bookmark not defined. Table 3.2-2 Summary of Sour ce Category Level Risks for Marine Tank Vessel Loading Operations ..................................................................................... Error! Bookmark not defined. Table 3.2-3 Source Category Contribution to Facility-Wide Cancer Risks – Marine Tank
Vessel ............................................................................................ Error! Bookmark not defined. Table 3.3-1 Summary of Emi ssions and Availability of Dose-Response Values for the Pharmaceuticals Production Source Category .............................. Error! Bookmark not defined. Table 3.3-2 Summary of Source Cate gory Level Risks for Pharmaceuticals Error! Bookmark not defined. Table 3.3-3 Summary of Ac ute Refined Results for Pharmaceuticals Production Error! Bookmark not defi n Table 3.3-4 Summary Category Contribution to Faci lity-Wide Cancer Risks -
Pharmaceuticals ............................................................................ Error! Bookmark not defined. Table 3.4-1 Summary of Emi ssions and Availability of Dose-Response Values for the Epichlorohydrin Elastomers Production Source Category ........... Error! Bookmark not defined. Table 3.4-2 Summary of Sour ce Category Level Risks for Epichlorohydrin Elastomers
Production ..................................................................................... Error! Bookmark not defined. Table 3.4-3 Source Category Contribution to Facility-Wide Cancer Risks - Epichlorohydrin Error! Bookma r Table 3.5-1 Summary of Emi ssions and Availability of Dose-Response Values for the Polybutadiene Rubber Source Category ....................................... Error! Bookmark not defined. Table 3.5-2 Summary of Sour ce Category Level Risks for Po lybutadiene Rubber Production Error! Bookm a Table 3.5-2 Source Category Contribution to Facility-Wide Cancer Risks - Polybutadiene Error! Bookmark Table 3.6-1 Summary of Emissions and Availa bility of Dose-Response Values for Styrene
Butadiene Rubber and Latex Production ...................................... Error! Bookmark not defined. Table 3.6-2 Summary of Source Category Level Risks for Styrene Butadiene – Rubber and
Latex Production ........................................................................... Error! Bookmark not defined. Table 3.6-2 Source Category Contribution to Facility-Wide Cancer Risks - Styrene Error! Bookmark not d e Table 3.7-1 Summary of Emissions and Availa bility of Dose-Response Values for Nitrile
Butadiene Rubber Production ....................................................... Error! Bookmark not defined. Table 3.7-2 Summary of S ource Category Level Risks for Nitrile Butadiene Rubber
Production ..................................................................................... Error! Bookmark not defined. Table 3.7-2 Source Category Contribution to Faci lity-Wide Cancer Risks – Nitrile Butadiene Error! Bookm aAppendices

Appendix 1 Emissions Inventory Support Memorandums Appendix 2 Technical Support Docu ment for HEM-AERMOD Modeling Appendix 3 Meteorological Da ta 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 Re fined 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

### 1 Introduction

Section 112 of the Clean Air Act (CAA) establ ishes a two-stage regu latory process for addressing emissions of hazardous air pollutants ( HAPs) from stationary sources. In the first stage, section 112(d)(2) requires the Environmental Protectio n Agency (EPA, or the Agency) to develop technology-based standards for categ ories of industrial sources (e.g., petroleum refineries, pulp and paper mills, etc.) [ 1 ]. EPA has largely completed the initial Maximum Achievable Control Technology (MACT) standa rds as required under this provision. Under section 112(d)(6), EPA must review each of thes e technology-based standards at least every eight years and revise a sta ndard, as necessary, “taking in to account developments in practices, processes and control technologies.” In the second stage, EPA is required under section 112(f)(2) to assess th e health and environmental risks that remain after implementation of the MACT standards. If addi tional risk reductions ar e 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 st age 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 (R TR) Assessment Plan” and in June of 2007,
we received a letter with the results of that c onsultation. 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) A ssessment 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 assessm ents by incorporating updates based on the SAB recommendations as they are developed and be come 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 result s 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 ButadieneThe 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 de scriptions of the methods used to screen for acute health risks, chronic non-inhalati on health risks, and adverse environmental effects. Since none of the screening assessments indicated any signifi cant potential for chroni c non-inhalation health effects, or environmental impacts including eff ects to threatened and endangered species, no
further refinement of these assessments was performed. Screening assessments indicated a
concern for acute health effect s for all 5 of the source categor ies. 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 Inventor y (NEI) which were used and published as part of the 2005 National-Scale Air Toxics A ssessment (NATA) served as the starting point
for this assessment. The 2005 NEI contains in formation on actual emissions during the entire 2005 base year. Using the process MACT code 1 , 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 inform ation using EPA engineers who were directly involved in the development of the MACT standa rds 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 av ailable. The goal of the engi neering review was to identify readily-apparent limitations and issues with the emissions data (particularly those that would greatly influence risk estimates) and to make ch anges to the data set wh ere possible to address
these issues and decrease the uncertainti es associated with the assessment.

Details on the development of the emissions a nd source data for thes e source categories are
discussed in Section 3. The emissions data and modifications made to the NEI data are discussed in the Appendix 1, entitled “Emi ssions Inventory Support Memorandums.”



### 2.2 Dispersion modeling for in halation exposure assessment
Both long- and short-term inhalation exposure co ncentrations and associated health risk from each facility in each of the s ource categories of interest we re estimated using the Human Exposure Model in combination with the Amer ican Meteorological So ciety/EPA Regulatory Model dispersion modeling system (HEM-AERMOD) . The approach used in applying this modeling system is outlined below, and furt her details are provided in Appendix 2. HEMAERMOD performs three main operations: at mospheric dispersion modeling, estimation of individual human exposures and health risks, an d 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 de termine 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 pro cess level or at the site level in the point source data (e.g., the MACT code for municipal waste combustors (M WCs) is assigned at the site level whereas the MACT code for petroleum refinery catalytic crack ing is assigned at the process level).The dispersion model in the HEM-AERMOD sy stem, AERMOD version 09292, is a state-ofthe-science Gaussian plume di spersion model that is prefer red by EPA for modeling point, area, and volume sources of continuous ai r 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 concentr ation through the simu lation of hour-by-hour dispersion from the emission sources into the su rrounding 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 NW S from nearest site (158 stations)

In HEM-AERMOD, meteorological data are ordinarily select ed from a list of 158 National Weather Service (NWS) surface observation stat ions 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. Idea lly, when considering off-site meteorological data most site specific disp ersion modeling efforts will employ up to five years of data to capture variabil ity in weather patterns from ye ar to year. However, because we had insufficient number of appropriately formatted model input files derived from available meteorological data, we modeled onl y a single year, typica lly 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 over-predicti on at others. For each facility identified by its characteristic latitude and long itude coordinates, the closest meteorological station was used in the dispersion modeling. The average dist ance between a modele d facility and the applicable meteorological station was 40 miles (72 km). Appendix 3 (Meteorological Data Processing Using AERMET for HEM-AERMOD) provi des a complete listing of stations and assumptions along with further details used in processing the data through AERMET. Thesensitivity of model results to the selection of the nearest weather station and the use of one year of meteorological data is discussed in “Risk and Technology Review (RTR) Risk Assessment Methodologies” [ 2 ].

The HEM-AERMOD system estimates ambient con centrations at the ge ographic centroids of census blocks (using the 2000 Census), and at othe r receptor locations that can be specified by
the user. The model accounts for the effect s of multiple facili ties when estimating concentration impacts at each block centroid. Typically we combined only the impacts of facilities within the same source category, and assessed chronic exposur e 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 fi nest resolution availa ble in the census data, are typically comprised of approximately 40 people or about ten households.

In contrast to the developmen t of ambient concentrations fo r evaluating long-term exposures, which was performed only for occupied censu s blocks, worst-case short-term (one-hour)
concentrations were estimated both at the censu s 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 tota ls, we applied the gene ral assumption to all source categories that the maxi mum 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 us ing a short-term emi ssions dataset from a
number of sources located in Texa s (originally reported on by Allen et al. 2004)[ 7]. In that report, the Texas Environmental Research C onsortium Project compared hourly and annual emissions data for volatile organic compounds fo r 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 an d 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 99 th percentile ratio of peak hourly emission rate to the annual hourly emissi on rate was 9. Based on these results, we
chose the factor of ten for all initial screeni ng; it is intended to c over routinely-variable emissions as well as startup, shutdown, and ma lfunction (SSM) emissions. While there are
some documented emission excursions above this level, our analysis of the data from the Texas Environmental Research Consortium suggest s that this factor s hould cover more than99% of the short-term peak gaseous or vol atile HAP emissions from typical industrial

sources.

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 shortand long-term ambient concentrations were assu med 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 th e 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 pa tterns. 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 con centration of each HAP at each census block centroid as a surrogate for the lifetime inhalati on exposure concentration of all the people who
reside in the census block. That is, this risk analysis did not c onsider either the short-term or long-term behavior (mobility) of the exposed populations and its poten tial 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 cu rrent understanding of microenvironment concentrations and daily activ ities, modeling short-term ac tivity 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, ba sing 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 be havior 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 assumpti on 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 inci dence. This assumpti on 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 populati on number remains the same. It does, however, affect the shape of the distribution of individual risks across the affected population, shifting it to ward higher estimated individua l risks at the upper end andreducing the number of people estimated to be at lower risks, thereby biasing the risk estimates high.

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 concen tration for any individual.



### 2.4 Acute risk screening and refined assessments

In establishing a scientifically defensible approa ch for the assessment of potential health risks due to acute exposures to HAP, we followed the same general appr oach that has been used for developing chronic health risk assessments under the residual risk program. That is, we developed a tiered, iterative approach. This a pproach to risk assessment was endorsed by the National Academy of Sciences in its 1993 pub lication “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 el iminate 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 tier ed, iterative approach to the assessment. This means that we began with a screening assessmen t, which relies on read ily available data and uses conservative assumptions that in combina tion approximate a worst-case exposure. The result of this screening process is that either the facility be ing 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 pa ttern of emissions, the layout of emission points at the facility, th e boundaries of the facil ity, and/or the local meteorology. In some cases, all of these site-s pecific data would be needed to refine the assessment; in others, lesser amounts of site-spe cific data could be used to determine that acute exposures are not a con cern, 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, an d 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 possi ble acute health risk might exist. These
benchmarks are described in section 2.6 of this report.

As mentioned above, when we identify acu te impacts which exceed their relevant benchmarks, we pursue refining our acute screeni ng 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 ca tegories in the document, we conducted a review of the layout of emission points at the facilities with the facility boundaries to determine the maximum offsite acute impact for the facilitie s 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 envi ronmental risk screening

The potential for significant hum an health risks due to expos ures via routes other than inhalation (i.e., multipathway exposures) or adve rse environmental impacts were screened by first determining whether any sources emitte d any hazardous air pollutants known to be persistent and bioaccumulative in the envir onment (PB-HAP). The PB-HAP compounds or compound classes are identified for the scre ening 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, polyc yclic organic matter (POM), t oxaphene, 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-devel oped screening scenario whic h was developed for use with
the TRIM.FaTE 2 model. This screening scenario us es environmental media outputs from the peer-reviewed TRIM.FaTE to estimate the maximum potential ingestion risks for any specified emission scenario by using a generi c farming/fishing exposure scenario that
simulates a subsistence environment. The scr eening scenario retains many of the ingestion and scenario inputs developed for EPA’s Human Health Risk Assessment Protocols (HHRAP) for hazardous wast e 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 c oncentrations 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 a nd 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

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/hazwa ste/combust/riskvol.htm#volume1for our multi-pathway screening, we derived em ission 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 ev aluating 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 Stan dard (NAAQS) for lead. Values below the NAAQS were considered to have a low potentia l for multi-pathway risks of any significance.

In all instances, modeling of emissions of cad mium, mercury, and POM associated with the 7 source categories using our screening scenar io 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 fo r lifetime cancer risk a nd a hazard quotient of 1.0 for noncancer impacts. In evaluating emi ssions of lead compounds, since an ingestion reference dose has not been established for chronic noncancer effects, we compared maximum chronic atmospheric concentrations w ith 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 significan t ecological exposures to non PB-HAP
from exceedances of chronic human health inhala tion 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 rodent s) 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 th e 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 shoul d 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 impact s 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 do se-response information Dose-response assessment information (car cinogenic and non-carcinogenic) for chronic exposure (either by inhalation or ingestion) for the HAPs reporte d in the emissions inventory were based on the EPA Office of Air Qu ality 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 assessm ent guidelines and (2) level of peer reviewreceived. The prioritization process was aimed at incorporating into our assessments the best available science with respect to dose-response information. The recommendations are based on the following sources, in order of priority:

1) US Environmental Protection Agency (EPA). EPA has developed dose-response assessments for chronic exposure for many of th e pollutants in this risk assessment. These assessments typically provide a qualitative stat ement regarding the st rength of scientific data and specify a reference concentration (RfC, for inhalation) or reference dose (RfD, for ingestion) to protect against effects othe r than cancer and/or a unit risk estimate (URE, for inhalation) or slope factor (SF, for ingestion) to estimat e the probability of developing cancer. The RfC is defined as “an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation e xposure to the human population (including sensitive subgroups) that is likely to be without an appreciabl e 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 appr eciable risk of deleterious effects during a lifetime.” The URE is defined as “the uppe r-bound excess cancer risk estimated to result from continuous lifetime exposure to an agent at a concentration of 1 μg/m 3 in air.” The SF is “an upper bound, approximating a 95% co nfidence 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) aff ected 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 cu rrent IRIS process includes review by EPA scientists, interagency reviewers from other federal agencies, and the public, and peer review by independe nt scientists external to EPA. New IRIS values are developed and old IRIS values are upda ted as new health effects data become
available. Refer to the “IRIS Track” webs ite for detailed information on status and scheduling of current individua l IRIS assessments and updates ( http://cfpub.epa .gov/ncea/iristrac/index.cfm). EPA’s science policy appr oach, 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 Huma n Services, develops and publishes Minimum Risk Levels (MRLs) [ 12 ] for inhalation and oral exposur e to many toxic substances. As stated on the ATSDR web site: “Following di scussions 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 Refere nce 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 subs tance that is likelyto 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 environm ental contaminants for further evaluation. Exposures above an MRL do not necessarily re present 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 ha s developed dose-response assessments for many substances, based both on carcinogenicity a nd health effects other than cancer. The process for developing these assessments is si milar to that used by EPA to develop IRIS values and incorporates signifi cant external scientific peer review. As cited in the CalEPA Technical Support Document fo r developing their chronic assessments 4 : “The guidelines for developing chronic inhala tion exposure levels incorporate many recommendations of the U.S. EPA [ 13 ] and NAS [ 14 ].” The non-cancer information
includes available inhalation hea lth risk guidance values expr essed as chronic inhalation reference exposure levels (RELs) [ 15 ]. CalEPA defines the R EL as “the concentration
level at or below which no adverse health e ffects are anticipated in the general human population.” CalEPA's quantitative dose-re sponse information on carcinogenicity by inhalation exposure is expre ssed in terms of the URE [ 16 ], defined similarly to EPA's
URE.

In developing chronic risk estimates, we adju sted dose-response values for some HAPs based on professional judgment, as follows:

1) In the case of HAP categories such as glyc ol 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 valu es were not available. This is done in order to examine, under conservative a ssumptions, 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 cat egory to develop a composite dose-response value for the category.

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

per μ g/m 3 ) was based on better science than the IRIS dose-response value (1.3 x 10 -5 per
μ g/m 3 ), and we switched from using the IRIS valu e to the CIIT value in risk assessments supporting regulatory actions. This determination was ba sed on a substantial body of research on the inhalation dosimetry for formal dehyde in rodents and primates by the CIIT Centers for Health Research (f ormerly the CIIT), with a focus on use of rodent data for

4 Air Toxics Hot Spots Program, Risk Assessment Guidelines, Part III - Technical Support Document
for the Determination of Noncancer Chronic Referen ce 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)refinement of the quantitative can cer 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 va ried, resulting dose-re sponse estimates can vary by several orders of magnitude [ 18, 19, 20, 20 ]. These findings are not supportive of interpreting the CIIT model results as pr oviding a conservative (health-protective) estimate of human risk [ 21 ]. The recent EPA research also examined the contribution of the two-stage modeling for formaldehyde toward s characterizing the relative weights of key events in the mode-of-action of a carcinoge n. For example, in the EPA research, the
model-based inference in the published CIIT study that form aldehyde’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 petition to use the CIIT URE value rather
than its 1992 cancer risk value of 6 X 10 -6 per ug/m 3 . 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, a nd 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 re-assessment 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 deri ved from evidence of the carcinogenic effects of insoluble nickel compounds in crystalline fo rm. Soluble nickel species, and insoluble species in amorphous form, do not appear to pr oduce genotoxic effects by the same toxic
mode of action as insoluble cr ystalline nickel. Nickel speci ation information for some of the largest nickel-emitting sources (incl uding oil combustion, coal combustion, and others) suggests that at leas t 35% of total nickel emissi ons 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 al l insoluble nickel is crystalline. The nickel URE (based on nickel subsulfide, and represen tative of pure insoluble crysta lline 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 assessm ent that were used for the 1999 NATA study [ 25 ]. The NATA approach partitions POM in to 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, (isophoron e and propylene dichloride) that lack
inhalation assessments from the sources evaluated in this document, oral carcinogenic potency estimates were c onverted to inhalation UREs. The conversion from oral risk (p er mg/kg/d oral intake) to inhalation risk (per μ g/m 3

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

m 3 

### /d inhalation rate, as follows:

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

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

EPA understands that conversion of oral dose-response information to inhalation exposure may add significant uncertainty to the resulting risk estimates. However,
the alternative to this would have been to omit these substances from quantitative
inhalation risk estimates a ltogether, 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 abov e to screen these ca rcinogens for their potential contributions to risk. If a substa nce 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 catego ries include emissions of 85 HAP. Of these, 34 are classified as known, probabl e, or possible carcinogens, with quantitative cancer doseresponse values available. These 34 HAP, thei r quantitative inhalation chronic cancer doseresponse values, and the source of each va lue are listed in Table 2.6-1.A. The POM compounds with chronic oral cancer dose-respon se values available (for which multipathway screening assessments were performed) are listed in Table 2.6-1.B.

The emissions inventories for the 7 source ca tegories include emi ssions of 75 HAP with quantitative inhalation chronic noncancer thresh old 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. 

## ( ) ⎟ ⎟ ⎠ ⎞ ⎜ ⎜ ⎝ ⎛

× ⎟ ⎟ ⎠ ⎞ ⎜ ⎜ ⎝ ⎛

× × ⎟ ⎟ ⎠ ⎞ ⎜ ⎜ ⎝ ⎛

⋅ = ⎟ ⎠ ⎞ ⎜ ⎝ ⎛ −

−

g mg
d m kg d kg

mg CPS

m

g URE μ μ
1000 1 20 70 1 3 1 1

3Table 2.6-1.A Dose-Response Values for Ch ronic Inhalation Exposure to Carcinogens

URE (unit risk estimate for cancer) = cancer risk per μ g/m 3 of average lifetime exposure. Sources : IRIS = EPA Integrated Risk Information System, CAL = Ca lifornia 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 Number 5 URE (1/ μ g/m 3 ) 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 7440 020 1.6E-04 EPA OAQPS 8
p-Dichlorobenzene 106467 1.1E-05 CAL Polycyclic organic matter (POM) 246 11 EPA OAQPS 11 - Benzo(a)anthracene 56553 1.0E-04 EPA OAQPS 9

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

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

URE (unit risk estimate for cancer) = cancer risk per μ g/m 3 of average lifetime exposure. Sources : IRIS = EPA Integrated Risk Information System, CAL = Ca lifornia 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 Number 5 URE (1/ μ g/m 3 ) Source - Benzo(a)pyrene 50328 1.0E-03 EPA OAQPS 11
- Benzo(b)fluoranthene 205992 1.0E-04 EPA OAQPS 11
- Benzo(k)fluoranthene 207089 1.0E-04 EPA OAQPS 11
- Chrysene 218019 1.0E-05 EPA OAQPS 11
- Dibenz(a,h)anthracene 53703 1.0E-03 EPA OAQPS 11
- Indeno(1,2,3-cd)pyrene 193395 1.0E-04 EPA OAQPS 11
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 lif etime exposure. Sources : IRIS = EPA Integrated Risk Information System, CAL = Ca lifornia EPA Office of Environmental Health Hazard Assessment, EPA/OAQPS = interim value recommended by the EPA Office of Air Quality Planning and Standards.

Pollutant CAS Number 11 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)fluoranth ene 205992 1 EPA OAQPS - Benzo(k)fluoranth ene 207089 1 EPA OAQPS - Chrysene 2180 19 0.1 EPA OAQPS - Dibenz(a,h)anthrac ene 53703 10 EPA OAQPS

- Indeno(1,2,3-cd)py rene 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/nata19 99/99pdfs/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 PO M emissions (e.g., total PAH).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 i nhalation 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/m 3 ) Source 13
1,1,1-Trichloroethane 71556 5 IRIS 1,2-Epoxybutane 106887 0.02 IRIS -- M 1,2,4-Trichlorobenze ne 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 compounds 14 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 compounds 15 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 cyan ide used as a surrogate.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 i nhalation 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/m 3 ) 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 ethers 18 171 0.02 IRIS -- M - 2-Butoxyethyl acetate 16 112072 0.02 IRIS -- M - Ethylene glycol ethy l ether 110805 0.2 IRIS -- M - Ethylene glycol methyl ether 109864 0.02 IRIS -- M - Diethylene glycol monobutyl ether 18 112345 0.02 IRIS -- M - n-Hexyl carbitol 18 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.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 i nhalation 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/m 3 ) 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-Xylene 17 108383 0.1 IRIS -- M - o-Xylene 19 95476 0.1 IRIS -- M - p-Xylene 19 106423 0.1 IRIS -- M

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

RfD (reference dose) = an estimate (wit h 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 chloride 19 7439976 0.0003 IRIS – H - Methyl mercury 21 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 recommenda tions of OAQPS for HAPs [ 26 ]. Depending on availability, the result s from screening acute assessments are

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.compared to both “no effects” reference levels for the general public, such as the California Reference Exposure Levels (RELs), as well as emergency response levels, such as Acute Exposure Guideline Levels (AEGLs) and Emergency Response Planning Guidelines (ERPGs), with the recognition that the ultimate interpretation of any potential risks associated with an estimated exceedance of a particular refe rence level depends on the definition of that level and any limitations expressed therein. Comparisons among different available inhalation health effect reference values (bot h acute and chronic) for selected HAPs can be
found in a newly released an EPA document (Reference: U.S. EPA. Graphical Arrays of Chemical-Specific Health Effect Reference Valu es 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 acu te dose-response refe rence 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 litera ture. RELs are designed to protect the most sensitive individuals in th e population by the incl usion of margins of safety. Since margins of safety are incorpor ated to address data gaps and uncertainties, exceeding the REL does not automatically indica te an adverse health impact.” Acute RELs are developed for 1-hour (and 8-hou r) 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 Exposur e Guideline Levels (NAC/AEGL) for Hazardous Substances, and then reviewed a nd published by the National Research Council
As described in the Committee’s “Sta nding Operating Procedures (SOP)” ( http://www.epa.gov/op ptintr/aegl/pubs/sop.pdf ), AEGLs “represent threshold exposure limits for the general public and are applicable to emer gency 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 fixe d facilities and from tran sport carriers.” The document states that “the primary purpos e of the AEGL program and the NAC/AEGL Committee is to develop guideli ne 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 antic ipated 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 c onjunction with chemical emergency response, planning, and prevention programs. More spec ifically, 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 emerge ncy response actions, for accidental chemical
releases at fixed facilities a nd from transport carriers.”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 Revi ew (RTR) Risk Assessm ent Methodologies: For

Review by the EPA’s Science Advisory Board wi th Case Studies – MACT I Petroleum Refining
Sources and Portland Cement Ma nufacturing. EPA-452/R-09-006. http://www.epa.gov/ttn/a tw/rrisk/rtrpg.html.

3 . US EPA, 2010. SAB’s Response to EPA’s RTR Risk Assessment Methodologies.

http://yosemite.epa.gov/ sab/sabproduct.nsf/4AB3966E 263D943A8525771F00668381 /$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 Ac tions 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: Adop tion of a Preferred General Purpose (Flat and Complex Terrain) Dispersion Model and Ot her Revisions; Final
Rule. 40 CFR Part 51. http://www.epa.gov/EPA-AIR/2005 /November/Day-09/a21627.htm

6 . US EPA, 2004. Users’ gui de 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. Variab le 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/Proj ects/AirQuality/Pr ojects/H013.2003/H 13FinalReport.pdf

8 . US EPA, 2004. Air Toxics Risk Assessment Re ference 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 Chr onic 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/t tn/atw/nata1999

11 . US EPA, 2008. Integrated Risk Information System. http://www.epa.gov/iris/index.html

.

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