Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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## Draft Residual Risk Assessment for the Mineral Wool Production
and Wool Fiberglass Manufacturing Source Categories

by EPA’s Office of Air Quality Planning and Standards

Office of Air and Radiation February 2013Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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### Table of Contents

1 Introduction

................................ ................................ ................................ .................... 4

2 Methods

................................ ................................ ................................ .......................... 5
2.1 Emissions and source data

................................ ................................ ........................ 5
2.2 Dispersion modeling for inhalation exposure assessment

................................ .......... 6
2.3 Estimating human inhalation exposure

................................ ................................ ..... 9
2.4 Acute Risk Screening and Refined Assessments

................................ ....................... 9
2.5 Multipathway and environmental risk screening

................................ ..................... 11
2.6 Dose

- Response Assessment

................................ ................................ .................... 13
2.6.1 Sources of chronic dose

- response information

................................ ................. 13
2.6.2 Sources of acute dose

- response infor mation

................................ .................... 18
2.7 Risk Characterization

................................ ................................ ............................. 21
2.7.1 General

................................ ................................ ................................ ............ 21
2.7.2 Mi xtures

................................ ................................ ................................ .......... 23
3 Risk Results for the Mineral Wool Production

................................ .......................... 24
3.1 Source Category Description and Results

................................ ............................... 24
3.2 Risk Characterization

................................ ................................ ............................. 26
4 Risk Results for the Wool Fiberglass Manufacturing Source Category

...................... 30
4.1 Source Category Description and Results

................................ ............................... 30
4.2 Risk Characterization

................................ ................................ ............................. 32
4.3 Auxiliary Risk Characterization

................................ ................................ .............. 37
5 General Discussion of Uncertainties and How They Have Been Addressed

................... 39
5.1 Exposure Modeling Uncertainties

................................ ................................ ........... 39
5.2 Uncertainties in the Dose

- Response Relationships

................................ .................. 40
5 References

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

Index of Tables

Table 2.2

- 1 AERMOD version 11103 model options for RTR modeling

............................... 7
Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcino gens

..... 17
Table 2.6

- 1 (b) Dose

- Response Values for Chronic Inhalation Exposure to Noncarcinogens

................................ ................................ ................................ ................................ ............. 18
Table 2.6

- 2 Dose

- Response V alues for Acute Exposure

................................ ....................... 21
Table 3.1

- 1 Summary of Emissions from the Mineral Wool Production Category and Availability of Dose

- Response Values

................................ ................................ .................. 26
Table 3.2

- 1 Summary of Source Category Level Inhalation Risks for Mineral Wool
Production

................................ ................................ ................................ ............................ 29
Table 4.2

- 1 Summary of Source Category Level Inhalation Risks for Wool Fiberg lass Manufacturing

................................ ................................ ................................ ...................... 36
Table 4.2

- 2 Summary of Refined Acute Results for Wool Fiberglass Manufacturing Facilities

................................ ................................ ................................ ................................ ............. 37
Table 4.2

- 3 Summary of Source Category Level Cancer Risks for the Wool Fiberglass Manufacturing Auxiliary Analysis

................................ ................................ ........................ 38Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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Appendices

Appendix 1 Emissions Inventory Support Memorandum

Appendix 1a

- Emissions Data Used in Residual Risk Mo deling for Mineral
Wool Production Appendix 1b

- Emissions Data Used in Residual Risk Modeling for Wool Fiberglass Manufacturing Appendix 2 Technical Support Document for HEM 3 Modeling Appendix 3 Meteorological Data for HEM 3 Modeling Appendix 4 Analysis of data on short

- term emission rates relative to long

- term emission

rates Appendix 5 Technical Support Document for TRIM

- Based Multipathway Screening

Scenario for RTR: Summary of Approach and Evaluation Appendix 6 Detailed Risk Modeling Results Appendix 7 Ac ute Impacts Refined Analysis Appendix 8 Development of the Chronic Screening Level for Carbonyl Sulfide

Index of Acronyms
AERMOD American Meteorological Society/EPA Regulatory Model
AEGL Acute exposure guideline level
ASTDR US Agency for Toxic Substanc es 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 Ac hievable Control Technology

MIR Maximum Individual Risk
MOA Mode of action
NAC National Advisory Committee NAAQS National Ambient Air Quality Standard

NATA National Air Toxics Assessment

NEI National Emissions Inventory

NPRM Notice of Proposed Rulema king

PB

- HAP Persistent and Bioaccumulative

- HAP
POM Polycyclic organic matter

REL Reference exposure level
RfC Reference concentration
RfD Reference dose

RTR Risk and Technology
TOSHI Target

- organ

- specific hazard index

URE Unit risk estimateDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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## 1 Intro duction

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

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

- based standards for categories of sources (e.g., petroleum refineries, pulp and paper mills, etc.) [ 1 ]. EPA has largely completed the initial Maximum Achievable Control Technology ( MACT ) standards as required und er 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,

processe s and control technologies.” In t he 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 safe ty 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) Asses sment 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 assessment s and we will be continuing our efforts to improve our assessments by incorporating updates based on the SAB recommendations as they are developed and become available . Our responses to the key
recommendations of the SAB are outlined in the memo entitled, “EPA’s Actions in Response to Key Recommendations from the SAB Review of RTR risk Assessment Methodologies” [ 4 ].

This document contains the methods and the results of baseline risk assessments (i.e., after the implementation of the respective MACT standards) performed for the Wool Fiberglass
Manufacturi ng and Mineral Wool Production source categories. The methods discussion includes descriptions of the methods used to develop refined estimates of chronic inhalation exposures and human health risks for cancer and noncancer endpoints, as well as descripti ons of the methods used to screen for acute health risks, chronic non

- inhalation health risks, and
adverse e nvironmental effects.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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## 2 Methods

2.1 Emissions and source data

Mineral Wool The 2002 National Emissions Inventory (NEI) data served as the starting poi nt for the mineral wool assessment. Using the process MACT code, 1 a subset of the NEI was developed that contained facility, process, and emissions data for each facility in the Mineral Wool Production source category. Those data were based on an emissio n factor developed from one source test; emissions were estimated for all facilities based on their production data reported in NEI, and were supplemented with other emissions estimates in NEI. In the 2008 proposal EPA requested comment and new data that could inform that proposal. After proposal, EPA learned that the one plant for which we had test data had closed, some facilities were missing from the NEI and others, listed in NEI, had since closed. As a result, EPA
decided to collect 2010 industry pro cess and source test data under an information collection request that would inform the risk review, the technology review (under 112(d)(6)), start up and shutdown issues that emerged after the General Provisions vacature 2 , and a petition 3

raised to the co urt following the vacature of the Brick MACT 4 . These data underwent an extensive QA/QC procedure, and revisions were made to the dataset as necessary. The
Mineral Wool ICR emissions data and modifications made to the NEI data are discussed in the Appendi x 1 a , entitled “ Emissions Data Used in Residual Risk Modeling for Mineral Wool
Production

. ”

Wool Fiberglass A voluntary ICR was sent out in March 2010 to the 29 wool fiberglass facilities currently operating in the US. ICR responses from all the facili ties were compiled in the project database and included information on each facility, process, process equipment, control equipment, costs, and HAP emissions. Facility

- specific production rate information was also
included and was claimed as confidential business information (CBI), which resulted in much of the project database being treated as CBI.

Emissions test data provided by the wool fiberglass industry varied widely by facility. Companies were allowed to, in lieu of new testing, submit existing an d well documented test data that was representative of current operations and used the recommended test methods. A number of facilities submitted existing test reports on one or more of the following emission sources: glass melting furnaces, curing ovens, forming, and collection operations. In order to fill data gaps in existing data, new test data was also required. Companies were, however, allowed to test a subset of facility operations, if the facilities were able to demonstrate that the
tested subset w as representative of the untested subset. Test results were typically presented

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

2 SierraClub v. EPA , 551 F. 3d 1019 (D.C. Cir. 2008), cert. denied, 130 S. Ct. 1735 (2010).

3 SierraClub v. Stephen L. Johnson, Petition for Rulemaking

, January 14, 2009

4 SierraClub v. EPA

, 479 F. 3d 875 (D.C. Cir. March 13, 2007)Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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as three test runs and provided in units of mass of pollutant per mass of production (e.g., lbs of HAP/ton of glass pulled). A combination of new and existing test data was u sed to populate the wool fiberglass residual risk modeling file. Using the glass pull rates (generally given in tons of glass pulled/day) that each facility provided in its ICR response and the source emission rates (lb/ton) from emission testing, annual emissions (tpy) were calculated for each pollutant and emission source. For each source, stack heights, diameters and coordinates were compiled from ICR responses and then sent to each facility for
confirmation.

The Wool Fiberglass ICR emissions data an d modifications made to the NEI data are discussed in the Appendix 1b, entitled “ Emissions Data Used in Residual Risk Modeling for Wool Fiberglass Manufacturing. ”



### 2.2 Dispersion modeling for inhalation exposure assessment

Both long

- and short

- term inhalation exposure concentrations and associated health risk from each facility in the source category of interest were estimated using the Human Exposure Model in combination with the American Meteorological Society/EPA Regulatory Model (AERMOD) dispersion modelin g system (HEM 3 ). The approach used in applying this modeling system is outlined below, and further details are provided in Appendix 2

. The

HEM 3 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.

The dispersion model in the HEM 3 syste m, AERMOD version 11103 , is a state

- of

- the

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

- by

- hour dispersion from the emission sources into the surrounding atmosphere. Hourly emission rates used for
this simulation are 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 3 modeling system is to predict ambient
concentrations at locations of interest. The AERMOD mode l options employed are
summarized in Table 2.2

- 1 and are discussed further below.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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Table 2.2

- 1 AERMOD version 11103 mo del options for RTR modeling

Modeling Option Selected Parameter for chronic exposure

T ype of calculations Hourly Ambient Concentration

Source type Point

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

Terrain characterization Actual from USGS 1 /3 Arc Second NED data

Building downwash Not Included

Plume deposition/depletion Not Included

Urban source option No

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

In HEM 3 , meteorological data are ordinarily selected from a list of over 200 National Weather Service (NWS) surf ace 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 d ata most site specific dispersion modeling efforts will employ up to five years of data to capture variability in weather patterns from year to year. However, because
we had an insufficient number of appropriately formatted model input files derived from available meteorological data, we modeled only a single year, typically 1991. While the selection of a single year may result in under

- prediction of long

- term ambient levels at some locations, likewise it may result in over

- prediction 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 52 miles ( 84 km). Appendix 3 (Meteorological Data Processing Using AERMET for HEM 3 ) 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 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 3 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 facilit y). Chronic ambient concentrations were calculated as the annual average of all estimated short

- term (one

- hour) concentrations at each block centroid. Possible future residential use of currently uninhabited areas was notDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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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 occupi ed 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 m eters 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 emissions data contains only annual emission totals, we generally apply the assumption to all source categories that the maximum one

- hour emission rate from any source
is ten times the average annual hourly emission rate for that source.

Th e average hourly emissions rate is defined as the total emissions for a year divided by the total number of operating hours in the year. The choice of a factor of ten for acute screening was originally based on engineering judgment

. To develop a more rob ust peak

- to

- mean emissions factor, and in response to one of the key messages from the SAB consultation on our RTR Assessment Plan, we performed an analysis using a short

- term emissions data set from a number of source s located in Texas (originally reported on by Allen et al

. 2004)[ 7 ]. In that report, the Texas Environmental Research Consortium Project compared hourly and
annual emissions data for volatile organic compound s for all facilities in a heavily

industrialized 4

- county area (Harris, Galveston, Cha mbers, 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 99 th percentile ratio of peak hourly emission rate to the annual hourly emission rate was 9 . Based on these results, we typically chose a factor of ten for the initial screening . These factors are
intended to cover all possible hourly peaks associated with routinely

- variable emissions.
Wh ile there have been 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 emission s from typical
industrial sources.

Census block elevations for HEM 3 modeling were determined nationally from the US Geological Service 1 /3 Arc Second National Elevation Dataset , which have a spatial
resolution of about 1 0 meters. Elevations of polar grid points used in estimating short

- and long

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

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In addition to using receptor elevation to deter mine 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 expos ure

We used the estimated annual average ambient air concentration of each HAP at each census block centroid as a surrogate for the lifetime inhalation exposure concentration of all the people who reside in the census block. That is, the risk analysis did not consider either the
short

- term or long

- term behavior (mobility) of the exposed populations and its potential influence on their exposure.

We did not address short

- term human activity for two reasons. First, our experience with the
NATA assessment s (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 HAP; it will also reduce risk estimates for gaseous HAP, 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

re sidences. Further reducing exposure estimates for the most highly exposed residents by modeling their short

- term behavior could add a systematic low bias to these results.

We did not address long

- term migration nor population growth or decrease over 70 y ears, 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 individu al risk (MIR), which is defined as the risk associated with a lifetime of exposure at the highest concentration; the population risk distribution; and the cancer incidence. The 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, shi fting it toward higher estimated individual risks at the upper end and reducing the number of people estimated to be at lower risks, thereby increasing the estimated number of people at specific risk levels

.

When screening for potentially significant ac ute exposures, we used an estimate of the highest hourly ambient concentration at any off

- site location as the surrogate for the maximum potential acute exposure concentration for any individual.



### 2.4 Acute Risk Screening and Refined Assessments
In establishing a scientifically defensible approach for the assessment of potential health risks due to acute exposures to HAP, we f ollowed the same general approach that has been used for developing chronic health risk assessments under the residual risk program. That is, we developed a tiered, iterative approach. This approach to risk assessment was endorsed by the National Academy of Sciences in its 1993 publication “Science and Judgment in Risk Assessment” and subsequently was adopted in the EPA’s “Residual Risk Re port to Congress”
in 1999.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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The assessment methodology is designed to eliminate from further consideration those
facilities for which we have confidence that no acute adverse health effects of concern will occur. To do so, we use what is called a tiered , iterative approach to the asse ssment. This
means that we begin with a screening assessment, which relies on readily available data and uses conservative assumptions that in combination approximate a worst

- case exposure . The result of this screening pro cess is that either the facility being assessed poses no potential acute health risks (i.e., it “screens out”), or that it requires further , more refined assessment.
A more refined acute assessment could u s e 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 are used to refine the assessment; in others, lesser amount s of site

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

necessary.

Acute health risk screening was performed as the first step. We used conservative assumptions for emission rates, meteo rology, 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 emiss ions 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 whet her 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 worst

- case 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

HAP being assessed to determine if a possible acute health risk might exist. These benchmarks are described in section 2.6 of this report.

As mentioned above, when we identify acute impacts which exceed their relevant
benc hmarks, we pursue refining our acute screening estimates. For the Mineral Wool
Production source category we use d a refined emissions multiplier of 3 to estimate the peak hourly emission rates from the average rates . Refer to a separate memorandum in the docket
for a detailed description of how the refined emissions multiplier was developed for the

M ineral W ool Production source category

. For the Wool Fiberglass Manufacturing source category data were not available to develop a refined emissions multipli er, therefore, the default emissions multiplier of 10 was used.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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### 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) was screened b y 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 A ssessment 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)

, toxaphene, and trifluralin

. Emissions of lead, cadmium, and mercury were identified in the
emissions inventor ies for both the Mineral Wool Production and Wool Fiberglass Manufacturing source categor ies

.

These PB

- HAP emission s were evaluated for potential non

- inhalation risks and adverse environmental impacts using our screening scenario which was developed for use with the

TRIM.FaTE 5 model. This screening scenario uses environmental media outputs from the

peer

- reviewed TRIM. FaTE to estimate the maximum potential ingestion risks for any specified emission scenario by using a generic farming/fishing exposure scenario that simulates a subsistence environment. The screening scenario retains many of the ingestion and scenario inp uts developed for EPA’s Human Health Risk Assessment Protocols (HHRAP) for hazardous waste combustion facilities. 6 In the development of the screening scenario a sensitivity analysis was conducted to ensure that its key design parameters were
established such that environmental media concentrations were not underestimated, and to also minimize the occurrence of false positives for human health endpoints. See Appendix 5 for a complete discussion of the development and testing of the screening scenario, as well as for the values of facility

- level emission rates developed for screening potentially significant
multi

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

- pathway screening, we derived emission levels for each PB HAP at whic h the maximum human health risk would be 1 in a million for lifetime cancer risk or a hazard quotient of 1.0 for noncancer impacts.

In evaluating the potential multi

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

- pathway risks.

None of the facilities in the Mineral Wool Production or the Wool Fiberglass Manufacturing source categories reported emissions of PB HAP that were greater than the emission
thresholds

. Therefore, multi

- pathway exposures and environmental risks were deemed

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

6 EPA’s Human Health Risk Assessment Protocol (HHRAP) for Hazardous Waste Combustion Facilities; http://www.epa.gov/epaoswer/hazwaste/combust/riskvol.htm#volume1Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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negli gible and no further analysis was performed.

In section 3 we present our inhalation exposure results separate from the multipathway screening assessment results. We have been questioned as to why we do not add these two risk results together. We do n ot believe it is appropriate to add a multipathway screening result to a refined quantitative inhalation risk result. The purpose of the multipathway screen is not to provide a quantitative value. This multipathway screening approach is designed to point out facilities and pollutants that we are confident do not have a multipathway effect and for those that do not screen out, more effort can be focused on them. The multipathway screening scenario is a hypothetical scenario that does not have a real

- world counterpart. The real world result would be less than the screening result value, but we cannot say how much less it would be. In addition, the inhalation assessment is quite refined and the multipathway screen is a less rigorous assessment. It might b e mathematically logical to add these values together, but it is not scientifically appropriate. It is also highly unlikely that the receptor exposed to the maximum inhalation risk is also the receptor exposed to the maximum multipathway risk. Therefore, we do not believe that it is appropriate to sum the inhalation risk assessment results and the multipathway screening result. However, in certain cases where we perform a refined multipathway assessment on facilities that have failed the Tier 1
and Tier 2 multipathway screen it may be appropriate to combine this refined multipathway result with the inhalation result. Compatibility is a major factor in deciding the appropriateness of combining the two risk results. For instance if the refined multipathwa y risk results and the inhalation results are associated with the same target organ (e.g. liver cancer) then it may be appropriate to add the results together. It should be noted that any decision to add these results will bring additional new uncertainti es into the assessment.

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 do se

- 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 up to 3000. As a result, these human threshold values are often signif

icantly 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 th e maximum inhalation hazard in an ecosystem is below the level of concern for humans, we have generally concluded that mammalian receptors should be at no risk of adverse effects due to inhalation exposures from non PB

- HAP, and have assurance that other ec ological 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 HA Ps, 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.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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### 2.6 Dose

- Response Assessment

2.6.1 Sources of chronic dose

- response information

Dose

- response assessment (carcinogenic and non

- carcinogenic) for chronic exposure (either by inhalation or ingestion) for the HAPs reported in the emissions inventories for Wool Fiberglass Manufacturing and for Mineral Wool Production sources were based on the EPA
Off ice of Air Quality Planning and Standards’ existing recommendations for HAPs [ 9 ], also used for NATA [ 10 ]. This information has been obtained from various sources and prioritized according to (1) conceptual consistency with EPA risk assessment guidelines a nd (2) level of peer review received. The prioritization process was aimed at incorporating into our assessments the best available science with respect to dose

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

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

- response assessments for chronic exposure for many of the pollutants in this study. These assessments typically provide a qualitative statement regarding the strength of scientific data and specify a reference concentration (RfC, for inhalation) or reference dose (RfD, for ingestion) to protect against effects other than cancer and/or a unit risk estimate (URE, for inhalation) or slope factor (SF, for ingestion) to estimate the prob ability 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 apprecia ble risk of deleterious effects during a lifetime. ” The RfD is “a n estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without an apprecia ble 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/m 3 in air. ” The
SF is “a n upper bound, approximati ng 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 underg one 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 no t 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

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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 sim ilar 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 evaluati on. 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 o f 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 develo p IRIS values and incorporates significant external scientific peer review. As cited in the CalEPA Technical Support Document for developing their chronic assessments 7 : “The guidelines for developing chronic inhalation exposure levels incorporate many

rec ommendations 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 a t or below which no health effects are anticipated in the general human population.” CalEPA's quantitative dose

- response information on carcinogenicity by inhalation exposure is expressed in terms of the URE [ 16 ], defined similarly to EPA's URE.

In dev eloping 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 chemica l category i s used as a surrogate for other compounds in the group f or which dose

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

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

out from further assessment.

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

- specific chemical speciation profiles appropriate

to the source category to develop a composite dose

- response value for the category.

7 Air Toxics Hot Spots Program, Risk Assess ment Guidelines, Part III

- Technical Support Document
for the Determination of Non

- cancer Chronic Reference Exposure Levels. Air Toxicology and Epidemiology Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Ag ency. February 2000 ( http://www.oehha.ca.gov/air/chronic_rels/pdf/relsP32k.pdf )Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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

- response value for formaldehyde (5.5 x 10 - 9 per μg/m 3 ) was based on bette r science than the IRIS cancer dose

- response value (1.3 x 10 - 5 per μg/m 3 ), and we switched from using the IRIS value to the CIIT value in risk assessments supporting regulatory
actions. S ubsequent research published by EPA suggested that the CIIT model wa s not appropriate and in 2010 EPA returned to using 1991 IRIS value

. EPA has been working on revising the formaldehyde IRIS assessment and the National Academy of Sciences (NAS) completed its review of the EPA’s draft assessment in April of 2011

. 8 EPA wil l follow the NAS Report recommendations and will present results obtained by implementing the biologically

- based dose

- response (BBDR) model for formaldehyde. EPA will compare these estimates with those currently presented in the External Review
draft of t he assessment and will discuss their strengths and weaknesses. As recommended by the NAS committee, appropriate sensitivity and uncertainty analyses will be an integral component of implementing the BBDR model. The draft IRIS assessment will be revised
i n response to the NAS peer review and public comments and the final assessment will be posted on the IRIS database. In the interim, we will present findings using the 1991 IRIS value as a primary estimate, and EPA may also consider other information as th e science
evolves.

4) In the case of nickel compounds, to provide a health

- protective estimate of potential cancer risks, we used the IRIS URE value for nickel subsulfide in this assessment. Based on past scientific and technical considerations, the determi nation of the percent of nickel subsulfide was considered a major factor for estimating the extent and magnitude of the
risks of cancer due to nickel

- containing emissions. Nickel speciation information for some of the largest nickel

- emitting sources (incl uding oil combustion, coal combustion, and others) suggested that at least 35 percent of total nickel emissions may be soluble compounds and that the URE for the mixture of inhaled nickel compounds (based on nickel subsulfide, and representative of pure in soluble crystalline nickel) could be derived to reflect the assumption that 65 percent of the total mass of nickel may be carcinogenic. Based on consistent views of major scientific bodies (i.e., National Toxicology Program (NTP) in their 12 th Report of t he Carcinogens (ROC) 9 , International Agency for Research on Cancer (IARC) 10 , and other international agencies) 11 that consider all nickel compounds to be carcinogenic, we currently consider all nickel compounds to have the potential of being as carcinogenic to humans. The 12 th Report of the Carcinogens states that the “combined results of epidemiological studies, mechanistic studies, and carcinogenic studies in rodents support the concept that nickel compounds generate nickel ions in target cells at sites cr itical for carcinogenesis, thus allowing consideration and

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

9 National Toxicology Program (NTP), 2011. Report on carcinog ens. 12 th ed. Research Triangle Park, NC: US Department of Health and Human Services (DHHS), Public Health Service. Available online at http://ntp.niehs.nih.gov/ntp/roc/twelfth/roc12.pdf

10 International Agency for Research on Cancer (IARC), 1990. IARC monographs on the evaluation of carcinogenic risks to humans. Chromium, nickel, and welding. Vol. 49. Lyons, France: International Agency for Research on Cancer, World Health Organizati on Vol. 49:256.

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

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evaluation of these compounds as a single group.” Although the precise nickel compound (or compounds) responsible for the carcinogenic effects in humans is not always clear,
studies indicate that nickel sulfate and the combinations of nickel sulfides and oxides encountered in the nickel refining industries cause cancer in humans (these studies are summarized in a review by Grimsrud et al., 2010 12 ). The major scientific bodies
mentioned above have a lso recognized that there are differences in toxicity and/or carcinogenic potential across the different nickel compounds. In this inhalation risk assessment, to take a conservative approach, we have considered all nickel compounds to be as carcinogenic a s nickel subsulfide and have applied the IRIS URE for nickel subsulfide without a factor to reflect the assumption that 100 percent of the total mass of nickel may be as carcinogenic as pure nickel subsulfide. In addition, given that there are
two additio nal URE 13 values derived for exposure to mixtures of nickel compounds, as a group, that are 2

- 3 fold lower than the IRIS URE for nickel subsulfide, the EPA also considers it reasonable to use a value that is 50 percent of the IRIS URE for nickel
subsulfide for providing an estimate of the lower end of the plausible range of cancer potency values for different mixtures of nickel compounds.

5) A substantial propo rtion of POM reported to EPA’s N ati onal E mission I nventory (NEI) is not speciated into individua l co mpounds. As a result, it i s necessary to apply the same simplifying assumptions to assessment s that are used in NATA. [ 17 ] The NATA approach partitions POM into eight different non

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

5) A chronic screening level of 163 ug/m 3 was developed for carbonyl sulfide (COS) from a No Observed Adverse Effects Level (NOAEL) of 200 ppm based on brain lesi ons and neurophysiological alterations in r odents. A more detailed discussion of the studies used to develop the COS chronic screening level is provided in Appendix 8. The screening level includes a total uncertainty factor (UF) of 3,000: 10x for extrapo lation for interspecies differences, 10x for consideration of intraspecies variability, 10x for extrapolation from subchronic to chronic duration, and 3x for database insufficiencies. See section 5 of this document for a detailed discussion of exposure mo deling
uncertainties.

The chronic screening level for COS is used only as a screening level assessment to identify areas with significant inhalation risk potential. A high COS chronic risk based on the screening level does not necessarily indicate that further action is required.

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

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

- 7. Available online at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2868037/?tool=pubmed

13 Two UREs (other than the current IRIS values) have been d erived for nickel compounds as a group: one developed by the California Department of Health Services ( http://www.arb.ca.gov/toxics/id/summary/nickel_tech_b.pdf ) and the other by the Texas Commission on Environmental Quality ( http://www.epa.gov/ttn/atw/nata1999/99pdfs/healtheffectsinfo.pdf ).Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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The emissions inventory for the Wool Fiberglass Manufacturing and for the Mineral Wool
Production source categor ies includes emissions of 14 HAP with available chronic quantitative inhalation dose

- response values. These HAP , their dose

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

- 1 (a) and ( b ).

Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcinogens

URE (unit risk estimate for cancer) 14 = cancer risk per μg/m 3 of a verage lifetime exposure. Sources: IRIS = EPA Integrated Risk Information System, CAL = California
EPA Office of Environmental Health Hazard Assessment.

Pollutant CAS Number 15 URE 5 (1/μg/m3) Source

Arsenic compounds 7440382 4.3E

- 03 IRIS Beryllium compo unds 7440417 2.4E

- 03 IRIS Cadmium compounds 7440439 1.8E

- 03 IRIS Chromium (VI) compounds 18540299 1.2E

- 02 IRIS Formaldehyde a 50000 1.3E

- 05 IRIS

a

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

14 The URE is the upper

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

15 Chemical Abstract Services 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.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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Table 2.6

- 1 (b) Dose

- Response Values for Chronic Inhalation Exposure to Noncarcinogens

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation exposure to t he human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL =
California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry, EPA OAQPS = EPA Office of Air Quality Planning
and Standards.

Pollutant CAS Number 6 RfC (mg/m3) Source 16

Arsenic compounds 7440382 1.5E

- 05 CAL Beryllium compounds 7440417 2.0E

- 05 IRIS

- M Cadmium compounds 7440439 1.0E

- 05 ATSDR

- D Carbonyl sulfide 463581 0.163 ORD Screening Chromium (VI) compounds 18540299 1.0E

- 04 IRIS

- M Formaldehyde 50000 0.0098 ATSDR Hydrochloric acid 7647010 0.02 IRIS

- L Lead compounds 7439921 1.5E

- 04 EPA OA QPS Manganese 7439965 5.0E

- 05 IRIS

- M

Methanol 67561 4 CAL Mercury (elemental) 7439976 3.0E

- 4 IRIS

- M Nickel compounds 7440020 0.00048 EPA OAQPS 17

Phenol 10952 0.2 CAL Selenium compounds 7782492 0.02 CAL

2.6.2 Sources of acute dose

- response information

Hazard identification and dose

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

. Depending on availability, the results from screening acute assessments are compared to both “no effects” reference levels for the general public, such as the California Reference Exposure Levels (RELs), as well as emergency response levels, such as Acute Exposure Guideline Levels (AEGLs) and Emergency Response Planning Guidel ines (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 a mong different available

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

ov erall level of confidence in the RfC value, as reported in IRIS.

17 The EPA IRIS assessments for nickel compounds provide a range of plausible UREs. This assessment used the highest value in that range which is equal to the URE for nickel subsulfide, 4.8E

- 04 per ug/m 3 . The low end of the range is equal to 50% of the URE for nickel subsulfide, 2.4E

- 04 per ug/m 3

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inhalation health effect reference values (both acute and chronic) for selected HAPs can be
found in a n EPA document [ 19 ].

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

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

The acute REL ( http://www.oehha.ca.gov/air/pdf /acuterel.pdf

) is defined by CalEPA as

“ t he concentration level at or below which no adverse health effects are anticipated for a specified exposure duration [ 20 ]

. RELs are based on the most sensitive, relevant, adverse
health effect reported in the medic al 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 exp osures (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) f or Hazardous
Substances , and then revi ewed and published by the National Research Council A s described
in the Committee’s “Standing Operating Procedures (SOP) ” ( http://www.epa.gov/opptintr/aegl/pubs/sop.pdf ), AEGLs “represent thresho ld 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 we ll 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 regula tory and nonregulatory purposes by U.S. Federal and State agencies, and possibly the international community in conjunction with chemical emergency response, planning, and prevention programs. More specifically, the AEGL values will be used for conducting various risk assessments to aid in the development of emergency preparedness and prevention plans, as well as real

- time emergency response actions, for accidental chemical releases at fixed facilities and from transport carriers.”

The NAC/AEGL defines AEGL

- 1 and AEGL

- 2 as:

“ AEGL

- 1 is the airborne concentration (expressed as ppm or mg/m 3 ) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic nonsensory effects. However, the effects are not disabling and are transient and reversible upon cessation of

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“ AEGL

- 2 is the airborne concentration (expressed as ppm or mg/m 3 ) of a substance above which it is predicted that the ge neral population, including susceptible individuals, could experience 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 m ild 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, an d those with other illnesses, it is recognized that individuals, subject to unique or idiosyncratic responses, could experience the effects described at concentration s below the corresponding AEGL.”

Emergency Response Planning Guidelines (ERPGs). The Ame rican Industrial Hygiene Association (AIHA) has developed Emergency Response Planning Guidelines (ERPGs) [ 21 ] for acute exposures at three different levels of severity. These guidelines represent concentrations for exposure of the general population (but n ot particularly sensitive persons) for up to 1 hour associated with effects expected to be mild or transient (ERPG

- 1), irreversible or serious (ERPG

- 2), and potentially life

- threatening (ERPG

- 3).

ERPG values ( http://www.aiha.org/insideaiha/GuidelineDevelopment/ERPG/Pages/default.aspx ) are described in their supporting documentation as follows: “ERPGs are air concentration guidelines for single exposures to agents a nd are intended for use as tools to assess the adequacy of accident prevention and emergency response plans, including transportation emergency planning, community emergency response plans and incident prevention and mitigation.”

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 percei ving a clearly defined, objectionable
odor. ”

“ ERPG

- 2 is the maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing or developing
irreversible or other serious health ef fects or symptoms which could impair an individual's ability to take protective action. ”

The emissions inventory for the Wool Fiberglass Manufacturing and for the Mineral Wool
Production source categories includes emissions of 9 HAP with relevant and avai lableDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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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

- 2.

Table 2.6

- 2 Dose

- Response Values for Acute Exposure

Pollutant CAS
Number AEGL

- 1

(1

- hr) (mg/m 3 ) AEGL

- 2

(1

- hr) (mg/m 3 ) ERPG

1 (mg/m 3 ) ERPG

2 (mg/m 3 ) REL Arsenic compounds 7440382 0.0002 Beryllium com

p ounds 7440417 0.025 Carbonyl sulfide 463581 140 Formaldehyde 50000 1.1 17 1.1 17 0.055 Hydrochloric acid 7647010 2.7 33 2.7 33 2.1 Mercury (elemental) 7439976 1.7 2 0.0006

Methanol 67561 690 2700 690 2700 28
Nickel 7440020 0.006

Phenol 108952 58 89 58 89 5.8



### 2.7 Risk Characterization

2.7.1 General

The final product of the risk assessment is the risk characterization, in which the in formation 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, t he 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 Charact erization [ 22 ] specifies that a risk characterization “be prepared in a manner that is clear, transparent, reasonable, and consistent with other risk characterizations of similar scope prepared across programs in the Agency.” These principles of transparen cy and consistency have been reinforced by the Agency’s Risk Characterization
Handbook [ 23 ], in 2002 by the Agency’s information quality guidelines [ 24 ], and in the OMB/OSTP September 2007 Memorandum on Updated Principles for Risk Analysis 18 , and are incorpor ated 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

18 Memorandum f

or t he Heads o f Executive Departments a nd Agencies

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

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the limitations of available time and resources. We provide summaries of risk metrics (including maximum individual cancer risks and noncancer hazards, as well as cancer incidence estimates) along wit h 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 the assessment that has a potency estimate availabl e, individu al and population cancer risks we re calculated by multiplying the corresponding lifetime average exposure estimate by the appropriate URE. This calculated cancer risk is defined as the upper

- bound probability of developing cancer over a 70

- y r p eriod (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 muta genic mode

- of

- action [ 25 ], we applied
EPA’s Supplemental Guidance for Assessing Susceptibility from Early

- Life Exposure to Carcinogens [ 26 ]

. This guidance has the effect of adjusting the URE by factors of 10 (for children aged 0

- 1), 3 (for children aged 2

- 1 5), 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 on evidence that carcinogenic POM have the same mutagenic mechanism
of action as does benzo[a]pyrene. For this reason

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

Increased cancer incidence for the entire receptor population within the area of analysis wa s estimated by multiplying the estimated lifetime cancer risk for each census block by the number of people residing in that block, then su mming the results for the entire modeled
domain. This lifetime population incidence estimate wa s divided by 70 years to obtain an estimate of the number of cancer cases per year.

In the case of benzene, the high end of the reported cancer URE range was u sed in our assessments to provide a conservative estimate of potential cancer risks. Use of the high end of the range provides risk estimates that are approximately 3.5 times higher than use of the equally plausible low end value. If the estimated benzen e

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

Unlike linear dose

- response assessments for cancer, 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,

expos ures at or below the reference level (HQ≤1) are not likely to cause adverse healthDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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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

r isk 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 ch ronic effects other than cancer is expressed in terms of the HQ for inhalation, calculated for each HAP at each census block centroid. As discussed above, RfCs incorporate generally conservative uncertainty factors in the face of uncertain extrapolations, such that an HQ greater than one does not necessarily suggest the onset of adverse effects. The HQ cannot be translated to a probability that adverse effects will occur, and is unlikely to be proportional to adverse health effect outcomes in a population

.

Screening for potentially significant acute inhalation exposures also followed the HQ approach. We divided the maximum estimated acute exposure by each available short

- term threshold value to develop an array of HQ values relative to the various acute endpoints and thresholds. In general, when none of these HQ values are greater than one, there is no potential for acute risk. In those cases where HQ values above one are seen, additional information is used to determine if there is a potential for sign ificant 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 cate gory combined.

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

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

In a ssessing 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, th e 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) t hat 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. A ll TOSHI calculations pre sented 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 onl y 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 theDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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potential for adverse health outcomes associated with pollutant exposure, and needs t o 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
ba sis, not using the TOSHI approach.



### 3 Risk Results for the Mineral Wool Production

3.1 Source Category Description and Results

Mineral wool is a fibrous, glassy substance made from natural rock (such as basalt), blast furnace slag, or other similar materials an d consisting of silicate fibers typically 4 to 7 micrometers in diameter. In the mineral wool manufacturing process, rock and/or blast furnace slag and other raw materials (e.g., gravel) are melted in a furnace (cupola) using coke
as fuel. The molten mat erial is then formed into fiber. Mineral wool is manufactured as either a “bonded” product that incorporates a binder to increase structural rigidity or a less rigid “nonbonded” product. The production of bonded mineral wool involves the application
of a HAP

- based binder to the fiber, where the binder is typically composed of a phenol

formaldehyde resin, water, urea, silane, ammonia, and ammonium sulfate. The application of binder is followed by thermosetting in a curing oven and cooling of the finished product. Sources that manufacture only nonbonded fibers would not include the processes of binder application and curing. Emission sources at mineral wool production facilities include the cupola furnace where the mineral charge is melted; a blow chamb er, in which air or a binder is drawn over the fibers, forming them into a screen; a curing oven that bonds th e fibers (for bonded products); and a cooling oven.

In 1997 when the mineral wool MACT rule was proposed, EPA estimated that there were 16 majo r source mineral wool production facilities in the United States that would be subject to
the rule. Currently, there are seven mineral wool production facilities nationwide

. Based on emissions data collected from the industry, t hese 7 facilities emitted a reported total of 3 6 3 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 Mineral Wool Production source category.
Based on the se data , the HAP emitted in largest quantities in total from these facilities are carbonyl sulfide, formaldehyde, phenol, hydrochloric acid, methanol, and hydrogen fluoride ; emissions of these 6 pollutants account for 99

. 7 percent of the total HAP emissions by ma ss from the data set. Carbonyl sulfide , hydrochloric acid, and hydrogen fluoride were reported
as an emission for all o f the facilities. Formaldehyde and phenol are also emitted in large quantities, but from fewer facilities; no more than three facilitie s report emissions of any one
of these HAP. Formaldehyde and p henol are emitted only from bonded mineral wool fiber manufacturing, which includes emissions from the application of t he binder, curing, and cooling. Raw material feed rates in mineral wool p rocesses are essentially constant with minimal fluctuation (approximately ± 10 percent). Consequently, emissions also haveDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 25

minimal fluctuation [ 30 ]. In refining the acute risk assessment, a short

- term emissions multiplier of 3 was used to estimate the max imum hazard from acute exposures

. See separate
memo on the Mineral Wool Acute Factor in the project docket for a detailed description of how the refined emissions multiplier was developed for the Mineral Wool Production source
category. Emissions of PB H AP reported in the data set for the mineral wool production source category include lead, cadmium, and mercury compounds.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 26

Table 3.1

- 1 Summary of Emissions from the Minera l Wool Production Category and Availability of
Dose

- Response Values

HAP Emi ssions (tpy) Number

of
Facilities Reporting
HAP (7
facilities
in data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS a

PB

HAP? Unit Risk
Estimate for
Cancer? Reference

Concentration
for Noncancer? Health

Benchmark
Values for Acute
Noncancer?

Carbonyl Sulfide 224 7 Y
Formaldehyde 45 3 Y Y Y

Phenol 35 3 Y Y
Hydrochloric acid 23 7 Y Y

Methanol 18 3 Y Y
Hydrogen Fluoride 17 7

Selenium 0.28 7 Y
Manganese 0.14 7 Y

Chromium III 0.04 7

Lead 0.03 7 Y Y

A rsenic 0.03 7 Y Y Y

Nickel 0.024 7 Y Y
Antimony 0.002 7

Cadmium 0.002 7 Y Y Y

Cobalt 0.0013 7 Y Elemental Gaseous Mercury 0.0005 6 Y Y Y
Chromium (VI) 0.0003 7 Y Y Berylium 0.0002 7 Y Y Y
Gaseous Divalent Mercury 0.0001 6 Y

Parti culate Divalent Mercury 0.0001 6 Y

a Tables 2.6

- 1 (a) and (b) of this report contain the URE and RfC values for the HAP emitted from mineral wool production
facilities. Table 2.6

- 2 of this report contains the acute noncancer values for the HAP emitte d from mineral wool production
facil ities. 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/a tw/toxsource/summary.html

.



### 3.2 Risk Characterization

This section presents the results of the risk assessment for the Mineral Wool Production

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

- inhalat ion risks from PB HAP. Also presented are the HAP “drivers,” which are the HAP that collectively contribute 90 percent of the maximum cancer risk or maximum hazard index at the highest exposure location

.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 27

Table s 3 .2

- 1 and 3.2

- 2 summarize the chronic and a cute inhalation risk results for this source
category. The results for the Mineral Wool Production source category indicate that maximum lifetime individual cancer risks could be as high as 10 in a million. The major
contributor to th is risk is formaldeh yde

. A pproximately 1 0

, 30 0 people were estimated to have
cancer risks above 1 in a million as a result of the emissions from 1 facilit y . The maximum
chronic non

- cancer TOSHI value for the source category could be up to 0. 1 with emissions of formaldehyde d ominating t hose impacts, indicating no sig nificant potential for chronic noncancer impacts.

Worst

- case screening a cute hazard quotients (HQs) were calculated for every HAP shown in
Table 3.1

- 1 that has an acute benchmark, and the high est acute HQ (REL o f 20 for formaldehyde ) is shown in Table 3 .2

- 1

. A refined emissions multiplier of 3 was used to estimate the peak hourly emission rates from the average rates . Refer to a separate memorandum in the docket for a detailed description of how the refined emi ssions multiplier was developed for the M ineral W ool Production source category. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries. In this case, the refined analysis did not change the acute analysis results. Table 3

. 2

- 2 provides more information on the acute risk
estimates for formaldehyde, the only HAP that had a worst

- case screening acute HQ greater than 1 for any benchmark.

To better characterize the potential health risks associated with estimated worst

- case acute exposures to HAP, and in response to a key recommendation from the Science Advisory Board’s peer review of EPA’s RTR risk assessment methodologies 19 , we examine a wider

range of available acute health metrics than we do for our chronic risk assessments. This is in response to the acknowledgement that there are generally more data gaps and inconsistencies
in acute reference values than there are in chronic reference values. B y definition, the acute
CA

- REL represents a health

- protective level of exposure, with no risk anticipated below those levels, even for repeated exposures; however, the health risk from higher

- level exposures is unknown. Therefore, when a CA

- REL is exceede d and an AEGL

- 1 or ERPG

- 1 level is available (i.e., levels at which mild effects are anticipated in the general public for a single exposure), we have used them as a second comparative measure. Historically, c omparisons of
the estimated maximum off

- site o ne

- hour exposure levels have not been typically made to occupational levels for the purpose of characterizing public health risks in RTR assessments

. This is because o ccupat ional ceiling values are not generally considered protective for the general publi c since they are designed to protect the worker population (presumed healthy adults) for short duration (<15 minute) increases in exposure 20

. As a result, f or most

19 The SAB peer review of RTR Risk Assessment Methodologies is available at: http://yosemite.epa.gov/sab/sabproduct.nsf/4AB3966E263D943A8525771F00668381/$File/EPA

- SAB

- 10

- 007

- unsigned.pdf

20 U.S. EPA. (2009) Chapter 2.9 C hemical Specific Reference Values for Formaldehyde in Graphical Arrays of
Chemical

- Specific Health Effect Reference Values for Inhalation Exposures (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R

- 09/061, and available on

- lin e at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 28

chemicals, the 15

- minute occupational ceiling values are set at levels higher than a one

- hou r AEGL

- 1 , making comparisons to them irrelevant unless the AEGL

- 1 or ERPG

- 1 levels are
exceeded 13

. Such is not the case when comparing the available acute inhalation health effect reference values for formaldehyde 13

.

The worst

- case maximum estimated 1

- ho ur exposure to formaldehyde outside the facility
fence line for the mineral wool production source category is 1.21 mg/m 3

. This estimated

worst

- case exposure exceeds the 1

- hour REL by a factor of 20 (HQ REL = 20 ) and exceeds the
1

- hour AEGL

- 1 by a factor of 1 (HQ AEGL

- 1 = 1 ). T his exposure estimate exceed s the workplace ceiling level guideline for the formaldehyde value developed by National Institutes for Occupational Safety and Health (NIOSH) 21 “for any 15 minute period in a work day” by a
factor of 10 (NIO SH REL

- ceiling value of 0.12 mg/m 3 ; HQ NIOSH = 10 ). T he estimate exceeds the value developed by the American Conference of Governmental Industrial Hygienists (ACGIH) 22 as “not to be exceeded at any time” by a factor of 3 (ACGIH TLV

- ceiling value of 0.37 mg/ m

3 ; HQ ACGIH = 3 ). Additionally, the estimated maximum acute exposure exceeds the Air Quality Guideline value that was developed by the World Health Organization 23 for 30

- minute exposures by a factor of 12 (0.1 mg/m 3 ; HQ WHO = 12 )

.

Chronic noncancer target organ specific hazard indices (HIs) were calculated for every HAP
shown in Table 3.1

- 1 that has a chronic benchmark, and the highest target organ specific HI ( 0.1 for formaldehyde ) is shown in Table 3.2

- 1. There were no HIs greater than 1 for this

source category.

We conducted a screening

- level evaluation of the potential human health risks associated with emissions of PB HAP. Reported emissions of PB HAP were compared to emission thresholds established by EPA for the purposes of the RTR risk assessm ents. 24 The PB HAP s emitted by facilities in this category are lead, cadmium, and mercury . All lead, cadmium, and

mercury emissions were below the threshold levels , indicating no potential for significant
multi

- pathway risks from these facilities

.

Analy sis of potential differences between actual emissions 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 emissions levels. Considering this difference, the risk results
from the inhalation risk assessment indicate that the maximum excess lifetime individual

21 National Institutes for Occupational Safety and Health (NIOSH). Occupational Safety and Health Guideline for Formaldehyde; http://www.cdc.gov/niosh/docs/81

- 123/pdfs/0293.pdf

22 ACGIH (200 1) Formaldehyde. In Documentation of the TLVs® and BEIs® with Other Worldwide Occupational Exposure Values. ACGIH, 1300 Kemper Meadow Drive, Cincinnati, OH 45240 (ISBN: 978

- 1

- 882417

- 74

- 2) and available on

- line at http://www.acgih.org.

23 WHO (2000). Chapter 5.8 Formaldehyde, in Air Quality Guidelines for Europe, second edition. World Health Organization Regional Publications, European Series, No. 91. Copenhagen, Denmark. Available on

- line at http://www.euro.who.int/__data/assets/pdf_file/0005/74732/E71922.pdf

.

24 ICF International. TRIM

- Based Multipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 29

cancer risk could be up to 3 0 in a million, and that the maximum chronic noncancer TOSHI value could be as high as 0. 4 at the MACT

- allowable emission s level.

Table 3.2

- 1 Summary of Source Category Level Inhalation Risks for Mineral Wool Production

Result HAP
“Drivers” Facilities in Source Category

Number of Facilities Estimated to be in Source Category 7 n/a

Number of Facilities Identified in the NEI and Modeled in Preliminary
Risk Assessment 7 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 1 0 25 formaldehyde 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 formaldehyde Greater than or equal to 1 in 1 million 1 formaldehyde

Chronic Noncancer Risks

Maximum Hazard Index 0.1 formaldehyde

Num ber of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a

Refined Acute Noncancer Screening Results

Maximum Acute Hazard Quotient [using scali ng factor of 3 ] 20
1 formaldehyde

(REL) formaldehyde (AEGL

- 1

, ERPG

- 1) )
Number of Facilities With Potential for Acute Effects 1 formaldehyde Population E xposure Number of People Living Within 50 Kilometers of Facilities Modeled 3 ,70 0 ,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 14 n/a Greater than or equal to 1 in 1 million 10,300 n/a

Number of People Exposed to Noncancer Respiratory Hazard Index:

Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.0007 18 n/a Contribution of HAP to Cancer Incidence:
Formaldehyde Arsenic compounds 80%

19% n/a

25 We not e that the MIR for this source category would be 0.3

- in

- 1 million if the CIIT URE for formaldehyde
had been used in the assessment. The total cancer incidence would decrease by 80%. There is an ongoing IRIS reassessment for formaldehyde, and future RTR r isk assessments will use the cancer potency for formaldehyde that results from that reassessment. As a result, the current results may not match those of future assessments.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 30

Table 3.2

- 2 Summary of Refined Acute Results for Mineral Wool Production Facilities

Refined Results MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE

- RESPONSE VALUES

Based

on REL Based on

AEGL

- 1/
ERPG

- 1 Based on

AEGL

- 2/
ERPG

- 2 REL

(mg/m 3 ) AEGL

- 1 (1

-

hr) (mg/m 3 ) ERPG

- 1

(mg/m 3 ) AEGL

- 2

(1

- hr) (mg/m 3 ) ERPG

2 (mg/m 3 )
HAP Max. 1

- hr.

Air Conc. (mg/m 3 )

Formaldehyde 1.21 22 1 0.0 65 0.055 1.1 1.1 17 17

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

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

- response values which are not in the table do no t carry any potential for posing acute health risks, based on an analysis of currently available emissions data.
Notes on Acute Dose

- Response Values:

REL

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

- hour exposures.

AEGL

– Acute exposure guideline levels represent emergency exposure (1

- hour) limits for the general public.
AEGL

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

exp erience effects t hat are notable discomfort, but which are transient and reversible upon cessation of exposure.

AEGL

- 2 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience irreve rsible or other serious, long

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

– Emergency Removal Program guidelines represent emergency exposure (1

- hour) limits for the general public.

ERPG

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

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



### 4 Risk Results for the Wool Fiberglass Manufacturing Source Category

4.1 Source Category De scription and Results

Wool fiberglass is manufactured in a process that forms thin fibers from molten glass. A typical wool fiberglass manufacturing line consists of the following processes: (1) Preparation of molten glass, (2) formation of fibers into a wool fiberglass mat, (3) curing the binder

coated fiberglass mat, (4) cooling the mat (not always present), and (5) backing, cutting, and packaging. Typically, the binder consists of a solution of phenol

- formaldehyde resin, water, urea, lignin, silane, an d ammonia. Wool fiberglass products are primarily used as thermal and acoustical insulation for buildings, automobiles, aircraft, appliances, ductwork, and pipes. Other uses include liquid and air filtration. Approximately 90 percent of the wool fiberglass currently produced is for building insulation products.

The NESHAP for the Wool Fiberglass Manufacturing source category was promulgated on June 14, 1999 (62 FR 31695) and codified at 40 CFR part 63, subpart DDD. The 1999 NESHAP (40 CFR 63.1381) defines a “wool fiberglass manufacturing facility” as “anyDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 31

facility manufacturing wool fiberglass on a rotary spin manufacturing line or on a flame attenuation manufacturing line.” The MACT rule for the Wool Fiberglass Manufacturing source category does not appl y to facilities that manufacture mineral wool from rock, slag,
and other similar materials . Wool fiberglass is currently manufactured in the United States by 6 companies operating 29 plants in 16 States. Ten of these facilities are major sources and 19

a re area sources

.

HAP are emitted from wool fiberglass glass

- melting furnaces, including arsenic, chromium, and lead. Organic HAP (formaldehyde, phenol, and methanol) are released from RS forming, curing, and cooling processes and FA forming and curing p rocesses. Formaldehyde, phenol, and methanol are emitted from wool fiberglass plants that use HAP in their binders. Some furnaces also emit high risk metals including hexavalent chromium.

The emissions for the Wool Fiberglass Manufacturing source cate gory data set (of 29 facilities) are summarized in Table 4.1

- 1. The total HAP emissions for the sou rce category are approximately 1,874 tons per year. Based on these data, the HAP emitted in the largest quantities across these 29 facilities are: methanol , formaldehyde, phenol, hydrogen fluoride, and hydrochloric acid . Emissions of these 5 HAP make up 99.9 percent of the total emissions by mass. For the Wool Fiberglass Manufacturing source category, data were not available to develop a refined emissions multiplier. Therefore, the default emissions multiplier of 10 was used for the acute risk analysis. Persistent and bioaccumulative HAP (PB HAP) reported as
emissions from these facilities include lead, cadmium, and mercury compounds

. 26

26 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Ass essment Library , Volume 1,

EPa

- 453K

- 04

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

.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 32

Table 4.1

- 1 Summary of Emissions from the Wool Fiberglass Manufacturing Category and Availability of Dose

- Response Values

HAP Emissions (tpy) Number

of
Facilities Reporting
HAP (29
facilities
in data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS a

PB

HAP? Unit Risk
Estimate for
Cancer? Reference

Concentration
for Noncancer? Health

Benchmark
Values for Acute
Noncancer?

Methanol 820 26 Y Y
Formaldehyde 618 26 Y Y Y

Phenol 403 26 Y Y
Hydrogen Fluoride 20 29 Hydrochloric acid 12 29 Y Y
Chromium (VI) 0.38 29 Y Y

Selenium 0.15 29 Y

Lead 0.14 29 Y Y
Manganese 0.13 29 Y

Nickel 0.12 29 Y Y

Chromium III 0.05 29

Arsenic 0.05 29 Y Y Y
Elemental Gaseous Mercury 0.04 29 Y Y Y Antimony 0.04 29

Cadmium 0.0 2 29 Y Y Y

Cobalt 0.02 29 Y Berylium 0.009 29 Y Y Y
Gaseous Divalent Mercury 0.005 29 Y Particulate Divalent Mercury 0.005 29 Y

a Notes for how HAP were speciated for risk assessment:

For emissions of any chemicals or chemical groups class ified 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
ht tp://www.epa.gov/nata2002/methods.html#pom ( Approach to Modeling POM ).

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

.



### 4.2 Risk Characterization

This section presents the results of the risk assessment for the W ool F iberglass Manufacturing source category. The basic chronic inhalation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients, as well as the results of our prelimi nary screen for potential non

- inhalationDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 33

risks from PB HAP. Also presented are the HAP “drivers,” which are the HAP that collectively contribute 90 percent of the maximum cancer risk or maximum hazard index at the highest exposure location.

Table s 4.2

- 1 and 4.2

- 2 summarize the chronic and acute inhalation risk results for this source
category. The results for the Wool Fiberglass Manufacturing source category indicate that maximum lifetime individual cancer risks could be as high as 2 0 in a million. The major
contributor to the risk is formaldehyde . Approximately 650 ,000 people were estimated to
have cancer risks above 1 in a million as a result of the emissions from 15 facilities. The
maximum chronic non

- cancer TOSHI value for the source category coul d be up to 0.2 with
emissions of formaldehyde dominating those impacts, indicating no significant potential for chronic noncancer impacts.

Worst

- case a cute hazard quotients (HQs) were calculated for every HAP shown in Table 4.1

- 1 that has an acute bench mark, and the highest acute HQ REL of 30 for formaldehyde is
shown in Table 4.2

- 1. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries.
In thi s case, the refined analysis did not change the acute analysis results. Table 4.2

- 2 provides more information on the acute risk estimates for formaldehyde, the only HAP that
had a worst

- case screening acute HQ greater than 1 for any benchmark.

To bette r characterize the potential health risks associated with estimated worst

- case acute exposures to HAP, and in response to a key recommendation from the Science Advisory Board’s peer review of EPA’s RTR risk assessment methodologies 27 , we examine a wider

ran ge of available acute health metrics than we do for our chronic risk assessments. This is in response to the acknowledgement that there are generally more data gaps and inconsistencies
in acute reference values than there are in chronic reference values. By definition, the acute
CA

- REL represents a health

- protective level of exposure, with no risk anticipated below those levels, even for repeated exposures; however, the health risk from higher

- level exposures is unknown. Therefore, when a CA

- REL is excee ded and an AEGL

- 1 or ERPG

- 1 level is available (i.e., levels at which mild effects are anticipated in the general public for a single exposure), we have used them as a second comparative measure. Historically, c omparisons of
the estimated maximum off

- site one

- hour exposure levels have not been typically made to occupational levels for the purpose of characterizing public health risks in RTR assessments

. This is because o ccupat ional ceiling values are not generally considered protective for the general pub lic since they are designed to protect the worker population (presumed healthy adults) for short duration (<15 minute) increases in exposure 28 . As a result, f or most chemicals, the 15

- minute occupational ceiling values are set at levels higher than a one

- h our

27 The SAB peer review of RTR Risk Assessment Methodologies is available at: http://yosemite.epa.gov/sab/sabproduct.nsf/4AB3966E263D943A8525771F00668381/$File/EPA

- SAB

- 10

- 007

- unsigned.pdf

28 U.S. EPA. (2009) Chapter 2.9 Chemica l Specific Reference Values for Formaldehyde in Graphical Arrays of
Chemical

- Specific Health Effect Reference Values for Inhalation Exposures (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R

- 09/061, and available on

- line at
h ttp://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 34

AEGL

- 1 , making comparisons to them irrelevant unless the AEGL

- 1 or ERPG

- 1 levels are
exceeded 21 . Such is not the case when comparing the available acute inhalation health effect reference values for formaldehyde 21

.

T he worst

- case maximum estimated 1

- hour exposure to formaldehyde outside the facility
fence line for the wool fiberglass manufacturing source category is 1. 92 mg/m 3 . This
estimated worst

- case exposure exceeds the 1

- hour REL by a factor of 30 (HQ REL = 30) and
the 1

- hour AEGL

- 1 (HQ AEGL

- 1 = 2 ). T his exposure estimate also exceeds multiple workplace ceiling level guidelines for formaldehyde , including the value developed by the American Conference of Governmental Industrial Hygienists (ACGIH) 29 as “not to be exceeded at any time” (ACGIH TLV

- cei ling value of 0.37 mg/m 3 ; HQ ACGIH = 5 ) , and the value developed by the National Institutes for Occupational Safety and Health (NIOSH) 30 “ for any 15 minute period in a work day ” (NIOSH REL

- ceiling value of 0.12 mg/m 3 ; HQ NIOSH = 16 ). Additionally, the estima ted maximum acute exposure exceeds the Air Quality Guideline value that was developed by the World Health Organization 31 for 30

- minute exposures (0.1 mg/m 3 ; HQ WHO = 19 )

.

Chronic noncancer target organ specific hazard indices (HIs) were calculate d for every HAP
shown in Table 4.1

- 1 that has a chronic benchmark, and the highest t arget organ specific HI (0.2 for formaldehyde) is shown in Table 4.2

- 1. There were no HIs greater than 1 for this
source category.

For this source category, EPA conducted a scre ening

- level evaluation of the potential human health risks associated with emissions of PB HAP. Reported emissions of PB HAP were compared to emission thresholds established by EPA for the purposes of the RTR risk

assessments. 32 The PB HAP emitted by faci lities in this category are lead, cadmium, and

mercury

. All lead, cadmium, and mercury emissions were below the threshold levels

, indicating no potential for significant multi

- pathway risks from these facilities

.

Analysis of potential differences between actual emissions 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 emissions levels for phenol, methanol, and formaldehyde
emissions. For hexavalent chromium emissions the allowable emissions are equal to actual
emissions since there is no hexavalent chromium emission limit in the MACT standard. Considering this difference, the risk results from the inhalation risk assessment indicate that

29 ACGIH (2001) Formaldehyde. In Documentation of the TLVs® and BEIs® with Other Worldwide Occupational Exposure Values. ACGIH, 1300 Kemper Meadow Drive, Cincinnati, OH 45240 (ISBN: 978

- 1

- 882417

- 74

- 2 ) and available on

- line at http://www.acgih.org.

30 National Institutes for Occupational Safety and Health (NIOSH). Occupational Safety and Health Guideline for Formaldehyde; http://www.cdc.gov/niosh/docs/81

- 123/pdfs/0293.pdf

31 WHO (2000). Chapter 5.8 F ormaldehyde, in Air Quality Guidelines for Europe, second edition. World Health Organization Regional Publications, European Series, No. 91. Copenhagen, Denmark. Available on

- line at http://www.euro.who.int/__data/assets/pdf_file/0005/74732/E71922.pdf

.

32 ICF International. TRIM

- Based Multipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 35

the maximum excess lifetime individual cancer risk could be up to 60 in a million, and that the maximum chronic noncancer TOSHI value could be as high as 0.5 at the MACT

allowable emissions level.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

Manufacturing Source Categories

– FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 36

Table 4.2

- 1 Summary of Source Category Le vel Inhalation Risks fo r Wool Fiberglass Manufacturing

Result HAP “Drivers”

Number of Facilities Estimated to be i n Source Category 29 n/a

Number of Facilities Identified in NEI and
Modeled in Preliminary Risk Assessment 29 n/a

Cancer Risks
Maximum Individual Lifetime Canc er Risk (in 1 million) 20 33 formaldehyde

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 formaldehyde, Cr (VI)

Greater than or equal to 1 in 1 million 15 formaldehyde, Cr (VI), Ni, As

Chronic Noncancer Risks

Maximum Respiratory Hazard Index 0. 2 formaldehyde

Num ber of Facilities with Maximum Respiratory Hazard Index:

Greater than 1 0 n/a Acute Noncancer Screening Results

Maximum Acute H azard Quotient 30

2 formaldehyde (REL)

formaldehyde (AEGL

- 1,
ERPG

- 1)

Number of Facilities With Potential for Acute
Effects 7 formaldehyde

Population Exposure Number of People Living Within 50 Kilometers
of Facilities Modeled 27,000,000 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 1, 800 n/a Greater than or equal to 1 in 1 million 650 ,000 n/a Number of People Exposed to Noncancer Respiratory Hazard Index:

G reater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.0 4 26 n/a

Contribution of HAP to Cancer Incidence Formaldehyde Cr (VI) Arsenic Compounds 64 %
35 %
1% n/a

33 We note that the MIR for this source category would change to 10 in a million (driven by Cr(VI)) if the CIIT URE for formaldehyde had been used in the assessment, and the total cancer incidence would decrease by 64%. There is an ongoing IRIS reassessment for formalde hyde, and future RTR risk assessments will use the cancer potency for formaldehyde that results from that reassessment. As a result, the current results may not match
those of future assessments.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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Table 4.2

- 2 Summary of Refined Acute Results for W ool Fiberglass Manufacturing
Facilities

Refined Results MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE

- RESPONSE VALUES

Based on

REL Based on

AEGL

- 1/
ERPG

- 1 Based on

AEGL

- 2/
ERPG

- 2 REL

(mg/m 3 ) AEGL

- 1

(1

- hr) (mg/m 3 ) ERPG

- 1

(mg/m 3 ) AEGL

- 2

(1

- hr) (mg/m 3 ) ERPG

- 2

(mg/m 3 )

HAP Max. 1

- hr.

Air Conc. (mg/m 3 )

Formaldehyde 1.77 30 2 0.1 0.055 1.1 1.1 17 17

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

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

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

- Response Values:

REL

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

- hour exposures.

AEGL

– Acute exposure guideline levels represent emergency exposure (1

- hour) limits for the general public.
AEGL

- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience effects t hat are notable discomfort, but which are transient and reversible upon cessation of exposure.

AEGL

- 2 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long

- lasting adverse health effects of an impaired ability to es cape. EPRG

– Emergency Removal Program guidelines represent emergency exposure (1

- hour) limits for the general public.

ERPG

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

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



### 4.3 Auxiliary Risk Characterization

As indicated in Section 4.2, the maximum lifetime individual cancer risks for the Wool Fiberglass Manufacturing source category could be as hig h as 2 0 in a million based on actual emissions. The major contributor to this cancer risk is formaldehyde, although c hromium (VI) is also a risk driver. Chromium i s emitted from the furnace refractory brick as it breaks down over time. The greatest amou nt of c hromium (VI) is emitted from the Certainteed Facility in Kansas City, Kansas that uses a type of refractory brick that is almost 100%
chromium.

Furnace refractory brick are essential to the structure and function of the furnace, providing
thermal insulation and corrosi on protection. Refractory bricks in the glass melting industry are typically composed of Al 2 O 3 , Al 2 0 3 - SiO 2 , ZrO 2 , with or without Cr 2 O 3 added, and dense
Cr 2 O 3 .[ 31

, 32 ] Refractory brick breaks down over time, and therefore, must be re placed periodically (approximately every 7

- 14 years depending on the type of brick).

Since there are currently no regulations preventing the use of high chromium refractory brick or limiting emissions of c hromium in the Wool Fiberglass Manufacturing Indus try, it is reasonable to assume that another Wool Fiberglass Manufacturing facility might replace its current furnace refractory brick with high chromium refractory brick sometime in the future.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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Therefore, we performed an auxiliary risk characterization analysis to assess the maximum
individual lifetime cancer risks of the o ther 28 Wool Fiberglass facilit ies switching to high

c hromium brick. For the auxiliary risk characterization analysis it was assumed that the Cr (VI) would be emitted from the other f acilities at the same as rate (in lbs Cr (VI) emitted per ton of glass pulled) as for the K2 furnace at the Certainteed Facility in Kansas City, Kansas.

The results of the auxiliary analysis (Table 4.2

- 3) show that 4 facilities would have maximum
indivi dual lifetime cancer risks greater than 100 in a million, with the highest facility at 4 00 in
a million. Under this scenario

, 5 4 ,000 people would be exposed to risks of greater than 10 in
a million and over 2.2 million people would be exposed to cancer ri sks of greater than 1 in a
million

.

Table 4.2

- 3 Summary of Source Category Le vel Cancer Risks for the Wool Fiberglass Manufacturing Auxiliary Analysis

Result HAP “Drivers”

Number of Facilities Estimated to be i n Source Category 29 n/a

Number of F acilities Identified in NEI and
Modeled in Auxiliary Risk Assessment 29 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 4 00 Cr (VI)

Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1 million 4 Cr (VI), formaldehyde Greater than or equal to 10 in 1 million 24 Cr (VI) , formaldehyde Greater than or equal to 1 in 1 million 29 Cr (VI), formaldehyde Population Exposure Number of People Living Within 50 Kilometers
of Facilities Mo deled 27,000,000 n/a

Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1 million 200 n/a Greater than or equal to 10 in 1 million 54 ,000 n/a Greater than or equal to 1 in 1 million 2,200,000 n/a Estimated Cancer Incidence (ex cess cancer cases per year) 0. 14 n/a

Contribution of HAP to Cancer Incidence Formaldehyde Cr (VI) 18 %
82 % n/aDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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## 5 General Discussion of Uncertainties and How They Have
Been Addressed

5.1 Exposure Modeling Uncertainties

Although every effo rt 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 e xposure modeling estimates. The chronic ambient modeling uncertainties are considered relatively small in comparison, since we are using EPA’s refined local dispersion model with site

specific parameters and reasonably representative meteorology. If anyt hing, the population exposure estimates are biased high by not accounting for short

- or long

- term population mobility, and by neglecting processes like deposition, plume depletion, and atmospheric degradation. Additionally, estimates of the maximum indivi dual risk (MIR) contain uncertainty , because they are deriv ed at census block centroid locations rather than actual
residences. This uncertainty is known to create potential underestimates and overestimates of
the actual MIR values for individual faciliti es, 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 upw ard bias in both the MIR and population risk estimates; nor did we factor in the possibility of population growth during the 70

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

A sensitivity analysis performed for the 1999 NATA found that the selection of the meteorology dataset location could result in a range of chronic ambient concentrations which varied from as much as 17% below the predicted value to as much as 84% higher than the predic ted 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 resul ts 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 acce ptable we have chosen the most conservative of these threshold
values , 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,

w e have refined our assessment by developing a better understanding of the geography of the facility relative to potential exposure locations.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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### 5.2 Uncertainties in the Dose

- Response Relationships

In the sections that follow, separate discussions are pro vided 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), bu t may also be derived for acute (

- term (>24 hours up to 30 days), and subchronic (>30 days up to 10% of lifetime) exposure durations, all of which are derived based on an assumption of continuous exposure throughout the duration specified. For the purposes of assessing all potential health risks associated wit h
the emissions included in an assessment, we rely on both chronic (cancer and noncancer) and acute ( noncancer ) benchmarks, which are described in more detail below.

Although every effort is made to identify peer

- review ed dose

- response values for all HAPs
emitted by the source category included in an assessment, some HAP have no peer

- reviewed cancer potency values or reference values for chronic non

- cancer or acute effects (inhalation or ingestion) . Since exposure s to these pollutants cannot be included in a quantitative risk estimate, an understatement of risk for these pollutants at environmental exposure levels is possible.

Additionally, chronic dose

- response values for certain compounds included in the assessm ent 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 u sed by the EPA to develop cancer potency factors. In general, these same uncertainties attend the development of cancer potency factors by CalEPA, the source of peer

- reviewed cancer potency factors
used where EPA

- developed values are not yet available. T o place this discussion in context, we provide a quote from the EPA’s Guidelines for Carcinogen Risk Assessment [ 33 ] (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 Guidel ines

.

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. De pending 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 CancerDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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Guidelines , EPA uses animal cancer bioassays as indicators of po tential 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 doc uments 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 Cance r 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). 34 In some circumstances, the true risk could be as low as zero; however, in other circumstances the risk could also be greater. 35 When developing an upper bound estimate of risk and to provide risk values that do not underestimate risk, EPA generally re lies on conservative default approaches. 36 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 benefit s analysis).

Such health risk assessments have associated uncertainties, some which may be considered quantitatively, and others which generally are expressed qualitatively. Uncertainties may vary substantially among cancer risk assessments associated wi th 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 [ 34 ]. 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

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

35 T he 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.

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

- assessment process when the correct scientific model is unknown or uncertain. ” The 1983 NRC report Risk Assessment in the Federal Government: Managing the Process defined default option as “the option chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to the contrary” (NRC, 1983 a, 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 publ ic 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 Practice s, EPA/100/B

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

- final.pdf.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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tumors would occur in humans. 37 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 agen t 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 t o 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 un certainties associated with limitations in the
test data and the correctness of scaled estimates.

(4) EPA cancer risk estimates, whether based on epidemiological or experimental animal data, are generally developed using a benchmark dose (BMD) analysis to estimate a dose at which there is a specified excess risk of cancer, which is used as the point of departure (or POD) for the remainder of the calculation. Statistical uncertainty in developing a POD using a benchmark dose (BMD) approach is generally addressed though use of the 95% lower confidence limit on the dose at which the specified excess risk occurs (the BMDL), decreasing the likelihood of understating risk. EPA has generally utilized the multistage model for estimation of the BMDL using cance r 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 p ollutant 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 manne r in which a

37 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 hum ans.” and “Target organ concordance is not a prerequisite for evaluating the implications of animal study results for humans.”Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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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 thresh old 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 extrap olation 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. P ollutants 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

a pproach.

EPA most frequently utilizes a linear low

- dose extrapolation approach as a baseline science

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

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

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

- dose nonlinear, non

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

- probit models) in representing dos e response relationships due to the variability in response within human populations. Another National Research Council (NRC) report [ 35 ] suggests that models based on distributions of individual thresholds are likely to lead to sigmoidal

- shaped
dose

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

processes.

As noted above, EPA’s current approach to cancer risk assessment typically utilizes a straight line approach from the BMDL. This is equivalent to using an upper confidence limit on the slope of the straight line extrapolation. The impact of the choice of the BMDL on bottom line 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 contrib utor to uncertainty in risk assessment (Subramaniam et. al., 2006) [ 36 ]. 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 extrapo late 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 notDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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show large differences from those based on the u pper 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 div erse 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

s tage 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 lev els 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 . Uncertaint y factors are commonly default values 38 e.g., factors of 10 or 3, used in the absence of compound

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

- specific information. When data are limited, more assumption s 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 a re 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 inhala tion exposures.

38 According to the NRC report Science and Judgment in Risk Assessment (NRC, 1994) “[Default] options are generic approaches, bas ed 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.pd f.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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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. 39 To derive values that are intended to be “without appreciable risk,” EPA’s methodology relies upon an uncertainty factor (UF) approach [ 37 ],[ 38 ] which includes consideration of both uncertainty and variability.

EPA begins by evaluating all of the available peer

- reviewed literature to determine non

cancer endpoints of concern, evaluating the quality, strengths and limitations of the available studies. EPA typically chooses the rel evant 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
l evel (LOAEL).

A series of downward adjustments using default UFs is then applied to the POD to estimate
the reference value [ 39 ] . 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 extrapola ting 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 ext rapolating 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, defa ult adjustment values are selected for the individual UFs. For each type of uncertainty (when relevant to the assessment) , EPA typically applies an UF value of 10 or 3 with the cumulative UF value leading to a downward adjustment of 10

- 3000 fold from the selected POD. An UF of 3 is used when the data do not support the use of a 10

- fold factor. If an extrapolation step or adjustment is not relevant to an assessment (e.g., if applying human toxicity data and an interspecies extrapolation is not required) t he 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 fr om 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

39 See IRIS glossaryDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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situations, a smaller UF of 3 may be appli ed 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 concentr ation 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

un certainties 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 s pecific chemical, differences in species responses may be greater or less than this value

.

Pharmacokinetic models are useful to examine species differences in pharmacokinetic processing and associated uncertainties; however, such dosimetric adjustments are not always possible. Information may not be available to quantitatively assess toxicokinetic or toxicodynamic differences bet ween 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 h umans 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 t he available scientific information supports use of a different value.

4) Toxicity data are typically limited as to the dose or exposure levels that have been tested in individual studies; in an animal study, for example, treatment groups may differ in

ex posure 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 pre ferred 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 limite d 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.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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There is no RfD or other comparable chronic health benchmark value for lead compounds. Thus, to address multipathway human health and environmental risks ass ociated with emissions of lead from these facilities, ambient lead concentrations were compared to the NAAQS for lead. In developing the NAAQS for lead, EPA considered human health evidence reporting adverse health effects associated with lead exposure, a s well as an EPA conducted multipathway risk assessment that applied models to estimate human exposures to
air

- related lead and the associated risk (73FR at 66979). EPA also explicitly considered the
uncertainties associated with both the human health evid ence and the exposure and risk analyses when developing the NAAQS for lead. For example, EPA considered uncertainties in the relationship between ambient air lead and blood lead levels (73FR at 66974), as well as
uncertainties between blood lead levels an d loss of IQ points in children (73FR at 66981). In considering the evidence and risk analyses and their associated uncertainties, the EPA
Administrator noted his view that there is no evidence

- or risk

- based bright line that indicates a single appropriat e level. Instead, he noted, there is a collection of scientific evidence and judgments and other information, including information about the uncertainties inherent in many relevant factors, which needs to be considered together in making this public healt h policy judgment and in selecting a standard level from a range of reasonable values (73FR at 66998). In so doing, the Administ rator decided that, a level for the primary lead standard of 0.15 μg/m 3 , in combination with the specified choice of indicator, averaging time, and form, is requisite to protect public health, including the health of sensitive groups, with an adequate

marg in of safety (73FR at 67006). A thorough discussion of the health evidence, risk and exposure analyses, and their associated uncertainties can be found in EPA’s final rule revising the lead NAAQS (73 FR 66970

- 66981, November 12, 2008).

We also note the uncertainties associated with the health

- based (i.e., primary) NAAQS are likely less than the uncertainties associated with dose

- response values developed for many of the other HAP, particularly those HAP for which no human health data exist. In 1988, E PA’s IRIS program reviewed the health effects data regarding lead and its inorganic compounds and determined that it would be inappropriate to develop an RfD for these compounds, saying, “A great deal of information on the health effects of lead has been o btained through
decades of medical observation and scientific research. This information has been assessed in the development of air and water quality criteria by the Agency's Office of Health and Environmental Assessment (OHEA) in support of regulatory de cision

- making by the Office of Air Quality Planning and Standards (OAQPS) and by the Office of Drinking Water (ODW). By comparison to most other environmental toxicants, the degree of uncertainty about the health effects of lead is quite low. It appears that some of these effects, particularly changes in the levels of certain blood enzymes and in aspects of children's neurobehavioral development, may occur at blood lead levels so low as to be essentially without a threshold. The Agency's RfD Work Group di scussed inorganic lead (and lead compounds) at two meetings (07/08/1985 and 07/22/1985) and considered it inappropriate to develop an RfD for inorganic lead.” EPA’s IRIS assessment for Lead and compounds (inorganic) (CASRN 7439

- 92

- 1), http://www.epa.gov/iris/subst/0277.htm

.

We note further that because of the multi

- pathway, multi

- media impacts of lead, the risk assessment supporting the NAAQS considered direct inhalation exposures and indirect air

rela ted multi

- pathway exposures from industrial sources like primary and secondary leadDraft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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smelting operations. It also considered background lead exposures from other sources (like contaminated drinking water and exposure to lead

- based paints). In revising the NAAQS for lead, we note that the Administrator placed more weight on the evidence

- based framework and less weight on the results from the risk assessment, although he did find the risk estimates to be roughly consistent with and generally supportive of th e evidence

- based framework applied in the NAAQS determination (73FR at 67004). Thus, when revising the NAAQS for lead to protect public health with an adequate margin of safety, EPA considered both the
evidence

- based framework and the risk assessment, albe it to different extents.

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 U F values that may be less than 10. UFs are applied based on chemical

specific or health effect

- specific information (e.g., simple irritation effects do not vary appreciably between human individuals, hence a value of 3 is typically used), or based on the purpose for the reference value (see the following paragraph). The UFs applied in acute reference value derivation include: 1) heterogeneity among humans; 2) uncertainty in extrapolating from animals to humans; 3) uncertainty in LOAEL to NOAEL adjustment s; 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 heal th effects relative to the reference value or values being exceeded. W here 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.Draft Risk Assessment for the Mineral Wool Production and Wool Fiberglass

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## 5 References

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