**Draft Risk Ass essment 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 September**  **2011 Draft Risk Ass**  **essment 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
................................ ................................ ...................... 12 2.6.1 Sources of chronic dose
- response information
................................ .................. 12 2.6.2 Sources of acute dose
- response info rmation
................................ ...................... 16 2.7 Risk Characterization
................................ ................................ ................................ 19 2.7.1 General
................................ ................................ ................................ ............... 19 2.7.2 M ixtures
................................ ................................ ................................ ............. 21 3 Risk Results for the Mineral Wool Production
................................ ............................ 22 3.1 Source Category

Description and Results
................................ ................................ . 22 3.2 Risk Characterization
................................ ................................ ................................ 23 4 Risk Results for the Wool Fiberglass Manufacturing Source Category
...................... 28 4.1 Source Category

Description and Results
................................ ................................ . 28 4.2 Risk Characterization
................................ ................................ ................................ 30 4.3 Auxiliary

Risk Characterization
................................ ................................ ................ 35 5 General Discussion of Uncertainties and How They Have Been Addressed
................... 37 5.1 Exposure Modeling Uncertainties
................................ ................................ ............. 37 5.2 Uncertainties in the Dose
- Response Relationships
................................ ................... 38 5 References
................................ ................................ ................................ ........................ 46 **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 Carcin ogens .... 15 Table 2.6
- 1 (b) Dose
- Response Values for Chronic Inhalation Exposure to Noncarcinogens

................................ ................................ ................................ ................................ .................. 16 Table 2.6
- 2 Dose
- Response Values for Acute Exposure
................................ ........................ 19 Table 3.1
- 1 Summary

of Emissions from the Mineral Wool Production Category and Availability

of Dose
- Response Values
................................ ................................ .................... 23 Table 3.2
- 1 Summary

of Source Category

L evel Inhalation Risks for Mineral Wool Production
................................ ................................ ................................ ................................ 27 Table 4.2
- 1 Summary

of Source Category

L evel Inhalation Risks for Wool Fiber glass Manufacturing
................................ ................................ ................................ .......................... 34 Table 4.2
- 2 Summary

of Refined Acute Results for Wool Fiberglass Manufacturing Facilities

................................ ................................ ................................ ................................ .................. 35 Table 4.2
- 3 Summary

of Source Category

L evel Cancer Risks for the Wool Fiberglass Manufacturing Auxiliary Analy sis
................................ ................................ ........................... 36**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  3 **Appendices** Appendix 1 Emissions Inventory Support Memorandum Appendix 1a
- Emissions Data Used in Residual Risk M odeling 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 Analy sis o f 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 A cute Impacts Refined Analy sis 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 Substances and Disease Registry CalEPA California Environmental Agency ERPG Emergency Response Planning Guideline HAP Hazardous Air Pollutant HEM Human Exposure Model HI Hazard index HQ Hazard quotient IR IS Integrated Risk Information Sy stem MACT Maximum Achievable Control Technology MIR Maximum Individual Risk MOA Mode of action NAC National Advisory Committee NATA National Air Toxics Assessment NEI National Emissions Inventory NPRM Notice of Proposed Rulemaking PB
- HAP Persistent and Bioaccumulative
- HAP POM Polycyclic organic matter REL Reference exposure level RfC Reference concentration RfD Reference dose RTR Risk and Technology TOSHI Target
- organ - specific hazard index URE Unit risk estimate**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

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### 1 **Introduction** Section 112 of the Clean Air Act ( CAA) establishes a two
- stage regulatory process for addressing emissions of hazardous air pollutants (HAPs) from stationary sources. In the first stage, section 112(d) requires the Environmental Protection Agency (EPA, or the Agency) to develop technology
- based standards for categories of sources (e.g., petroleum refineries, pulp and paper mills, etc.) [ 1 ]. EPA has largel y completed the initial Maximum Achievable Control Technology

( MACT ) standards as required under this provision. Under section 112(d)(6 ), EPA must review each of these technology
- based standards at least every eight ye ars and revise a standard, as necessary , “taking into account developments in practices, processe s and control technologies.” In the second stage, EPA is required under sec tion 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 safet y or to prevent an adverse environmental effect, EPA must develop standards to address these remaining risks. This second stage of the regulatory process is known as the residual risk stage. For each source category for which EPA issued MACT standards, the residual risk stage must be completed within eight years of promulgation of the initial technology
- based standard. In December of 2006 we consulted with a panel from the EPA's Science Advisory Board (SAB) on the “Risk and Technology Review (RTR) Assessment Plan” and in June of 2007, we receiv ed 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 b ased 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 Manufacturing and Mineral Wool Production source cate gories. 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 descriptions of the methods used to screen for acut e health risks, chronic non
- inhalation health risks, and adverse e nvironmental effects. Since the screening assessments indicated low potential for chronic non
- inhalation health effects or environmental impacts, including effects to threatened and endange red species, no further refinement of these assessments was performed.**Draft Risk Ass essment 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 point 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 emission factor developed from one source test; emissions were esti mated 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 NEIand others, listed in NEI , had since closed. As a result, EPA decided to collect 2010 industry process and source test data under an information collection re quest 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 court 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 IC R emissions data and modifications made to the NEI data are discussed in the Appendix 1 a , entitled “ Emissions Data Used in Residual Risk Modeling for Mineral Wool Production
. ” **Wool Fiberglass** A voluntary

I CR was sent out in March 2010 to the 29 wool fiberglass facilities currentl y operating in the US. I CR responses from all the facilities were compiled in the project database and included info rmation 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 pr oject database being treated as CBI. Emissions test data provided by the wool fiberglass industry varied widel y by

facility
. Companies were allowed to, in lieu of new testing, submit existing and well documented test data that was representative of curre nt 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 ga

ps in existing data, new test data was also required. Companies were, however, allowed to test a subset of facilit y operations, if the facilities were able to demonstrate that the tested subset was representative of the untested subset. Test results were ty pically presented

1 Assigning data with MACT codes allow s EPA to determine reductions attributable to the MACT program. The NEI associates MACT codes corresponding to MACT source categories with st ationary 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 Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  6 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 used to populate the wool fiberglass residual risk modeling f ile. Using the glass pull rates (generall y given in tons of glass pulled/day) that each facility provided in its I CR response and the source emission rates (lb/ton) from emission testing, annual emissions (tpy) were calculated for each pollutant and emiss ion 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 and modifications made to the NEIdata are discussed in the Ap pendix 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 eac h facility

in the source category

of interest were estimated using the Human Exposure Model in combination with the American Meteorological Society/EPA Regulatory Model dispersion modeling s ys tem (HEM 3 ). The approach used in appl yi ng this modeling s ys tem 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 focus es 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 sy stem, AERMOD version 11103 , is a state
- of
- the
science Gaussian plume dis persion model that is preferred b y 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 aver age ambient concentrations through the simulation of hour
- by
- hour dispersion from the emission sources into the surrounding atmosphere. Hourl y emission rates used for this simulation are generated b y evenl y dividing the total annual emission rate from the inventory into the 8,760 hours of the y ear. The first step in the application of the HEM 3 modeling s ys tem is to predict ambient concentrations at locations of interest. The AERMOD model options employed are summarized in Table 2.2
- 1 and are discussed further below.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  7 **Table 2.2**  **- 1**  **AERMOD version 11103**  **mo del options for RTR**  **modeling** Modeling Option Selected Parameter for chronic exposure Type of calculations Hourly Ambient Concentration Source type Point, area represented as pseudo point source Receptor orientation Polar (13 rings and 16 radials) Discrete (census block centroids) Terrain characterization Actual from USGS 1
- degree DEM data Building downwash Not Included Plume deposition/depletion Not Included Urban source option No Meteorology 1 year representative NWS from nearest site ( over 200 stations) In HEM 3 , meteorological data are ordinaril y selected from a list of over 200 National Weather Service (NWS) surface observation stations across the continental United States, Alaska, Hawaii, and Puerto Rico. In most cases the nearest station is selected as representative of the conditions at the subject facility
. Ideall y, when considering off
- site meteorological data most site specific dispersion modeling efforts will employ up to five ye ars of data to capture variability in weather patterns from ye ar to ye ar. However, because we had an insufficient number of appropriatel y formatted model input files derived from available meteorological data, we modeled only a single year, t ypicall y 1991. While the selection of a single ye ar 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 chara cteristic latitude and longitude coordinates, the closest meteorological station was used in the dispersion modeling. The average distance between a modeled facility and the applicable meteorological station was 40 miles (72 km). Appendix 3 (Meteorologic al 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 ye ar of meteorological data is discussed in “ Risk and Technology Review (RTR) Risk Assessment Methodologies ” [ 2 ]. The HEM 3 sy stem estimates ambient concentrations at the geographic centroids of census blocks (using the 2000 Census), and at o ther 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. Ty pically we combined only

the impacts of facilities within the same source category, and assessed chronic exposure and risk onl y for census blocks with at least one resident (i.e., locations where people may reasonably

be assumed to reside rather than receptor points at the fenceline of a facility). Chronic ambient concentratio ns were calculated as the annual average of all estimated short
- term (one
- hour) concentrations at each block centroid. Possible future residential use of currentl y uninhabited areas was not**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  8 considered. Census blocks, the finest resolution available in th e census data, are t ypically comprised of approximately 40 people or about ten households. In contrast to the development of ambient concentrations for evaluating long
- term exposures, which was performed only for occupied census blocks, worst
- case short - term (one
- hour) concentrations were estimated both at the census block centroids and at points nearer the facility that represent locations where people may be present for short periods, but generall y no nearer than 100 meters from the center of the faci lity (note that for large facilities, this 100
- meter ring could still contain locations inside the facility property). Since short
- term emission rates were needed to screen for the potential for hazard via acute exposures, and since the NEI contains only annual emission totals, we generall y appl y the assumption to all source categories that the maximum one
- hour emission rate from an y source is ten times the average annual hourl y emission rate for that source. The average hourly

emissions rate is defined a s 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 robust peak
- to - mean emissions factor, and in re sponse to one of the key messages from the SAB consultation on our RTR Assessment Plan, we performed an anal ysis using a short
- term emissions data set from a number of source s located in Texas (originally reported on b y Allen et al
. 2004)[ 7]. In that report, the Texas Environmental Research Consortium Project compared hourly and annual emissions data for volatile organic compound s for all facilities in a heavily
industrialized 4
- county

area (Harris, Galveston, Chambers, and Brazoria Counties , TX) over an el even - month time period in 2001 . We obtained the dataset and performed our own anal ys is, focusing that analy sis on sources which reported emitting high quantities of HAP over short periods of time (see Appendix 4 , “Analy sis of data on short
- term emission r ates 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 hourl y emissi on rate was 9 . Based on these results, we chose the factor of ten for all initial screening; it is intended to cover routinely
- variable emissions as well as startup, shutdown, and malfunction (SSM) emissions. While there have been some documented emissio n excursions above this level, our anal ys is of the data from the Texas Environmental Research Consortium suggests that this factor should cover more than 99% of the short
- term peak gaseous or volatile HAP emissions from ty pical industrial sources. Cen sus block elevations for HEM 3 modeling were determined nationally from the US Geological Service 1
- degree digital elevation model (DEM) data files, which have a spatial resolution of about 90 meters. Elevations of polar grid points used in estimating shor t - 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. I f a sector does not contain an y blocks, the model defaults the elevation t o 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 Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  9 In addition to using receptor elevation to determine plume height, AERMOD adjusts the plume’s flow if nearb y el evated hills are expected to influence the wind patterns. For details on how hill heights were estimated and used in the AERMOD modeling , see Appendix 2
. 

### 2.3 **Estimating human inhalation exposure** We used the annual average ambi ent 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 anal ysis did not consider either the short
- term or long
- t erm behavior (mobility ) of the exposed populations and its potential influence on their exposure. We did not address short
- term human activity for two reasons. First, our experience with the NATA assessments (which modeled dail y activity using EPA’s H APEM model) suggests that, given our current understanding of microenvironment concentrations and daily activities, modeling short
- term activity would, on average, reduce risk estimates about 25% for particulate HAPs; it will also reduce risk estimates for gaseous HAPs, but typically by much less. Second, basing exposure estimates on average ambient concentrations at census block centroids may

underestimate or overestimate actual exposure concentrations at some residences. Further reducing exposure estimates for the most highl y exposed residents b y modeling their short
- term behavior could add a sy stematic low bias to these results. We did not address long
- term migration nor population growth or decrease over 70 years, instead basing the assessment on the assumption that each person’s predicted exposure is constant over the course of their lifetime which is assumed to be 70 years. In assessing cancer risk, we generall y estimated three metrics; the maximum individual risk (MIR), which is defined as the risk associated with a lifetime of exposure at the highest concentration; the population risk distribution; and the cancer incidence. The assumption of not considering short or long
- term population mobility does not bias the estimate of the theoretical MIR no r does it affect the estimate of cancer incidence since the total population number remains the same. It does, however, affect the shape of the distribution of individual risks across the affected population, shifting it toward higher estimated individual risks at the upper end and reducing the number of people estimated to be at lower risks, thereb y increasing the estimated number of people at specific risk levels
. When screening for potentially significant acute exposures, we used an estimate of the h ighest hourly ambient concentration at any off
- site location as the surrogate for the maximum potential acute exposure concentration for an y individual. 

### 2.4 **Ac ute Risk Screening and Refined A** **ssessments** 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 appro ach. This approach to risk assessment was endorsed b y the National Academ y of Sciences in its 1993 publication “Science and Judgment in Risk Assessment” and subsequently was adopted in the EPA’s “Residual Risk Report to Congress” in 1999.**Draft Risk Ass essment 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. Th is means that we begin with a screening assessment, which relies on readil y available data and uses conservative assumptions that in combination approximate a worst
- case exposure . The result of this screening process is that either the facility being asse ssed poses no acute health risks (i.e., it “screens out”), or that it requires further , more refined assessment. A refined assessment could u s e industry
- or site
- specific data on the temporal pattern of emissions, the layout of emission points at the faci lity , the boundaries of the facilit y, and /or the local meteorology . In some cases, all of these site
- specific data would be needed to refine the assessment; in others, lesser amount s of site
- specific data could be used to determine that acute exposures ar e not a concern, and significant additional data collection would not be necessary . Acute health risk screening was performed as the first step. We used conservative assumptions for emission rates, meteorology , and exposure location. We used the follo wing worst - case assumptions in our screening approach:

 Peak 1
- hour emissions were assumed to equal 10 times the average 1
- hour emission rates.  For facilities with multiple emission points, peak 1
- hour emissions were assumed to occur at all emission points at the same time.  For facilities with multiple emission points, 1
- hour concentrations at each receptor were assumed to be the sum of the maximum concentrations due to each emission point, regardless of whether those maximum concentrations occurred during the same hour.  Worst
- case meteorology (from one ye ar 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 per son was assumed to be located downwind at the point of maximum impact during this same 1
- hour period, but no nearer to the source than 100 meters.  The maximum impact was compared to multiple short
- term health benchmarks for the chemical being assessed to d etermine 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 benchmarks, we pursue refining our acute screening estimate s. 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 e missions 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 multiplier, therefore, the default emissions multiplier of 10 w as used.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

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### 2.5 **Multipathway**

**and env**  **ironmental 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 an y sources emitted an y haz ardous air pollutants known to be persistent and bioaccumulative in the environment (PB
- HAP). The PB
- HAP compounds or compound classes are identified for the screening from the EPA’s Air Toxics Risk Assessment L ibrary [ 8 ]. Examples of PB
- HAP are cadmium compounds, chlordane, chlorinated dibenzodioxins and furans, DDE, heptachlor, hexachlorobenzene, hexachlorocyclohexane, lead compounds, mercury compounds, methoxychlor, polychlorinated biphenyls, pol yc yclic organic matter (POM) , toxaphene, and trifluralin
. Emissions of lead, cadmium, and mercury were identified in the emissions inventories for both the Mineral Wool Production and Wool Fiberglass Manufacturing source categories
. These PB
- HAP emissions were evaluated for potential non
- inhalation risks and adverse environmental impacts using our recentl y - developed 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 potenti al ingestion risks for an y specified emission scenario by using a generic farming/fishing exposure scenario that simulates a subsistence environment. The screening scenario retains many of the ingestion and scenario inputs developed for EPA’s Human Health Risk Assessment Protocols (HHRAP) for hazardous waste combustion facilities. 6 In the development of the screening scenario a sensitivity

analy sis 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
- l evel 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 which the maximum human health risk woul d be 1 in a million for lifetime cancer risk or a hazard quotient of 1.0 for noncancer impacts. In evaluating the potential multi
- pathway risks from emissions of lead compounds, rather than developing a screening emission rate for them , we compared maxi mum estimated chronic (3
- month average) atmospheric concentrations with the current National Ambient Air Quality Standard (NAAQS) for lead. Values below the NAAQS were considered to have a low potential for multi
- pathway risks. 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 negligible and no furth er anal ys is was performed.

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/combus t/riskvol.htm#volume1**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  12 Additionally , we evaluated the potential for significant ecological exposures to non PB
- HAP from exceedances of chronic human health inhalation thresholds in the ambient air near these facilities. Human health dose
- response threshold values are generall y derived from studies conducted on laboratory

animals (such as rodents) and developed with the inclusions of uncertaint y factors that could be as high as 3000. As a result, these human threshold values are often significantl y lower than the level expected to cause an adverse effect in an exposed rodent. It should be noted that there is a scarcit y of data on the direct atmospheric impact of these HAPs on other receptors, such as plants, birds, and wildlife. Thus, if the maximum inhalation hazard in an ecosy stem is below the level of concern for humans, we have generall y concluded that mammalian receptors should be at no risk of adverse effects due to inhalation exposures from non PB
- HAP, and have assurance that other ecological receptors are also not at an y significant risk from direct atmospheric impact. In some isolated cases where we have data indicating potential adverse impacts on plants, birds, or other wildlife due to the direct atmospheric impacts of specific HAPs, we note that as an uncertainty and, where possible, refine our anal ysis by comparing our modeled impacts to available threshold values from the scientific literature. 

### 2.6 **Dose -**  **Response A ssessment**  **2.6.1 Sources of chronic dose**  **- response information**  Dose
- response assess ment (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 Office of Air Quality

Planning and Standards’ existing recommendations for HAPs [ 9 ], also used for NATA [ 10 ]. This information has been obtained from various sources and prioritized according to (1) conceptual consistency with EPA risk assessment guidelines and (2) level of peer review received. The prioritization process was aimed at incorporating into our assessments the best available science with respect to dose
- response information. The recommendations are based on the following sources, in order of priority : 1) US Environmental Protection Agency (EPA). EPA has developed dose
- response assessments for chronic exposure for many of the pollutants in this study . These assessments ty

pically provide a qualitative statement regarding the strength of scientific data and specify

a reference concentration (RfC, for inhalation) or reference dose (RfD, for ingestion) to protect against effects other than cancer and/or a unit risk estimate (URE, for inhalation) or slope factor (SF, for ingestion) to estimate the probability of developing cancer. The RfC is defined as an “ estimate (with uncertaint y spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable ris k of deleterious effects during a lifetime. ” The RfD is “an estimate (with uncertaint y spanning perhaps an order of magnitude) of a daily

oral exposure to the human population (including sensitive subgroups) that is likely

to be without an appreciable ris k 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 “an upper bound, approximating a 95 % confidence limit, on the increased cancer**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  13 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 Sy stem (IRI S) [ 11 ] is an EPA database that contains scientific health assessment information, including dose
- response information. All IRI S assessments since 1996 have also undergone ind ependent external peer review. The current IRI S process includes review b y EPA scientists, interagency reviewers from other federal agencies, and the public, and peer review by independent scientists external to EPA. New IRI S values are developed and old IR IS values are updated as new health effects data become available. Refer to the “IRI S Track” website for detailed information on status and scheduling of current individual IRI S assessments and updates ( http://cfpub.epa.gov/ncea/iristrac/index.cfm ). EPA’s science policy approach , under the current carcinogen guidelines, is to use linear low
- dose extrapolation as a default option for carcinogens for which the mode of action (MOA) has not been identified. We expect future EPA dose
- response assessments to identify nonlinear MOAs where appropriate, and we will use those analy ses (once they are peer reviewed) in our risk assessments. At this time, however, there are no available carcinogen dose
- r esponse assessments for inhalation exposure that are based on a nonlinear MOA
. 2) US Agency

for Toxic Substances and Disease Registry (ATSDR). ATSDR, which is part of the US Department of Health and Human Services, develops and publishes Minimum Risk L evels (MRLs) [ 12 ] for inhalation and oral exposure to man y toxic substances. As stated on the ATSDR web site: “ Following discussions with scientists within the Department of Health and Human Services (HHS) and the EPA, ATSDR chose to adopt a practice similar to that of the EPA's Reference Dose (RfD) and Reference Concentration (RfC) for deriving substance specific health guidance levels for non neoplastic endpoints .” The MRLis defined as “an estimate of dail y 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 MRL s as substance
- specific estimates to be used by health assessors to select environmental contaminants for further evaluation. Exposures above an MRL do not necessarily represent a threat, and MRLs are therefore not intended for use as predictors of adverse health effects or for setting cleanup levels. 3) California Environmental Protection Agency (CalEPA). The CalEPA Office of Envir onmental Health Hazard Assessment has developed dose
- response assessments for many substances, based both on carcinogenicity and health effects other than cancer. The process for developing these assessments is similar to that used by EPA to develop IRIS values and incorporates significant external scientific peer review. As cited in the CalEPA Technical Support Document for developing their chronic assessments 7 : “The guidelines for developing chronic inhalation exposure levels incorporate many recommendations of the U.S. EPA [ 13 ] and NAS [ 14 ].” The non
- cancer information includes available inhalation health risk guidance values expressed as chronic inhalation
7 Air Toxics Hot Spots Program, Risk Assessment Guidelines, Part III
- Technical Support Document for the Determination of Non
- cancer Chronic Reference Exposure Levels. Air Toxicology and Epidemiology Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. February 2000 ( http://www.oehha.ca.gov/air/chronic_rels/pdf/relsP32k.pdf )**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  14 reference exposure levels (REL s) [ 15 ]. CalEPA defines the RELas “the concentration level at or be low which no health effects are anticipated in the general human population.” CalEPA's quantitative dose
- response information on carcinogenicity by inhalation exposure is expressed in terms of the URE [ 16], defined similarly to EPA's URE. In developing chronic risk estimates, we adjusted dose
- response values for some HAPs based on professional judgment, as follows: 1) In the case of HAP categories such as gl ycol ethers and cyanide compounds, the most conservative dose
- response value of the chemical categ ory 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 unacceptable 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 appl y category - specific chemical speciation profiles appropriate to the so urce category

to develop a composite dose
- response value for the category
. 3) In 2004, the EPA determined that the Chemical Industry Institute of Toxicology

(CIIT) cancer dose
- response value for formaldehyde (5.5 x 10 - 9 per μg/m 3 ) was based on better science than the IRIS 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. Based on s ubsequent published research , however, EP A changed its determination regarding the CIIT model and in 2010 the EPA returned to using 1991 IR IS value
. [US EPA , 2010. ] [ 17 ] EPA has been working on revising the formaldeh yd e IRI S assessment and the National Academy of Sciences (NAS) completed its rev iew of the EPA’s draft assessment in May of 2011 and EPA has been working on revising the formaldehyde assessment (http://www.nap.edu/catalog.php?record_id=13142). EPA is reviewing the public comments and the NAS independent scientific peer review. EPA w ill follow the NAS Report recommendations and will present results obtained by implementing the BBDR model for formaldehyde. EPA will compare these estimates with those currently presented in the External Review draft of the assessment and will discuss th eir strengths and weaknesses. As recommended by the NAS committee, appropriate sensitivity and uncertaint y analyses will be an integral component of implementing the BBDR model. The draft IR IS assessment will be revised in response to the NAS peer review and public comments and the final assessment will be posted on the IRI S database. In the interim, we will present findings using the 1991 IRIS value as a primary estimate, and may

also consider other information as the science evolves. 4) A substantial pr oportion of POM reported to EPA’s nati onal emission inventory (NEI) are not speciated into individua l compounds. As a result, it i s necessary to apply the same simplifying assumptions to assessment s that are used in NATA. [ 18 ] The NATA approach partitions POM into eight different non - overlapping “groups” that are modeled as separate pollutants. Each POM group comprises POM species of similar carcinogenic potency , for which we can appl y the same URE.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  15 5) A chronic screening level of 163 ug/m 3 was developed fo r carbon ylsulfide (COS) from a No Observed Adverse Effects Level (NOAEL) of 200 ppm based on brain lesions and neuroph ys iological alterations in r odents. A more detailed discussion of the studies used to develop the COS chronic screening level is provide d in Appendix 8. The screening level includes a total uncertainty factor (UF) of 3,000: 10x for extrapolation for interspecies differences, 10x for consideration of intraspecies variability, 10x for extrapolation from subchronic to chronic duration, and 3 x for database insufficiencies. See section 5 of this document for a detailed discussion of exposure modeling 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 necessaril y indicate that further action is required. The emissions inventory

for the Wool Fiberglass Manufacturing and for the Mineral Wool Production source categories 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) 8 = cancer risk per μg/m 3 of average lifetime exposure. Sources: IRI S = EPA Integrated Risk Information Sy stem, CAL = California EPA Office of Environmental Health Hazard Assessment
. **Pollutant CAS Number**  **9 URE**  **5 (1/μg/m3)**  **Source** Arsenic compounds 7440382 4.3E
- 03 IR IS Beryl lium compounds 7440417 2.4E
- 03 IR IS Cadmium compounds 7440439 1.8E
- 03 IR IS Chromium (VI) compounds 18540299 1.2E
- 02 IR IS Formaldeh yd e a 50000 1.3E
- 05 IR IS a - The EPA has used the CIIT URE value, 5.5X10 - 9 per mg/m 3 , to characterize formaldehyde cancer risk in some instances.

8 The URE is the upper
- bound excess cancer risk estimated to result from continuous lifetime exposure to an ag ent 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. 9 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 Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  16

**Table 2.6 -**  **1 (b) Dose -**  **Response Values for Chronic Inhalation Exposure to Noncarcinogens**  RfC (reference inhalation concentration) = an est imate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IR IS = EPA Integrated Risk Information Sy stem, CAL= California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry , **Pollutant CAS Number**  **6 RfC**  **(mg/m3) Source**  **10** Arsenic compounds 7440382 1.5E
- 05 CA L Beryl lium compounds 7440417 2.0E
- 05 IR IS
- M Cadmium compounds 7440439 1.0E
- 05 ATSDR
- D Carbonyl sulfide 463581 0.163 ORD Screening Chromium (VI) compounds 18540299 1.0E
- 04 IR IS
- M Formaldeh yd e 50000 0.0098 ATSDR Hydrochloric acid 7647010 0.02 IR IS
- L Lead compounds 7439921 1.5E
- 04 EPA OAQPS Manganese 7439965 5.0E
- 05 IR IS
- M Methanol 67561 4 CAL Mercury (elemental) 7439976 3.0E
- 4 IR IS
- M Nickel compounds 7440020 9.0E
- 05 ATSDR Phenol 10952 0.2 CAL Selenium compounds 7782492 0.02 CAL **2.6.2 Sourc**  **es 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 [ 19 ]
. Depending on availability , the res ults from screening acute assessments are compared to both “no effects” reference levels for the general public, such as the California Reference Exposure Levels (REL s), as well as emergency response levels, such as Acute Exposure Guideline Levels (AEGLs) and Emergency Response Planning Guidelines (ERPGs), with the recognition that the ultimate interpretation of an y potential risks associated with an estimated exceedance of a particular reference level depends on the definition of that level and an y limitat ions expressed therein. Comparisons among different available inhalation health effect reference values (both acute and chronic) for selected HAPs can be found in an EPA document [ 20 ].

10 The descriptors L (low), M (medium), and H (high) have been added for IRIS RfC values to indicate the overall level of confidence in the RfC value, as reported in IRIS.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  17 **California Acute Reference Exposure Levels (RELs ).**  The California Env ironmental Protection Agency

(CalEPA) has developed acute dose
- response reference values for man y substances, expressing the results as acute inhalation Reference Exposure Levels (RELs). The acute REL (http://www.oehha.ca.gov/air/pdf/acuterel.pdf ) is defined by

CalEPA as “ the concentration level at or below which no adverse health effects are anticipated for a specified exposure duration [ 21 ]
. REL s are based on the most sensitive, relevant, adver se health effect reported in the medical and toxicological literature. RELs are designed to protect the most sensitive individuals in the population by the inclusion of margins of safet y. Since margins of safet y are incorporated to address data gaps and uncertainties, exceeding the RELdoes not automatically indicate an adverse health impact. ” Acute REL s are developed for 1
- hour (and 8
- hour) exposures. The values incorporate uncertaint y factors similar to those used in deriving EPA’s Inhalation Reference Concentrations (RfCs) for chronic exposures (and, in fact, California also has developed chronic RELs). **Acute Exposure Guideline Levels (AEGLs** ). AEGL s are developed by the National Advisory Committee (NAC) on Acute Exposure Guideline Levels (NAC/AEGL) f or Hazardous Substances , and then reviewed and published b y the National Research Council A s described in the Committee’s “Standing Operating Procedures (SOP) ” ( http://www.epa.gov/opptintr/aegl/pu bs/sop.pdf

), AEGLs “represent threshold exposure limits for the general public and are applicable to emergency exposures ranging from 10 min to 8 h.” Their intended application is “for conducting risk assessments to aid in the development of emergency

pr eparedness and prevention plans, as well as real time emergency response actions, for accidental chemical releases at fixed facilities and from transport carriers.” The document states that “the primary purpose of the AEGL program and the NAC/AEGL Committ ee is to develop guideline levels for once - in
- a - lifetime , short
- term exposures to airborne concentrations of acutel y toxic, high
- priority chemicals.” In detailing the intended application of AEGL values, the document states that , “ Itis anticipated that the AEGL values will be used for regulatory and nonregulatory

purposes by

U.S. Federal and State agencies, and possibly

the international community in conjunction with chemical emergency response, planning, and prevention programs. More specifically , the A EGL 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 transpo rt 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 notab le discomfort, irritation, or certain asy mptomatic nonsensory

effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure. ”

“ AEGL
- 2 is the airborne concentration (expressed as ppm or mg/m 3 ) of a substance a bove which it is predicted that the general population, including susceptible individuals, could**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  18 experience irreversible or other serious, long
- lasting adverse health effects or an impaired ability to escape. ”

“ Airborne concentrations below AEGL
- 1 repres ent exposure levels that can produce mild and progressivel y increasing but transient and nondisabling odor, taste, and sensory irritation or certain as ymptomatic, nonsensory effects. With increasing airborne concentrations above each AEGL, there is a progressive increase in the likelihood of occurrence and the severity of effects described for each corresponding AEGL
. Although the AEGL values represent threshold levels for the general public, including susceptible subpopulations, such as infants, children , the elderly , persons with asthma, and those with other illnesses, it is recognized that individuals, subject to unique or idiosy ncratic responses, could experience the effects described at concentration s below the corresponding AEGL.” **Emergency Response Planning Guidelines (ERPGs).**  The American Industrial Hygiene Association (AIHA) has developed Emergency Response Planning Guidelines (ERPGs) [ 22 ] for acute exposures at three different levels of severity . These guidelines represent concentrations for exp osure of the general population (but not particularly sensitive persons) for up to 1 hour associated with effects expected to be mild or transient (ERPG
- 1), irreversible or serious (ERPG
- 2), and potentially life
- threatening (ERPG
- 3). ERPG values ( http://www.aiha.org/1documents/Committees/ERP
- erpglevels.pdf ) are described in their supporting documentation as follows: “ Emergency Response Planning Guidelines (ERPGs) were developed for emergency planning and are intended as health based guideline concentrations for single exposures to chemicals. These guidelines (i.e., the ERPG Documents and ERPG values) are intended for use as planning tools for assessing the adequacy of accident prev ention and emergency response plans, including transportation emergency planning and for developing community emergency

response plans. The emphasis is on ERPGs as planning values: When an actual chemical emergency occurs there is seldom time to measure airborne concentrations and then to take action. ” ERPG
- 1 and ERPG
- 2 values are defined by AI HA as follows:

“ ERPG
- 1 is the maximum airborne concentration below which it is believed that nearl y all individuals could be exposed for up to 1 hour without experiencing other than mild transient adverse health effects or without perceiving a clearly defined, objectionable odor. ”

“ ERPG
- 2 is the maximum airborne concentration below which it is believed that nearl y all individuals could be exposed for up to 1 ho ur without experiencing or developing irreversible or other serious health effects or s ymptoms which could impair an individual's ability to take protective action. ” The emissions inventory

for the Wool Fiberglass Manufacturing and for the Mineral Wool Pr oduction source categories includes emissions of 9 HAP with relevant and available**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  19 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 Beryl lium comp ounds 7440417 0.025 Carbonyl sulfide 463581 140 Formalde hyde 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 information from the previous steps is integrated and an overall conclusion about risk is sy nthesized that is complete, informative, and useful for decision makers. In general, the nature of this risk characterization depends on the information available, the application of the risk information and the resources available. In all cases, major issues associated with determining the nature and extent of the risk are identified and di scussed. Further, the EPA Administrator’s March 1995 Policy for Risk Characterization [ 23 ] specifies that a risk characterization “be prepared in a manner that is clear, transparent, reasonable, and consistent with other risk characterizations of similar s cope prepared across programs in the Agency .” These principles of transparency

and consistency

have been reinforced by

the Agency’s Risk Characterization Handbook [ 24 ], in 2002 by the Agency ’s information quality guidelines [ 25 ], and in the OMB/OSTP Septemb er 2007 Memorandum on Updated Principles for Risk Analy sis 11 , and are incorporated in these assessments. Estimates of health risk are presented in the context of uncertainties and limitations in the data and methodology . Through our tiered, iterative anal yt ical approach, we have attempted to reduce both uncertainty

and bias to the greatest degree possible in these assessments, within the limitations of available time and resources. We provide summaries of risk metrics

11 Memorandum f

or the Heads o f Executive Departments and Agencies
- Updated Principles for Risk Analysis ( September 19, 2007 ), From Susan E. Dudley, Administrator, Office of Information and Regulatory Affairs, Office of Management and Bud get; and Sharon L. Hays, Associate Director and Deputy Director for Science, Office of Science and Technology Policy ( http://www.whitehouse.gov/omb/memoranda/fy2007/m07
- 24.pdf )**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  20 (including maximum individual cancer risks and noncancer hazards, as well as cancer incidence estimates) along with a discussion of the major uncertainties associated with their derivation to provide decision makers with the fullest picture of the assessment and its limitations. For each car cinogenic HAP included in an assessment that has a potency estimate available, individu al and population cancer risks we re calculated by multiplying the corresponding lifetime average exposure estimate by the appropriate URE. This calculated cancer risk i s defined as the upper
- bound probability of developing cancer over a 70
- y r period (i.e., the assumed human lifespan) at that exposure. Because UREs for most HAPs are upper
- bound estimates, actual risks at a given exposure level may be lower than predicted , and could be zero. For EPA’s list of carcinogenic HAPs that act b y a mutagenic mode
- of
- action [ 26], we applied EPA’s Supplemental Guidance for Assessing Susceptibility from Early
- Life Exposure to Carcinogens [ 27]
. This guidance has the effect of adjustin g the URE by factors of 10 (for children aged 0
- 1), 3 (for children aged 2
- 15), or 1.6 (for 70 ye ars 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 po llutants by a factor of 1.6. Inaddition, although onl y 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]py rene equivalence, based on ev idence that carcinogenic POM have the same mutagenic mechanism of action as does benzo[a]py rene. For this reason , EPA implem entation policy [ 28 ] recommends appl yi ng the Supplemental Guidance to all carcinogenic PAHs for which risk estimates are based on re lative potency . Accordingl y, we applied the Supplemental Guidance to all unspeciated POM mixtures. In creased cancer incidence for the entire receptor population within the area of anal ys is wa s estimated by

multiplying the estimated lifetime cancer risk f or each census block by

the number of people residing in that block, then summing the results for the entire modeled domain. This lifetime population incidence estimate wa s divided by 70 years to obtain an estimate of the number of cancer cases per ye ar. 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 rati o. The “hazard quotient” (HQ) is the estimated exposure divided by a refer ence level (e.g., the RfC). For a given HAP, exposures at or below the reference level (HQ ≤1) are not likel y to cause adverse health effects. As exposures increase above the reference level (HQs increasingl y greater than 1), the potential for adverse eff ects increases. For exposures predicted to be above the RfC, the risk characterization includes the degree of confidence ascribed to the RfC values for the compound(s) of concern (i.e., high, medium, or low confidence) and discusses the impact of this on possible health interpretations. The risk characterization for chronic effects other than cancer is expressed in terms of the HQ for inhalation, calculated for each HAP at each census block centroid. As discussed above,**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  21 RfCs incorporate generally conser vative 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

t o 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 va lue 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, additiona l information is used to determine if there is a potential for significant acute risks. **2.7.2 Mixtures**  Since most or all receptors in these assessments receive exposures to multiple pollutants rather than a single pollutant, we estimated the aggregate health ri sks associated with all the exposures from a particular source category combined. To combine risks across multiple carcinogens, our assessments use the mixtures guidelines’ [ 29 , 30 ] default assumption of additivity of effects, and combine risks by summing th em using the independence formula in the mixtures guidelines. In assessing noncancer hazard from chronic exposures, in cases where different pollutants cause adverse health effects via completel y different modes of action, it may be inappropriate to aggre gate HQs. In consideration of these mode
- of
- action differences, the mixtures guidelines support aggregating effects of different substances in specific and limited way s. To conform to these guidelines, we aggregated non
- cancer HQs of HAPs that act by sim ilar toxic modes of action, or (where this information is absent) that affect the same target organ. This process creates, for each target organ, a target
- organ - specific hazard index (TOSHI ), defined as the sum of hazard quotients for individual HAPs that affect the same organ or organ s ys tem. A ll TOSHI calculations presented here were based exclusively on effects occurring at the “ critical dose” (i.e., the lowest dose that produces adverse health effects). Although HQs associated with some pollutants have been aggregated into more than one TOSHI , this has been done only in cases where the critical dose affects more than one target organ . Because impacts on organs or s ys tems that occur above the critical dose have not been included in the TOSHI calculati ons, some TOSHIs may have been underestimated. As with the HQ, the TOSHI should not be interpreted as a probability of adverse effects, or as strict delineation of “safe” and “unsafe” levels. Rather, the TOSHI is another measure of the potential for adve rse health outcomes associated with pollutant exposure, and needs to be interpreted carefully

by health scientists and risk managers. Because of the conservative nature of the acute inhalation screening and the variable nature of emissions and potential e xposures, acute impacts were screened on an individual pollutant basis, not using the TOSHI approach.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  22 

### 3 **Risk Results for the Mineral**  **Wool Production**  **3.1 Source Category**  **Description and Results** Mineral wool is a fibrous, glass y substance made from natural rock (such as basalt), blast furnace slag, or other similar materials and 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 material 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 ty pically composed of a phenol
formaldeh yde resin, water, urea, silane, ammonia, and ammonium sulfate. The application of binder is foll owed b y 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 chamber, 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 major source mineral wool production facilities in the United States that would be subject to the rule. Currentl y, there are seven mineral wool production facilities nationwide
. Based on emis sions data collected from the industry , these 7 facilities emitted a reported total of 4 62 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 fo r the Mineral Wool Production source category
. Based on the se data, the HAP emitted in largest quantities in total from these facilities are carbon ylsulfide, formaldehyde, phenol, hydrochloric acid, and h ydrogen fluoride ; emissions of these 5 pollutants account for 99 .8 percent of the total HAP emissions by mass from the data set. Carbon ylsulfide , hydrochloric acid, and hydrogen fluoride were reported as an emission for all o f the facilities. Formaldeh yde and phenol are also emitted in large quantities , but from fewer facilities; no more than three facilities 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 the binder, curing , and cooling. Raw material feed rates in mineral wool processes are essentially constant with minimal fluctuation (approximately ± 10 percent). Consequently , emissions also have minimal fluctuation [ 31 ]. In refining the acute risk assessment, a short
- te rm emissions multiplier of 3 was used to estimate the maximum 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 Mi neral Wool Production source category . Emissions of PB HAP reported in the data set for the mineral wool production source category

include lead, cadmium, and mercury compounds.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  23

**Table 3.1**  **- 1**  **Summary of Emissions from the**  **Minera l Wool Production**  **Ca tegory and Availability of**  **Dose -**  **Response Values**

**HAP Emissions**  **(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** 

**Concen tration**  **for Noncancer? Health** 

**Benchm ark**  **Values for Acute Noncancer?**  Carbonyl Sulfide 224 7 Y Phenol 177 3 Y Y Hydrochloric acid 23 7 Y Y Formaldehyde 20 3 Y Y Y Hydrogen Fluoride 17 7 Selenium 0.28 7 Y Methanol 0.16 3 Y Y Manganes e 0.14 7 Y Chromium III 0.04 7 Lead 0.03 7 Y Y Arsenic 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 Particulate 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 r eport contains the acute noncancer values for the HAP emitted 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/atw/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 e stimates presented here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients, as well as the results of our preliminary screen for potential non
- inhalation risks from PB HAP. Also presented are the HAP “drivers,” which are the HAP that collectively

contribute 90 percent of the maximum cancer risk or maximum hazard index at the highest exposure l ocation
.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  24
Table s 3 .2
- 1 and 3.2
- 2 summarize the chronic and acute 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 4 in a million. The major contributor to th is risk is formaldeh yde
. Approximately 1 , 65 0 people were estimated to have cancer risks above 1 in a million as a result of the emissions from 1 facility . The maximum chronic non
- cancer TOSHI value for the source category could be up to 0.04 with emissions of formaldeh yd e dominating those impacts, indicating no significant 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 (RELof 8 for formaldeh yde ) 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 th e docket for a detailed description of how the refined emissions 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 b y determining the highe st HQ value that is outside facility boundaries. Inthis case, the refined anal ys is did not change the acute anal ys is results. Table 3
. 2
- 2 provides more information on the acute risk estimates for formaldehyde, the only HAP that had a worst - case screenin g acute HQ greater than 1 for an y 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 RT R risk assessment methodologies 12 , 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 generall y more data gaps and inconsistencies in acute refer ence values than there are in chronic reference values. By definition, the acute CA
- RELrepresents 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 exceeded 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. His torically , c omparisons of the estimated maximum off
- site one
- hour exposure levels have not been ty pically 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 generall y considered protective for the general public since they

are designed to protect the worker population (presumed healthy adults) for short duration (<15 minute) increases in exposure 13

. As a result, f or most

12 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 13 U.S. EPA. (2009) Chapter 2.9 Chemical 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 http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  25 chemicals, the 15
- minute occupatio nal ceiling values are set at levels higher than a one
- hour 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 formaldeh yde 13

. T he worst - case maximum estimated 1
- hour exposure to formaldeh yd e outside the facilit y fence line for the mineral wool production source category is 0. 47 mg/m 3 . This estimated worst - case exposure exceeds the 1
- hour REL b y a factor of 8 (HQ REL = 8) and is below the 1
- hour AEGL
- 1 (HQ AE GL
- 1 = 0.4). T his exposure estimate does not exceed the AEGL
- 1, or exceed the workplace ceiling level guideline for the formaldeh yd e value developed by National Institutes for Occupational Safet y and Health (NIOSH) 14 “ for any 15 minute period in a work day” (NIOSH REL
- ceiling value of 0.12 mg/m 3 ; HQ NI OSH = 4 ). T he estimate is at the value developed b y the American Conference of Governmental Industrial Hygienists (ACGIH) 15 as “not to be exceeded at an y time” ( ACGIH TLV
- ceiling value of 0.37 mg/m 3 ; HQ ACGIH = 1). Additionally , the estimated maximum acute exposure exceeds the Air Quality Guideline value that was developed b y the World Health Organization 16 for 30
- minute exposures (0.1 mg/m 3 ; HQ WHO = 5 )
. Chronic n oncancer 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 ( 0.04 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 assessments. 17 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 f

acilities
. 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

14 National Institutes for Occupational Safety and H ealth (NIOSH). Occupational Safety and Health Guideline for Formaldehyde; http://www.cdc.gov/niosh/docs/81
- 123/pdfs/0293.pdf 15 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. 16 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
. 17 ICF International. TRIM
-B ased Multipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  26 cancer risk could be up to 10 in a million, and that the maximum chronic noncancer TOSHI value could be as high as 0.1 at the MACT
- a llowable emissions level.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  27
**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) 4 18 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 0 n/a Greater than or equal to 1 in 1 million 1 formaldehyde **Chronic Noncancer Risks** Maximum Hazard Index 0. 0 4 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**  **]** 8 0. 4 formaldehyde

(REL) formaldehyde (AEGL
- 1 , ERPG
- 1) ) Number of Facilities With Potential for Acute Effects 1 formaldehyde **Po pulation Exposure**  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 0 n/a Greater than or equal to 1 in 1 million 1 , 7 0 0 n/a Number of People Exposed to Noncancer Respiratory Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.00 0 4 18 n/a Contribution of HAP to Cancer Incidence: Formaldehyd e Arsenic compounds 64 % 33 % n/a

18 We note that the MIR for this source category would be 0.7
- in
- 1 million if the CIIT URE for formaldehyde had been used in the assessment. The total cancer incidence would decrease by 64%. There is an ongoing IRIS reassessment for formaldehyde, 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 Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  28 **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**

**(m g/m** **3 )**  **AEGL -**  **1 (1 -** 

**hr) (mg/m 3**  **) ERPG**  **- 1** 

**(m g/m** **3 )**  **AEGL -**  **2**

**(1 -**  **hr) (m**  **g/m 3**  **) ERPG**  ****

**2 (m**  **g/m 3**  **) HAP**  **Max. 1 -**  **hr.**

**Air Conc. (m**  **g/m 3**  **)** Formaldehyde 0.47 8 0.4 0.0 27 0.055 1.1 1.1 17 17

Notes on Refined Process: 1) The screening was performed fo r all emitted HAP with available acute dose
- response values. Only those pollutants whose screening HQs were greater than 1 for at least one acute threshold value are shown in the table. 2) HAP with available acute dose
- response values which are not in the table do not carry any potential for posing acute health risks, based on an analysis of currently available emissions data. Notes on Acute Dose
- Response Values: REL

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

– Acute exposure guideline levels represent emergency exposure (1
- hour) limits for the general public. AE GL
- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience effects that are notable discomfort, but which are transient and reversible upon cessation of exposure. AE GL
- 2 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experien ce irreversible or other serious, long
- lasting adverse health effects of an impaired ability to escape. EPRG

– Emergency Removal Program guidelines represent emergency exposure (1
- hour) limits for the general public. ERPG
- 1 is the maximum level below whic h it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing other than mild, transient adverse health effects. ERPG
- 2 is the maximum exposure below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual’s abilit y to take protective action.



### 4 **Risk Results for the**  **Wool Fiberglass Manufacturing**  **Source Category**  **4.1 Source Ca**  **tegory Description and Results**  Wool fiberglass is manufactured in a process that forms thin fibers from molten glass. A ty pical wool fiberglass manufacturing line consists of the following processes: (1) Preparation of molten glass, (2) formation of fiber s into a wool fiberglass mat, (3) curing the binder
coated fiberglass mat, (4) cooling the mat (not alway s present), and (5) backing, cutting, and packaging. Ty

pically , the binder consists of a solution of phenol
- formaldehyde resin, water, urea, lignin, s ilane, and ammonia. Wool fiberglass products are primaril y 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 f

iberglass currentl y 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 “an y**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  29 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 apply

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. Nine of these facilities are not consider ed major sources. HAP are emitted from wool fiberglass glass
- melting furnaces, including arsenic, chromium, and lead. Organic HAP (formaldeh yde, phenol, and methanol) are released from RS forming, curing, and cooling processes and FA forming and curing processes. Formaldeh yde, 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 cat egory data set ( of 29 facilities) are summarized in Table 4.1
- 1 . The total HAP emissions for the source category are approximately 1,874 tons per ye ar. Based on these data, the HAP emitted in the largest quantities across these 29 facilities are: methano l, formaldeh yde, phenol, hydrogen fluoride, and hydrochloric acid . Emissions of these 5 HAP make up 99.93 percent of the total emissions by

mass. For the Wool Fiberglass Manufacturing source category, data were not available to develop a refined emission s multiplier. Therefore, the default emissions multiplier of 10 was used for the acute risk analy sis. Persistent and bioaccumulative HAP (PB HAP) reported as emissions from these facilities include lead, cadmium, and mercury compounds
. 19

19 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Volume 1, EPa
- 453K
- 04
- 001A, as referenced in the ANPRM and provided on the EPA’s Technology Transf er Network website for Fate, Exposure, and Risk Assessment at http://www.epa.gov/ttn/fera/risk_atra_vol1.html
.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  30

**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**

**Benchm ark**  **Values for Acute Noncancer?**  Phenol 403 26 Y Y Hydrochloric acid 12 29 Y Y Formaldehyde 618 26 Y Y Y Hydrogen Fluoride 20 29 Selenium 0.15 29 Y Methanol 820 26 Y Y Manganese 0.13 29 Y Chromium III 0.05 29 Lead 0.14 29 Y Y Arsenic 0.05 29 Y Y Y Nickel 0.12 29 Y Y Antimony 0.04 29 Cadmium 0.02 29 Y Y Y Cobalt 0.02 29 Y Elemental Gaseous Mercury 0.04 29 Y Y Y Chromium (VI) 0.52 29 Y 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 cla ssified as polycyclic organic matter (POM), emissions were grouped into POM subgroups as found on EPA’s Technology Transfer Network website for the 2002 National
- Scale Air Toxics Assessment at http://www.epa.gov/nata2002/methods.html#pom ( Approach to Modeling POM ). 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 he re 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 preli minary screen for potential non
- inhalation**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  31 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 40 in a million. T he major contributor to the risk is Chromium (VI) . Approximately 849 ,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 c ould be up to 0.2 with emissions of formaldeh yde 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 be nchmark, 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 b y determining the highest HQ value that is outside facility boundaries. In this case, the refined analy sis did not change the acute anal ys is 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 b etter 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 20 , 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 generall y more data gaps and inconsistencies in acute reference values than there are in chronic reference valu es. By definition, the acute CA
- RELrepresents 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 e xceeded 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 ty pically 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 generall y considered protective for the general public since they

are designed to protect the worker population (presumed healthy adults) for short duration (<15 minute) increases in exposure 21 . As a result, f or most chemicals, the 15
- minute occupational ceiling values are set at levels higher than a o ne - hour

20 The SAB peer review

of RTR Risk Assessment Methodologies is available at: http://yo semite.epa.gov/sab/sabproduct.nsf/4AB3966E263D943A8525771F00668381/$File/EPA
- SAB
- 10
- 007
- unsigned.pdf 21 U.S. EPA. (2009) Chapter 2.9 Chemical Specific Reference Values for Formaldehyde in Graphical Arrays of Chemical
- Specific Health Effect Reference Value s for Inhalation Exposures (Final Report). U.S. Environmental Protection Agency, Washington, DC, EPA/600/R
- 09/061, and available on
- line at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  32 AEGL
- 1 , making comparisons to them irrelevant unless the AEGL
- 1 or ERPG
- 1 levels are exceeded21 . Such is not the case when comparing the available acute inhalation health effect reference values for formaldeh yde 21

. T he worst - case maximum estimate d 1
- hour exposure to formaldeh yd e outside the facilit y fence line for the wool fiberglass manufacturing source category is 1. 92 mg/m 3 . This estimated worst
- case exposure exceeds the 1
- hour RELby a factor of 30 (HQ REL = 30) and the 1
- hour AEGL
- 1 (HQ AE GL
- 1 = 2). T his exposure estimate also exceeds multiple workplace ceiling level guidelines for formaldeh yd e , including the value developed by the American Conference of Governmental Industrial Hygienists (ACGIH) 22 as “not to be exceeded at an y time” (ACGIH TLV
- ceiling value of 0.37 mg/m 3 ; HQ ACGIH = 5 ) , and the value developed by the National Institutes for Occupational Safety and Health (NIOSH) 23 “ for any 15 minute period in a work day” (NI OSH REL
- ceiling value of 0.12 mg/m 3 ; HQ NIOSH = 16 ). Additionally , the es timated maximum acute exposure exceeds the Air Quality Guideline value that was developed b y the World Health Organization24 for 30
- minute exposures (0.1 mg/m 3 ; HQ WHO = 19 )
. Chronic noncancer target organ specific hazard indices (HIs) were calculate d for e very 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 screening
- level evaluation of the potential human health risks associated with emissions of PB HAP. Reported emissions of PB HAP were compared to emission thresholds established by EPA for the purposes of the RTR risk assessments. 25 The PB HAP 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 for phenol, methanol, and formaldeh yde emissions. For hexaval ent 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

22 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. 23 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 24 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
. 25 ICF International. TRIM
-Based M ultipathway Screening Scenario . Prepared for U.S. Environmental Protection Agency, Research Triangle Park, NC. October 2008.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  33 the max imum 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 Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  34
**Table 4.2 -**  **1 Summary of Source Category Le**  **vel Inhalation Risk s for**  **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 Cancer Risk (in 1 million) 40 26 Cr (VI) , 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 Hazard 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 11,641 n/a Greater than or equal to 1 in 1 million 849,000 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) 0.05 26 n/a Contribution of HAP to Cancer Incidence Formaldehyde Cr (VI) Arsenic Compounds 52% 47% 1% n/a

26 We note that the MIR for this source category would not change if the CIIT URE for formaldehyde had been used in the assessment , although the total cancer incidence would decrease by 52%. The MIR for the source category would remain at 40 due to Cr (VI). There is an ongoing IRIS reassessment for formaldehyde, and future RTR risk assessments will use the cancer potency for formal dehyde that results from that reassessment. As a result, the current results may not match those of future assessments.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  35

**Table 4.2 -**  **2 Summary of**  **Refined Acute**  **Results for Wool 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**

**(m g/m** **3 )**  **AEGL -**  **1**

**(1 -**  **hr) (m**  **g/m 3**  **) ERPG**  **- 1** 

**(m g/m** **3 )**  **AEG**

**L -**  **2 (1**  **- hr)**  **(m g/**  **m 3**  **) ERP**  **G -**  **2 (m**  **g/ m** **3 )**  **HAP Max. 1**  **- hr.** 

**Air Conc. (m**  **g/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 screening HQs were greater than 1 for at least one acute threshold value are shown in the table. 2) HAP with available acute dose
- response values which are not in the table do not carry any potential for posing acute health risks, based on an analysis o f 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. AE GL

– Acute exposure guideline levels represent emergenc y exposure (1
- hour) limits for the general public. AE GL
- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience effects that are notable discomfort, but which are transient and reversible upon cessation of exposure. AE GL
- 2 is the exposure level above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long
- lasting adverse health effects of an impaired ability to escape. EPRG

– Emergency Removal Program guidelines represent emergency exposure (1
- hour) limits for the general public. ERPG
- 1 is the maximum level below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing other than mild, transient adverse health effects. ERPG
- 2 is the maximum exposure below which it is believed that nearly all individuals could be exposed for up to 1 hour without experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual’s ability to take protective action. 

### 4.3 **Au xiliary** 

**Risk Characterization** As indicated in Section 4.2, the maximum lifetime individual cancer risks for the Wool Fiberglass Manufacturing source category c ould be as high as 40 in a million based on actual emissions. The major contributor to this cancer risk is c hromium (VI) that is emitted from the furnace refractory

brick as it breaks down over time. The greatest amount of c hromium (VI) is emitted from the Certainteed Facility in Kansas City , Kansas that uses a ty pe 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 t ypicall y composed of Al 2 O 3 , Al 2 0 3 - SiO 2 , ZrO 2 , with or without Cr 2 O 3 added, and dense Cr2 O 3 .[ 32 , 33 ] Refractory brick breaks down over time, and therefore, must be replaced periodicall y (approximately ev ery 7
- 14 years depending on the t yp e 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 Industry , 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. Therefore, we performed an auxiliary risk characterization analy sis to assess the maximum**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  36 indivi dual lifetime cancer risks of the o ther 28 Wool Fiberglass facilit ies switching to high c hromium brick. For the auxiliary risk characterization anal ys is it was assumed that the Cr (VI) emissions for each facility would be the same as that for the Certaint eed Facilit y in Kansas City , Kansas ( 420 lbs per year per furnace of Cr(VI))
. The results of the auxiliary anal ys is (Table 4.2
- 3) show that 14 facilities would have maximum individual lifetime cancer risks greater than 100 in a million, with the highest facility at 800 in a million. Under this scenario , 460 ,000 people would be exposed to risks of greater than 10 in a million and over 7 million people would be exposed to cancer risks of greater than 1 in a million
. **Table 4.2 -**  **3 Summary of Source Cat**  **egory 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 Facilities Identified in NEI and Modeled in Auxiliary Risk Assessment 29 n/a **Cancer Risks** Maximum Individual Lifetime Cancer Risk (in 1 million) 8 00 Cr (VI) Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1 million 14 Cr (VI), formaldehyde Greater than or equal to 10 in 1 million 28 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 Modeled 27,000,000 n/a Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1 million 8,100 n/a Greater than or equal to 10 in 1 million 460,000 n/a Greater than or equal to 1 in 1 million 7,300,000 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.29 n/a Contribution of HAP to Cancer Inc idence Formaldehyde Cr (VI) 6 % 94 % n/a**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  37


### 5 **General Discussion of Uncertainties and How They**  **Have Been Ad**  **dressed 5.1**  **Exposure Modeling Uncertainties** Although every

effort has been made to identify all the relevant facilities and emission po ints, as well as to develop accurate estimates of the annual emission rates for all relevant HAP, the uncertainties in our emission inventory likel y dominate the uncertainties in our exposure modeling estimates. The chronic exposure modeling uncertainties are considered relativel y small in comparison, since we are using EPA’s refined local dispersion model with site
specific parameters and reasonabl y representative meteorology. If an ything, the population exposure estimates are biased high b y not accounti ng for short
- or long
- term population mobility , and b y neglecting processes like deposition, plume depletion, and atmospheric degradation. Additionally , estimates of the maximum individual risk (MIR) contain uncertaint y , because they are deriv ed at census block centroid locations rather than actual residences. This uncertainty is known to create potential underestimates and overestimates of the actual MIR values for individual facilities, but, 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
- ye ar chronic exposure period, leading to a potential upward bias in both the MIR and population risk estimates; nor did we fact or 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

anal ys is performed for the 1999 NATA found that the selection of the m eteorology

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 predicted value. This variability translates directly to the predicted expos ures and risks in our assessment, indicating that the actual risks could vary from 17% lower to 84% higher than the predicted values. We have purposel y biased the acute screening results high, considering that they depend upon the joint occurrence of independent factors, such as hourly emissions rates, meteorology and human activity

patterns. Furthermore, in cases where multiple acute threshold values are considered scientificall y acceptable we have chosen the most conservative of these assessments, errin g on the side of overestimating potential health risks from acute exposures. In the cases where these results indicated the potential for exceeding short
- term health thresholds, we have refined our assessment b y developing a better understanding of the ge ography

of the facility

relative to potential exposure locations and the true variability of short
- term emission rates.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  38



### 5.2 **Uncertainties in the Dose**  **- Response Relationships**  Inthe sections that follow, separate discussions are provided on uncertainty a ssociated with cancer potency

factors and for noncancer reference values. Cancer potency values are derived for chronic (lifetime) exposures. Noncancer reference values are generally derived for chronic exposures (up to a lifetime), but may also be deriv ed for acute ( <24 hours), short
- term (>24 hours up to 30 day s), and subchronic (>30 day s up to 10% of lifetime) exposure durations, all of which are derived based on an assumption of continuous exposure throughout the duration specified. For the purposes of assessing all potential health risks associated with the emissions included in an assessment, we rel y 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 sources included in an assessment, some HAP have no peer
- reviewed cancer potency values or reference values for chronic non
- cancer or acute effects (inhalation or ingestion) . Since exposures to the se pollutants cannot be included in a quantitative risk estimate, an understatement of risk for these pollutants at environmental exposure levels is possible. Additionally , chronic dose
- response values for certain compounds included in the assessment may be under EPA IRI S 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 ris k assessment may significantl y 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 currentl y used by the EPA to develop cancer potency

factors. In general, these same uncertainties attend the development of cancer potency

factors by

CalEPA, the source of peer
- reviewed cancer potency factors used where EPA
- developed values are not yet available. To place this discussion in context, we provide a quote from the EPA’s Guidelines for Carcinogen Risk Assessment [ 34 ] (herein referred to as Cancer Guidelines ). “The primary goal of EPA actions is protection of human health; accordingl y, as an Agency policy , risk a ssessment procedures, including default options that are used in the absence of scientific data to the contrary , should be health protective.” The approach adopted in this document is consistent with this approach as described in the Cancer Guidelines
. F or cancer endpoints EPA usually derives an oral slope factor for ingestion and a unit risk value for inhalation exposures. These values allow estimation of a lifetime probability of developing cancer given long
- term exposures to the pollutant. Depending on the pollutant being evaluated, EPA relies on both animal bioassay and epidemiological studies to characterize cancer risk. As a science policy approach, consistent with the Cancer**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  39 Guidelines , EPA uses animal cancer bioassay s as indicators of potential human health risk when other human cancer risk data are unavailable. Extrapolation of study

data to estimate potential risks to human populations is based upon EPA’s assessment of the scientific database for a pollutant using EPA’s guidance documents and other peer
- reviewed methodologies. The EPA Cancer Guidelines describes the Agency ’s recommendations for methodologies for cancer risk assessment. EPA believes that cancer risk estimates developed following the procedures described in the Cancer Guidel ines 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). 27 In s ome circumstances, the true risk could be as low as zero; however, in other circumstances the risk could also be greater. 28 When developing an upper bound estimate of risk and to provide risk values that do not underestimate risk, EPA generall y relies on conservative default approaches. 29 EPA also uses the upper bound (rather than lower bound or central) estimates in its assessments, although it is noted that this approach can have limitations for some uses (e.g. priority setting, expected benefits anal ys is). Such health risk assessments have associated uncertainties, some which may be considered quantitatively , and others which generally are expressed qualitativel y. Uncertainties may vary substantially

among cancer risk assessments associated with expos ures to different pollutants, since the assessments employ different databases with different strengths and limitations and the procedures emplo yedmay differ in how well they

represent actual biological processes for the assessed substance. EPA’s Risk Ch aracterization Handbook also recommends that risk characterizations present estimates demonstrating the impact on the assessment of alternative choices, data, models and assumptions [ 35 ]. Some of the major sources of uncertaint y and variability

in deriving cancer risk values are described more full y below. (1) The qualitative similarities or differences between tumor responses observed in experimental animal bioassay s and those which would occur in humans is a source of uncertaint y in cancer risk assessm ent. In general, EPA does not assume that tumor sites observed in an experimental animal bioassay are necessarily

predictive of the sites at which

27 IRIS glossary (www.epa.gov/NCEA/iris/help_gloss.htm). 28 The exception to this is the URE for benzene, which is considered to cover a range of values, each end of which is considered to be equally plausible, and which is based on maximum likelihood estimates. 29 According to the NRC report Science and Judgment in Risk Assessment (NRC, 1994) “[Default] options are generic approaches, based on general scientific knowledge and policy judgment, that are applied to various elements of the risk
- assessment process when the correct scientific model is unknown or uncertain.” The 1983 NRC report Risk Assessment in the Federal Government: Managing the Process defined default option as “the option chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to the contrary” (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; r ather, 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 r isk to chemicals is not underestimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An Examination of EPA Risk Assessment Principles and Practices, EPA/100/B
- 04/001 available at: http://www.epa.gov/osa/pdfs/ratf
- final.pdf
.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  40 tumors would occur in humans. 30 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) Uncertai nties 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. Howeve r, data may support development of a pharmacokinetic model for the absorption, distribution, metabolism and excretion of an agent, which may result in improved dose metrics (e.g., average blood concentration of the pollutant or the quantity of agent metabo lized in the body). Quantitative uncertainties result when the appropriate choice of a dose metric is uncertain or when dose metric estimates are themselves uncertain (e.g., as can occur when alternative pharmacokinetic models are available for a compound). Uncertainty in dose estimates may lead to either over or underestimation of risk. (3) For the quantitative extrapolation of cancer risk estimates from experimental animals to humans, EPA uses scaling methodologies (relating expected response to differ ences in phy sical size of the species), which introduce another source of uncertaint y. These methodologies are based on both biological data on differences in rates of process according to species size and empirical comparisons of toxicity between experim ental 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 uncertaint ies 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) anal ys is to esti mate 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 addresse d 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 generall y utilized the multistage model for estimation of the BMDL using cancer bioass ay data (see further discussion below). (5) Extrapolation from high to low doses is an important, and potentially large, source of uncertaint y in cancer risk assessment. EPA uses different approaches to low dose risk assessment (i.e., developing estimate s of risk for exposures to environmental doses of an agent from observations in experimental or epidemiological studies at higher dose) depending on the available data and understanding of a pollutant’s mode of action (i.e., the manner in which a pollutant causes cancer). EPA’s Cancer Guidelines express a preference for the use of reliable, compound
- specific, biologicall y - based risk models when feasible; however, such models are rarel y available. The mode of action for a pollutant (i.e., the manner in whi ch a
30 Per the EPA Cancer Guidelines: “The default option is that positive effects in animal cancer studies indicate that the agent under study can have carcinogenic potential in humans.” and “Target organ concordance is not a prerequisite for evaluating the im plications of animal study results for humans.”**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  41 pollutant causes cancer) is a key consideration in determining how risks should be estimated for low
- dose exposure. A reference value is calculated when the available mode of action data show the response to be nonlinear (e.g., as in a threshold resp onse). 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. L inear extrapolation can be supported b y 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. Pollutant s whose effects are additive to background biological processes in cancer development can also be predicted to have low
- dose linear responses, although the slope of this relationship may not be the same as the slope estimated by the straight line approach. EPA most frequently

utilizes a linear low
- dose extrapolation approach as a baseline 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 generall y provide a health protective approach. Note that another source of uncertaint y is the characterization of low
- dose nonlinear, non
- threshold relationships. The National Academy of Sciences has encouraged the exploration of sigmoidal ty pe functions (e.g., log
- probit models) in representing dose respon se relationships due to the variability in response within human populations. Another National Research Council (NRC) report [ 36] suggests that models based on distributions of individual thresholds are likel y to lead to sigmoidal
- shaped dose
- response func tions for a population. This report notes sources of variability in the human population: “One might expect these individual tolerances to vary extensively

in humans depending on genetics, coincident exposures, nutritional status, and various other susceptibility

factors...” Thus, if a distribution of thresholds approach is considered for a carcinogen risk assessment, application would depend on ability of modeling to reflect the degree of variability

in response in human populations (as opposed to resp onses in bioassay s with geneticall y more uniform rodents). Note also that low dose linearit y 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 ty pically 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 BMDLon bottom line risk estimates can be quantified by comparing risk estimates using the BMDLvalue to central estimate BMD values, although these differences are generall y not a large contributor to uncertaint y in risk assessment (Subramaniam et. al., 2006) [ 37]. It is important to note that earlier EPA assessments, including the majorit y of those for which risk values exist today , were generally

developed using the multistage model to extrapolate down to environmental dose levels and did not involve the use of a POD. Subramaniam et. al. (2006) also provide comparisons indicating that slopes based on straight line extrapolation from a POD do not**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  42 show large differences from those based on the upper con fidence limit of the multistage model. (6) Cancer risk estimates do not generall y make specific adjustments to reflect the variability in response within the human population

— resulting in another source of uncertainty in assessments. In the diverse hum an population, some individuals are likely to be more sensitive to the action of a carcinogen than the typ ical individual, although compound
- specific data to evaluate this variability are generally

not available. There may also be important life stage dif ferences 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 generall y quantitatively address life stage di fferences. 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 ty pically in the highest URE whi ch can be supported by reliable data, thus supporting estimates that are designed not to underestimate risk in the face of uncertainty

and variability
. **Chronic noncancer assessment** Chronic noncancer reference values represent chronic exposure levels that are intended to be health
- protective. That is, EPA and other organizations which develop noncancer reference values (e.g., the Agency

for Toxic Substances and Disease Registry

– ATSDR) utilize an approach that is intended not to underestimate risk in the face of uncertainty and variability
. When there are gaps in the available information, uncertainty factors (UFs) are applied to derive reference values that are intended to be protective against appreciable risk of deleterious effects . Uncertainty factor s are commonly

default values 31 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 assumptions are ne eded and more default factors are used. Thus there may be a greater tendency to overestimate risk

—in the sense that further study might support development of reference values that are higher (i.e., less potent) because fewer default assumptions are neede d. However, for some pollutants it is possible that risks may be underestimated. For non
- cancer endpoints related to chronic exposures, EPA derives a Reference Dose (RfD) for exposures via ingestion, and a Reference Concentration (RfC) for inhalation exp osures. 31 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 ri sk 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 s pecific substance when it believes this to be appropriate. In keeping with EPA’s goal of protecting public health and the environment, default assumptions are used to ensure that risk to chemicals is not underestimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An examination of EPA Risk Assessment Principles and Practices, EPA/100/B
- 04/001 available at: http://www.epa.gov/osa/pdfs/ratf
- final.pdf.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  43 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 witho ut an appreciable risk of deleterious effects during a lifetime. 32 To derive values that are intended to be “without appreciable risk,” EPA’s methodology relies upon an uncertainty factor (UF) approach [ 38 ],[ 39 ] which includes consideration of both uncertai nty and variability
. EPA begins b y 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 ty

picall y chooses the relevant en dpoint 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 stati stical estimation using the benchmark dose (BMD) approach; (2) use of the dose or concentration at which the toxic response was not significantl y elevated (no observed adverse effect level

— NOAEL); or (3) use of the lowest observed adverse effect level (LO AEL). A series of downward adjustments using default UFs is then applied to the POD to estimate the reference value [ 40 ] . While collectively termed “UFs”, these factors account for a number of different quantitative considerations when utilizing observed animal (usually rodent) or human toxicity data in a risk assessment. The UFs are intended to account for: (1) variation in susceptibility among the members of the human population (i.e., inter
- individual variability); (2) uncertainty in extrapolating fro m 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) uncertaint y in extrapolati ng from a LOAE L in the absence of a NOAEL; and (5) uncertainty when the database is incomplete or there are problems with applicability of available studies
. When scientifically

sound, peer
- reviewed assessment
- specific data are not available, default adju stment values are selected for the individual UFs. For each t ype of uncertaint y (when relevant to the assessment) , EPA ty picall y applies an UF value of 10 or 3 with the cumulative UF value leading to a downward adjustment of 10
- 3000 fold from the selected POD. An UF of 3 is used when the data do not support the use of a 10
- fold factor. If an extrapolation step or adjustment is not relevant to an assessment (e.g., if applying human toxicity data and an interspecies extrapolation is not required) the assoc iated UF is not used. The major adjustment steps are described more full y below. 1) Heterogeneit y among humans is a key source of variability

as well as uncertaint y. Uncertaint y related to human variation is considered in extrapolating doses from a sub set or smaller
- sized population, often of one sex or of a narrow range of life stages (ty pical 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

32 See IRIS glossary**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  44 situations, a smaller UF of 3 may be applied to re flect a known lack of significant variability among humans. 2) Extrapolation from results of studies in experimental animals to humans is a necessary step for the majority

of chemical risk assessments . When interpreting animal data, the concentration at the POD (e.g. NOAEL, BMDL) in an animal model (e.g. rodents) is extrapolated to estimate the human response. While there is long
- standing scientific support for the use of animal studies as indicators of potential toxicity to humans , there are uncertaint ies in such extrapolations. Inthe absence of data to the contrary , the ty pical 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. Ty picall y , compound specific data to evaluate relative sensitivity in humans versus rodents are lacking, thus leading to uncertaint y in this extrapolation. Size
- related differences (allometric relationships) indicate that ty picall y humans are more sensitive than rodents when compare d 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 alway s possible. Information may not be available to quantitatively assess toxicokinetic or toxicody namic differences between ani mals and humans, and in many cases a 10
- fold UF (with separate factors of 3 for toxicokinetic and toxicody namic components) is used to account for expected species differences and associated uncertainty in extrapolating from laboratory

animals to humans in the derivation of a reference value. If information on one or the other of these components is available and accounted for in the cross
- species extrapolation, a UF of 3 may be used for the remaining component. 3) In the case of reference values for chronic exposures where onl y 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 ty picall y applied unless the avail able scientific information supports use of a different value. 4) Toxicity

data are t ypically limited as to the dose or exposure levels that have been tested in individual studies; in an animal study , for example, treatment groups may differ in exposure b y up to an order of magnitude. The preferred approach to arrive at a POD is to use BMD analy sis; however, this approach requires adequate quantitative results for a meaningful anal ys is, which is not alway s possible. Use of a NOAEL is the next preferred a pproach after BMD analy sis in determining a POD for deriving a health effect reference value. However, many studies lack a dose or exposure level at which an adverse effect is not observed (i.e., a NOAEL is not identified). When using data limited to a L OAEL, 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 ty

pically applied.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  45
**Acute noncancer assessment** Many of the UFs used to account for variabilit y and uncertaint y in the development of acute reference values are quite similar to those d eveloped for chronic durations, but more often using individual UF values that may be less than 10. UFs are applied based on chemical
specific or health effect
- specific information (e.g., simple irritation effects do not vary appreciably

between human ind ividuals, hence a value of 3 is ty picall y used), or based on the purpose for the reference value (see the following paragraph). The UFs applied in acute reference value derivation include: 1) heterogeneity among humans; 2) uncertainty in extrapolating from animals to humans; 3) uncertainty in LOAEL to NOAEL adjustments; and 4) uncertainty

in accounting for an incomplete database on toxic effects of potential concern. Additional adjustments are often applied to account for uncertainty in extrapolation fro m observations at one exposure duration (e.g., 4 hours) to arrive at a POD for derivation of an acute reference value at another exposure duration (e.g., 1 hour). Not all acute reference values are developed for the same purpose and care must be taken when interpreting the results of an acute assessment of human health effects relative to the reference value or values being exceeded. Where relevant to the estimated exposures, the lack of threshold values at different levels of severity should be factore d into the risk characterization as potential uncertainties.**Draft Risk Ass essment for the Mineral Wool Production and Wool Fiberglass** 

**Manufacturing Source Categories --**  **FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE**  46


### 5 **References** 1 . US EPA. National Emission Standards for Hazardous Air Pollutants
. http://www.epa.gov/ttn/atw/mactfnlalph.html
. 2 US EPA, 2009. Risk and Technology Review (RTR) Risk Assessment Methodologies: For Review by

the EPA’s Science Advisory Board with Case Studies

– MACT I Petroleum Refining Sources and Portland Cement Manufacturing
. EPA
- 452/R
- 09
- 006. http://www.epa.gov/ttn/atw/rrisk/rtrpg.html. 3 . US EPA, 2010. SAB’s Response to EPA’s RTR Risk Assessment Met hodologies. http://y osemite.epa.gov/sab/sabproduct.nsf/4AB3966E263D943A8525771F00668381/$File/EP A
- SAB
- 10
- 007
-unsigned.pdf 4 . US EPA, 2010. Memorandum from Dave Guinnup to RTR Wood Furniture Docket, entitled, “EPA’s Actions in Response to Key Recommendations of the SAB Review of RTR Risk Assessment Methodologies. 5
. US EPA, 2005. Revision to the Guideline on Air Quality Models: Adoption of a Preferred General Purpose (Flat and Complex Terrain) Dispersion Model and Other Revisions; Final Rule. 40 CFR Part 51. http://www.epa.gov/EPA
- AI R/2005/November/Day
- 09/a2 1627.htm 6 . US EPA, 2004. Users’ guide for the AMS/EPA regulatory model

– AERMOD. EPA
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03
- 001
. http://www.epa.gov/scram001/7thconf/aermod/aermodugb.pdf
. 7
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. Vizuete, T
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. Sy mons , 2004. Variable industrial VOC emissions and their impact on ozone formation in the Houston Galveston Area. Final Report: Texas Environmental Research Consortium Proje ct H
- 13. http://files.harc.edu/Projects/AirQuality/Projects/H013.2003/H13FinalReport.pdf 8 . US EPA, 2004. Air Toxics Risk Assessment Reference Library, Volume 1
. EPA
- 453
- K
- 04
- 001A. http://www.epa.gov/ttn/fera/risk_atra_vol1.html. 9
. US EPA, 2005. Table 1. Prioritized Chronic Dose
- Response Values (2/28/05). Office of Air Quality

Planning and Standards. http://www.epa.gov/ttn/atw/toxsource/table1.pdf 10 . US EPA, 2005. 1999 National Air Toxics Risk Assessment. http://www.epa.gov/ttn/atw/nata1999 11
. US EPA, 2006. I

ntegrated Risk I

nformation System. http://www.epa.gov/iris/index.html
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