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## Draft Residual Risk Assessment for the Chromic Acid Anodizing, Decorative Chromium Electroplating, and Hard Chromium

Electroplating Source Categor ies

by EPA’s Office of Air Quality Planning and Standards

Office of Air and Radiation January 201 2Draft Risk Assessment for Chrome Plating Source Categories

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### Table of Contents

1 Introduction

................................ ................................ ................................ ........................ 3 2 Methods

................................ ................................ ................................ .............................. 4 2.1 Emissions and source data

................................ ................................ ........................... 4 2.2 Dispersion modeling for inhalation exposure assessment

................................ ........... 4 2.3 Estimating human inhalation exposure

................................ ................................ ....... 7 2.4 Acute Risk Screening and Refined Assessments

................................ ........................ 7 2.5 Multipathway and environmental risk screening

................................ ........................ 8 2.6 Dose

- Response Assessment

................................ ................................ ........................ 8 2.6.1 Sources of chronic dose

- response information

................................ .................... 8 2.7 Risk Characterization

................................ ................................ ................................ 10 2.7.1 General

................................ ................................ ................................ ............... 10 2.7.2 Mixtures

................................ ................................ ................................ ............. 12 2.7.3 Facility

- Wide Risks

................................ ................................ ............................ 13 2.7.4 MACT

- Allowable Risks

................................ ................................ .................... 13 3 Risk Results for the Chromium Anodizing, Decorative Chromium Electroplating, and Hard Chromium Electroplating Source Categories

................................ .............................. 13 3.1 Source Category Descriptions and Results

................................ ................................ 13 3.2 Risk Characterization

................................ ................................ ................................ 16 4 General Discussion of Uncertainties and How They Have Been Addressed

................... 22 4.1 Exposure Modeling Uncertainties

................................ ................................ ............. 22 4.2 Uncertainties in the Dose

- Response Relationships

................................ ................... 23 5 References

................................ ................................ ................................ ........................ 30

Index of Tables

Table 2.2

- 1 AERMOD Version 11103 Model Options for RTR Modeling

............................. 5 Table 2.6

- 1 Dose

- Response Values for Chronic Inhalation Exposures

................................ .. 10 Table 3.1

- 1 Summary of Emissions from the Hard Chromium Electroplating Source Category

................................ ................................ ................................ ................................ .................. 15 Table 3.1

- 2 Summary of Emissions from the Decorative Chromium Electroplating Source Category

................................ ................................ ................................ ................................ ... 16 Table 3.1

- 3 Summary of Emissions from the Chromium Anodizing Source Category

......... 16 Table 3.2

- 1 Summary of Source Category Level Risks for Hard Chromium Electroplating

. 17 Table 3.2

- 2 Source Category Contribution to Facility

- Wide Cancer Ri sks

– Hard Chromium Electroplating

................................ ................................ ................................ ........................... 18 Table 3.2

- 3 Summary of Source Category Level Risks for Decorative Chromium Electroplating

................................ ................................ ................................ ........................... 18 Table 3.2

- 4 Source Category Contribution to Facility

- Wide Cancer Risks

– Decorative Chromium Electroplating

................................ ................................ ................................ ......... 20 Table 3.2

- 5 Summary of Source Category Level Risks for Chromium Anodizing

................ 20 Table 3.2

- 6 Source Category Contribution to Facility

- Wide Cancer Risks

– Chromium Anodizing

................................ ................................ ................................ ................................ . 22Draft Risk Assessment for Chrome Plating Source Categories

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Appendices

Appendix 1 Technical Support Document for HEM

- AERMOD Modeling Appendix 2 Meteorological Data for HEM

- AERMOD Modeling Appendix 3 Analysis of D ata on S hort

- T erm E mission R ates R elative to L ong

- T erm

E mission R ates Appendix 4 Detailed Risk Modeling Results

Index of Acronyms

AERMOD American Meteorological Society/EPA Regulatory Model AEGL Acute exposure guideline l evel ASTDR US Agency for Toxic Substances and Disease Registry CalEPA California Environmental Agency ERPG Emergency Response Planning Guideline HAP Hazardous Air Pollutant HEM Human Exposure Model HI Hazard index HQ Hazard quotient IRIS Integrated Risk Information System MACT Maximum Achievable Control Technology MIR Maximum Individual Risk MOA Mode of a ction NAC National Advisory Committee NATA National Air Toxics Assessment NED National Elevation Dataset NEI National Emissions Inventory NPRM Notice of Proposed Rulemaking PB

- HAP Persistent and Bioaccumulative HAP POM Polycyclic organic m at ter REL Reference exposure l evel RfC Reference c oncentration RfD Reference d ose RTR Risk and Technology TOSHI Target

- organ

- specific hazard index URE Unit risk e stimateDraft Risk Assessment for Chrome Plating Source Categories

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

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

- based standards for categories of sources (e.g., petroleum refineries, pulp and paper mills, etc.) [ 1 ]. EPA has largely completed the initial Maximum Achievable Control Technology ( MACT ) standards as required under this provision. Under section 112(d)(6), EPA must review each of these t echnology

- based standards at least every eight years and revise a standard, as necessary, ―taking into account developments in practices,
processe s and control technologies.‖ In the second stage, EPA is required under section 112(f)(2) to assess the healt h and environmental risks that remain after implementation of the MACT standards. If additional risk reductions are necessary to protect public health with an ample margin of safety or to prevent an adverse environmental effect, EPA must develop standards to address these remaining risks. This second stage of the regulatory process is known as the residual risk stage. For each source category for which EPA issued MACT standards, the residual risk stage must be completed within eight years of promulgation of the initial technology

- based standard.

In December of 2006 we consulted with a panel from the EPA's Science Advisory Board (SAB) on the ―Risk and Technology Review (RTR) Assessment Plan‖ and in June of 2007, we received a letter with the results of th at consultation. Subsequent to the consultation, in July of 2009 a meeting was held with an SAB panel for a formal peer review of the ―Risk and Technology Review (RTR) Assessment Methodologies‖ [ 2 ]. We received the final SAB report on this review in May of 2010 [ 3 ]. Where appropriate, we have responded to the key messages from this review in developing our current risk assessment s and we will be continuing our efforts to improve our assessments by incorporating updates based on the SAB recommendations as they are developed and become available . Our responses to the key recommendations of the SAB are outlined in the me mo entitled, ―EPA’s Actions in Response to Key Recommendations from the SAB Review of RTR R isk Assessment Methodologies‖ [ 4 ].

This docume nt contains the methods and results of baseline risk assessment s (i.e., after the implementation of the respective MACT standard s ) performed for the chromium a nodizing, d ecorative c hromium e lectroplating, and h ard c hromium e lectroplating s ource c ategories

. The methods discussion includes descriptions of the methods used to develop refined estimates of chronic inhalation exposures and human health risks for cancer and non

- cancer endpoints, as well as descriptions of the methods used to screen chronic non

- in halation health risks and adverse environmental effects. Since none of the screening assessments indicated any significant potential for chronic non

- inhalation health effects or environmental impacts

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

assess m ents w as performed. Because t here were no HAPs with an acute dose

- response benchmark value, we did not perform a quantitative risk assessment for acute exposures to these pollutants

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### 2 Methods

2.1 Emissions and source data We contacted 28 State and local air pollution control agencies to request information on the industry. The requested information included facility data (name, location, number of employees), process type, tank design and operating parameters, annual hours of operation, emission control technology, control device operating parameters, emission test data, and other available supporting documents, such as emission inventory reports and operating permits. Agencies were asked to provide data on the 5 to 1 0 facilities that represent the worst case, in terms of emissions and risk, and any additional facilities for which the data were readily available. We received data from a total of 24 agencies. We supplemented the se data with additional data from operat ing permits and other information downloaded from State websites. T o assess nationwide residual risk, it was necessary to estimate emissions for much of the industry. W e used a Monte Carlo procedure to simulate actual emissions for those facilities for which actual emissions data were not available. The simulation model used the pool of available data on actual emissions concentrations, exhaust flow rates, and annual operating hours for each process type (hard chromium electroplating, decorative ch romium electroplating, and chromium anodizing).

The development of the emissions and source data for these source categories is discussed in Section 3. Additional details on the simulation approach can be found in the emissions technical document ―Draft Development of the RTR Emissions Data Set for Chromium Electroplating and Chromic Acid Anodizing Source categories

, ‖ available in the docket for the rulemaking for these source categories.



### 2.2 Dispersion modeling for inhalation exposure assessment Both long

- and short

- term inhalation exposure concentrations and associated health risk s from each facility in the source category of interest were estimated using the Human Exposure Model in combination with the American Meteorological Society/EPA Regulatory Model d ispersion modeling system (HEM

- AERMOD , or HEM3 ). The approach used in applying this modeling system is outlined below, and further details are provided in Appendix 1

. The HEM 3 performs three main operations: atmospheric dispersion modeling, estimation of individual human exposures and health risks, and estimation of population risks. This section focuses on the dispersion modeling component. The exposure and risk characterization components a re discussed in other subsections of S ection s 2 and 3

.

The di spersion model in the HEM 3 system, AERMOD version 11103 , is a state

- of

- the

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

- by

- hour dispersion from the emission sources into the surrounding atmosphere. Hourly emission ra tes used for this simulation are generated by evenly dividing the total annual emission rate from the inventory into the 8,760 hours of the year.Draft Risk Assessment for Chrome Plating Source Categories

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The first step in the application of the HEM 3 modeling system is to predict ambient concentrations at locatio ns of interest. The AERMOD model options employed are summarized in Table 2.2

- 1 and are discussed further below.

Table 2.2

- 1 AERMOD V ersion 11103 M o del O ptions for RTR M odeling

Modeling Option Selected Parameter for chronic exposure
Type of calculations Hourly a mbient c oncentration

Source type Point

Receptor orientation Polar (1 3 rings a nd 16 radials ) Discrete (census block centroids)

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

Building downwash Not Included

Plume d eposition/ d epletion Not Included

Urban s ource o ption No

Meteorology 1 year representative NWS from nearest site

In HEM3, meteorological data are ordinarily selected from a list of approximately 200 National Weather Service (NWS) surface observation stations across the continental United States, Alaska, Hawaii, and Puerto Rico. In most cases

, the nearest station is selected as representative of the conditions at the subject facility. Ideally, when considering off

- site meteorological data most site

- specific dispersion modeling efforts will employ up to five years of data to capture variability in weather patterns from year to year. However, because we had an insufficient number of appropriately form atted model input files derived from available meteorological data, we modeled only a single year, typically 1991. While the selection of a single year may result in under

- prediction of long

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

- prediction at others. For each facility identified by its characteristic latitude and longitude coordinates, the closest meteorological station was used in the dispersion modeling. The average distance between a modeled facility and the applicable meteorological station was 52 miles ( 84 km ). Appendix 2 ( Meteorological Data Processing Using AERMET for HEM3 ) provides a complete listing of stations and assumptions along with further details used in processing the data through AERMET. The sensitivity of model results to the selection of the nearest weather station and the use of one year of meteorological data is discussed in ―Risk and Technology Review (RTR) Risk Assessment Methodologies‖ [ 2 ].

The HEM3 system estimates ambient concentrations at the g eographic centroids of census blocks (using the 20 1 0 Census) and at other receptor locations that can be specified by the user. The model accounts for the effects of multiple facilities when estimating concentration impacts at each block centroid. Typica lly

, we combined only the impacts of facilities within the same source category, and assessed chronic exposure and risk only for census blocks with at least one resident (i.e., locations where people may reasonably be assumed to reside ratherDraft Risk Assessment for Chrome Plating Source Categories

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than receptor points at the fenceline of a facility). Chronic ambient concentrations were calculated as the annual average of all estimated short

- term (one

- hour) concentrations at each block centroid. Possible future residential use of currently uninhabited areas was not considered. Census blocks, the finest resolution available in the census data, are typically comprised of approximately 40 people or about ten households.

In contrast to the development of ambient concentrations for evaluating long

- term exposures
, which was performed only for occupied census blocks, worst

- case short

- term (one

- hour) concentrations were estimated both at the census block centroids and at points nearer the facility that represent locations where people may be present for short period s, but generally no nearer than 100 meters from the center of the facility (note that for large facilities, this 100

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

- term emission rates were needed to screen for the pote ntial for hazard via acute exposures, and since the collected emissions data contain only annual emission totals, we generally apply the assumption to all source categories that the maximum one

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

The average hourly emissions rate is defined as the total emissions for a year divided by the total number of operating hours in the year. Th e choice of a factor of ten for screening was originally based on eng ineering judgment. To develop a more robust peak

- to

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

- term emissions dataset from a number of sour ces located in Texas (originally reported on by Allen et al. 2004) [ 7 ] . In that report, the Texas Environmental Research Consortium Project compared hourly and annual emissions data for volatile organic compounds for all facilities in a heavily

- industriali zed 4

- county area (Harris, Galveston, Chambers, and Brazoria Counties, TX) over an eleven

- month time period in 2001. We obtained the dataset and performed our own analysis, focusing that analysis on sources which reported emitting high quantities of HAPs over short periods of time (see Appendix 3 Analysis of data on short

- term emission rates relative to long

- term emission rates ). Most peak emission events were less than twice the annual average, the highest was a factor of 74 times the annual average, an d the 99th percentile ratio of peak hourly emission rate to the annual hourly emission rate was 9. Based on these results, we chose the factor of ten for all initial screening. These factors are intended to cover all possible hourly peaks associated with routinely

- variable emissions. While there have been some documented emission excursions above this level, our analysis of the data from the Texas Environmental Research Consortium suggests that this factor should cover more than 99% of the short

- term pea k gaseous or volatile HAP emissions from typical industrial sources. We have no data relating specifically to peak short

- term emissions of particulate HAPs . In the absence of source category

- specific data, we use this same default approach for particulat e emissions as well.

Census block elevations for HEM3 modeling were determined nationally from the US Geological Service 1/3 Arc Second National Elevation Dataset , which ha s a spatial resolution of about 1 0 meters. Elevations of polar grid points used in estimating short

- and long

- term ambient concentrations were assumed to be equal to the highest elevation of any census block falling within the polar grid sector corresponding to the grid point. If a sector does notDraft Risk Assessment for Chrome Plating Source Categories

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contain any blocks, the model defaul ts the elevation to that of the nearest block. If an elevation is not provided for the emission source, the model uses the average elevation of all sectors within the innermost model ring. AERMOD adjusts the plume’s flow if nearby elevated hills are expec ted to influence the wind patterns. For details on how hill heights were estimated and used in the AERMOD modeling

, see Appendix 1

.


### 2.3 Estimating human inhalation exposure

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

- term or long

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

We did not address short

- term human activity for two reasons. First, our experience with the National

- scale Air Toxics Assessment (NATA) (which model s daily activity using EPA’s HAPEM model) suggests th at, given our current understanding of microenvironment concentrations and daily activities, modeling short

- term activity would, on average, reduce risk estimates about 25% for particulate HAP; it will also reduce risk estimates for gaseous HAPs , but typic ally by much less. Second, basing exposure estimates on average ambient concentrations at census block centroids may underestimate or overestimate actual exposure concentrations at some residences. Further reducing exposure estimates for the most highly exposed residents by modeling their short

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

We did not address long

- term migration nor population growth or decrease over 70 years, instead basing the assessment on the assumption that each pers on’s predicted exposure is constant over the course of their lifetime which is assumed to be 70 years. In assessing cancer risk, we generally estimated three metrics; the maximum individual risk (MIR), which is defined as the risk associated with a lifeti me of exposure at the highest concentration; the population risk distribution; and the cancer incidence. The assumption of not considering short or long

- term population mobility does not bias the estimate of the theoretical MIR nor does it affect the esti mate 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 a nd reducing the number of people estimated to be at lower risks, thereby increasing the estimated number of people at specific risk levels.



### 2.4 Acute Risk Screening and Refined Assessments

In establishing a scientifically

- defensible approach for the assessmen t of potential health risks due to acute exposures to HAPs , we f ollow the same general approach that is used for developing chronic health risk assessments under the residual risk program. However, for these source categories, t here are no HAPs with an acute dose

- response benchmark value

. Therefore

, we did not perform a quantitative risk assessment for acute exposures to these pollutants

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### 2.5 Multipathway and environmental risk screening

The potential for significant human health risks due to expo sures via routes other than inhalation (i.e., multipathway exposures) w as screened by first determining whether any sources emitted any hazardous air pollutants known to be persistent and bioaccumulative in the environment (PB

- HAP) 1 . The PB

- HAP compounds or compound classes are identified for th e screening from the EPA’s Air Toxics Risk Assessment Library [ 8 ]. Examples of PB

HAP are cadmium compounds, chlordane, chlorinated dibenzodioxins and furans, DDE, heptachlor, hexachlorobenzene, hexachlorocyclohexa ne, lead compounds, mercury compounds, methoxychlor, polychlorinated biphenyls, polycyclic organic matter (POM)

, toxaphene, and trifluralin . PB

- HAP emissions were not identified from the chromium

a nodizing, d ecorative c hromium e lectroplating, and h ard c hromium e lectroplating s ource

c ategories , indicating that exposures due to non

- inhalation routes of exposure are not significant. The lack of PB

- HAP emissions from th ese source categor ies indicates a very low potential for adverse environmental effects du e to exposures resulting from atmospheric deposition of PB

- HAPs. Thus, even if sensitive species are present in the areas surrounding these facilities with no PB

- HAP emissions, it is reasonable to assume that there are no adverse effects to populations in the areas surrounding these facilities.

Additionally, we evaluated the potential for significant ecological exposures to non PB

- HAP from exceedances of chronic human health inhalation thresholds in the ambient air near these facilities. Human health dose

- response threshold values are generally derived from studies conducted on laboratory animals (such as rodents) and developed with the inclusions of uncertainty factors that could be as high as 3000. As a result, these human threshold values are often significantly lower than the level expected to cause an advers e effect in an exposed rodent. It should be noted that there is a scarcity of data on the direct atmospheric impact of these HAPs on other receptors, such as plants, birds, and wildlife. Thus, if the maximum inhalation hazard in an ecosystem is below the level of concern for humans, we have generally concluded that mammalian receptors should be at no risk of adverse effects due to inhalation exposures from non PB

- HAP, and have assur ance that other ecological receptors are also not at any significant risk fr om direct atmospheric impact. In some isolated cases where we have data indicating pote ntial adverse impacts on plants, birds, or other wildlife due to the direct atmospheric impacts of specific HAP , we note that as an uncertainty and , where possible, refine our analysis by comparing our modeled impacts to available threshold values from the scientific literature.



### 2.6 Dose

- Response Assessment

2.6.1 Sources of chronic dose

- response information

1 Although the two

- letter chemical symbol for lead is Pb, in this assessment PB

- HAP refers to the man y air pollutants known to be persistent and bioaccumulative in the environment. In instances where the report is specifically referring to lead, it is spelled out (i.e., the two

- letter chemical symbol for lead is not used in this document).Draft Risk Assessment for Chrome Plating Source Categories

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Dose

- response assessment s (carcinogenic and non

- carcinogenic) for chronic exposure (either by inhalation or ingestion) for the HAP s reported in the emissions i nventory for the source categories in this document were based on the EPA Office of Air Quality Planning and Standards’ (OAQPS) existing recommendations for HAP s [ 9 ], also used for NATA [ 10 ]. This information has been obtained from various sources and pri oritized 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

asses sments typically provide a qualitative statement regarding the strength of scientific data and specify a reference concentration (RfC, for inhalation) or reference dose (RfD, for ingestion) to protect against effects other than cancer and/or a unit risk es timate (URE, for inhalation) or slope factor (SF, for ingestion) to estimate the probability of developing

cancer. The RfC is defined as an ― estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. ‖ The RfD is ―an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime.‖ The URE is defined as ― the upper

- bound excess cancer risk estimated to result from continuous lifetime exposure to an agent at a concentration of 1 μg/m 3 in air. ‖ The SF is ―a n upper bound, approximating a 95% confidence limit, on the increased cancer risk from a lifetime exposure to an agent. This estimate, [is] usually expressed in units of proportion (of a populat ion) affected per mg/kg

- day ...‖ EPA disseminates dose

- response assessment information in several forms, based on the level of review. The Integrated Risk Information System (IRIS) [ 11 ] is an EPA database that contains scientific health assessment informatio n, including dose

- response information. All IRIS assessments since 1996 have also undergone independent external peer review. The current IRIS process includes review by EPA scientists, interagency reviewers from other federal agencies, and the public, an d peer review by independent scientists external to EPA. 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 id entified. We expect future EPA dose

- response assessments to identify nonlinear MOAs where appropriate, and we will use those analyses (once they are peer reviewed) in our risk assessments. At this time, however, there are no available carcinogen dose

- res ponse assessments for inhalation exposure that are based on a nonlinear MOA

.
2) US Agency for Toxic Substances and Disease Registry (ATSDR). ATSDR, which is part of the US Department of Health and Human Services, develops and publishes Minimum Risk Levels (MRLs) [ 12 ] for inhalation and oral exposure to many toxic substances. As stated on the ATSDR web site: ― Following discussions with scientists within the Department of Health and Human Services (HHS) and the EPA, ATSDR chose to adopt aDraft Risk Assessment for Chrome Plating Source Categories

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practice similar to that of the EPA's Reference Dose (RfD) and Reference Concentration (RfC) for deriving substance

- specific health guidance levels for non neoplastic endpoints .‖ The MRL is defined as ―an estimate of daily human exposure to a substance that is likely to be w ithout an appreciable risk of adverse effects (other than cancer) over a specified duration of exposure.‖ ATSDR describes MRLs as substance

- specific estimates to be used by health assessors to select environmental contaminants for further evaluation. Exp osures 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 Environ mental 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

va lues and incorporates significant external scientific peer review. As cited in the CalEPA Technical Support Document for developing their chronic assessments 2 : ―The guidelines for developing chronic inhalation exposure levels incorporate many recommendati ons of the U.S. EPA [ 13 ] and NAS [ 14 ] .‖ The non

- cancer information includes available inhalation health risk guidance values expressed as chronic inhalation reference exposure levels (RELs) [ 15 ]. CalEPA defines the REL as ―the concentration level at or below which no health effects are anticipated in the general human population.‖ CalEPA's quantitative dose

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

The emissions inventor ies for the source categor ies include emissions of one HAP with available quantitative inhalation dose

- response values. Th is HAP, its dose

- response values, and the sourc e of the value s are lis ted in Table 2 .6

- 1

.

Table 2.6

- 1 Dose

- Response Values for Chronic Inhalation Exposures

Pollutant CAS Number RfC

(mg/m 3 ) URE

(1/μg/m 3 ) Source a Chromium VI Compounds 18540299 0.0001 0.012 IRIS

-- L

a The descriptors L (low), M (medium), and H (high) have been added for IRIS RfC values to indicate the overall level of confidence in the RfC value, as reported in the IRIS file.



### 2.7 Risk Characterization

2.7.1 General

The final product of the risk assessment is the risk characterization, in which the information from the previous steps is integrated and an overall conclusion about risk is synthesized that is complete, informative, and useful for decision makers. In general, the nature of this risk characterizati on depends on the information available, the application of the risk information

2 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 Assessme nt, California Environmental Protection Agency. February 2000 ( http://www.oehha.ca.gov/air/chronic_rels/pdf/relsP32k.pdf )Draft Risk Assessment for Chrome Plating Source Categories

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and the resources available. In all cases, major issues associated with determining the nature and extent of the risk are identified and discussed. Further, the EPA Administ rator’s March 1995 Policy for Risk Characterization [ 17 ] specifies that a risk characterization ―be prepared in a manner that is clear, transparent, reasonable, and consistent with other risk characterizations of similar scope prepared a cross programs in th e Agency.‖ These principles of transparency and consistency have been reinforced by the Agency’s Risk Characterization Handbook [ 18 ], in 2002 by the Agency’s information quality guidelines [ 19 ] , and in the OMB/OSTP September 2007 Memo randum on Updated Princ iples for Risk Analysis 3 , and are incorporated in these assessments.

Estimates of health risk are presented in the context of uncertainties and limitations in the data and methodology. Through our tiered, iterative analytical approach, we have attempted to reduce both uncertainty and bias to the greatest degree possible in these assessments, within the limitations of available time and resources. We provide summaries of risk metrics (including maximum individual cancer risks and noncancer hazards, as wel l as cancer incidence estimates) along with a discussion of the major uncertainties associated with their derivation to provide decision makers with the fullest picture of the assessment and its limitations.

For each carcinogenic HAP included in an assess ment that has a potency estimate available, individual and population cancer risks are calculated by multiplying the corresponding lifetime average exposure estimate by the appropriate URE. This calculated cancer risk is defined as the upper

- bound probabi lity 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 by a mutagenic mode

- of

- action [ 20 ], we apply EPA’s Supplemental Guidance for Assessing Susceptibility from Early

- Life Exposure to Carcinogens [ 21 ]

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

- 1), 3 (for children aged 2

- 15), or 1.6 (for 70 years of exposure beginning at birth), as needed in risk assessments . In this case, this has the effect of increasing the estimated life time risks for these pollutants by a factor of 1.6. In addition, although only a small fraction of the total POM emissions may be reported as individual compounds, EPA expresses carcinogenic potency for compounds in this group in terms of benzo[a]pyrene equivalence, based on evidence that carcinogenic POM have the same mutagenic mechanism of action as does benzo[a]pyrene. For this reason

, EPA implem entation policy [ 22 ] recommends applyi ng the Supplemental Guidance to all carcinogenic PAH s for which risk estimates are based on relative potency. Accordingly, we apply the Supplemental Guidance to all unspeciated POM mixtures.

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

3 Memorandum f

or t he Heads o f Executive Departments a nd Agencies

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

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estimated by multiplyi ng the estimated lifetime cancer risk for each census block by the number of people residing in that block, then summing the results for the entire modeled domain. This lifetime population incidence estimate is divided by 70 years to obtain an estimate of the number of cancer cases per year.

Unlike linear dose

- response assessments for cancer, non

- cancer health hazards generally are not expressed as a probability of an adverse occurrence. Instead, ―risk‖ for non

- cancer effects is expressed by comparing an exposure to a reference level as a ratio. The ―hazard quotient‖ (HQ) is the estimated exposure divided by a reference level (e.g., the RfC). For a given HAP, exposures at or below the reference level (HQ ≤ 1) are not likely to cause adverse health effects . As exposures increase above the reference level (HQs increasingly greater than 1), the potential for adverse effects increases. For exposures predicted to be above the RfC, the risk characterization includes the degree of confidence ascribed to the RfC values for the compound(s) of concern (i.e., high, medium, or low confidence) and discusses the impact of this on possible health interpretations.

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

.

2.7.2 Mixtures

Since most or all receptors in these assessments receive exposures to multiple pollutants rather than a single pollutant, we estimated the aggregate health risks associated with all the exposures from a particular source category combined.

To combine risks across multiple carcinogens, our assessments use the mi xtures guidelines’ [ 23

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

In assessing non

- cancer hazard from chronic exposures, in cases where different pollutants cause adverse health effects via completely d ifferent modes of action, it may be inappropriate to aggregate HQs. In consideration of these mode

- of

- action differences, the mixtures guideli nes support aggregating effects of different substances in specific and limited ways. To conform to these guidelines, we aggregated non

- cancer HQs of HAPs that act by similar toxic modes of action, or (where this information is absent) that affect the sam e target organ. This process creates, for each target organ, a target

- organ

- specific hazard index (TOSHI), defined as the sum of hazard quotients for individual HAPs that affect the same organ or organ system. A ll TOSHI calculations presented here were b ased 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 is done only in cases where the cri tical dose affects more than one target organ

. Because impacts on organs or systems that occur above the critical dose have not beenDraft Risk Assessment for Chrome Plating Source Categories

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included in the TOSHI calculations, some TOSHIs may be underestimated. As with the HQ, the TOSHI should not be interprete d as a probability of adverse effects, or as strict delineation of ―safe‖ and ―unsafe‖ levels. Rather, the TOSHI is another measure of the potential for adverse health outcomes associated with pollutant exposure, and needs to be interpreted carefully by h ealth scientists and risk managers.

2.7.3 Facility

- Wide Risk s

To help place the source category risks in context, we examined ―facility

- wide‖ risks using the results of a risk assessment based on the 2005 National Emissions Inventory (NEI) that was used in the 2005 NATA . For the facilities in the se source categor ies , we extracted (based on facility ID) t he estimates of inhalation cancer and chronic non

- cancer risks associated with all HAP emissions sources at the facilit ies

, including emissions sources that are not part of th e source categor ies but that are located within a contiguous area and are under common control

. We replaced the inhalation cancer and chronic non

- cancer risks from chromium anodizing and chromium electroplating with the estimates from the c urrent risk assessment to provide a facility

- wide assessment as current as possible. We analyzed risks due to the inhalation of HAP for the populations residing within 5 0 kilometers of each facility. The results of this facility

- wide assessment are provi ded for the highest

- risk facility below in the Risk Results section of this document. The complete results of the facility

- wide assessment are provided in Appendix 4

.

2.7.4 MACT

- Allowable Risks

The emissions data in the data sets for these source catego ries are estimates of actual emissions on an annual basis , and t he results presented in the following sections focus on the risks based on these actual emissions. However, we also estimated MACT

- allowable emissions and the ir associated risks. T o estimat e allowable emissions for facilities for which actual emissions concentration data were available, we calculated the allowable emissions by assuming the emissions concentration is equal to the emissions limit. For other facilities , we used the same approac h used to estimate actual emissions described previously (i.e., a simulation model of the pool of available data on emissions concentrations, exhaust flow rates, and annual operating hours for each process type). However, instead of using the actual emiss ions concentration data in the simulation model, we used the corresponding emissions limit. Thus, we calculated the allowable emissions by using the pool of available data on exhaust flow rates and annual operating hours for each process type and assumed each sources had emissions concentrations equal to the emissions limit (i.e., we assumed they were emitting at the maximum level allowed by the MACT standard). As was used for calculating actual emissions estimates, 5,000 simulations were performed for ea ch facility , and the average of simulated values was used to represent allowable emissions for the facility

.


### 3 Risk Results for the Chromium Anodizing, Decorative Chromium Electroplating, and Hard Chromium Electroplating Source Categories

3.1 Source Category Des cription s and ResultsDraft Risk Assessment for Chrome Plating Source Categories

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The h ard c hromium e lectroplating source category consists of facilities that plate base metals with a relatively thick layer of chromium using an electrolytic process. Hard chromium electroplating provides a finish that is resistant to wear, abrasion, heat, and corrosion. These facilities plate large cylinders and industrial rolls used in construction equipment and printing presses, hydraulic cylinders and rods, zinc die castings, plastic molds, engine components, and marine hardwar e.

The d ecorative c hromium e lectroplating source category consists of facilities that plate base materials such as brass, steel, aluminum, or plastic with layers of copper and nickel, followed by a relatively thin layer of chromium to provide a bright, ta rnish

- and wear

- resistant surface. Decorative chromium electroplating is used for items such as automotive trim, metal furniture, bicycles, hand tools, and plumbing fixtures.

The c hromium a nodizing source category consists of facilities that use chromi c acid to form an oxide layer on aluminum to provide resistance to corrosion. The chromium anodizing process is used to coat aircraft parts (such as wings and landing gears) as well as architectural structures that are subject to high stress and corrosive conditions.

The HAP emission sources subject to the c hromium e lectroplating MACT standards are the tanks in which the chromium deposition takes place. For hard chromium and decorative chromium electroplating facilities, the emission sources are elect roplating tanks. For the

c hromium a nodizing source category, the emission sources are anodizing tanks.

The primary emission controls used by the facilities in these source categories include packed bed scrubbers, mesh pad mist eliminators, composite me sh pad (CMP) systems, high efficiency particulate air (HEPA) filters, and wetting agent/fume suppressants (WAFS). Most decorative chromium electroplating facilities comply with the MACT standards by using WAFS in the tank bath to control surface tension, which in turn reduces emissions. Some facilities use a combination of WAFS and add

- on control to meet the MACT emission limits. If a facility controls emissions using an add

- on control device, the tank is generally equipped with a hood and duct work to e xhaust emissions through the control device and out the stack. However, when WAFS are used as the only means of emission control, the tanks often are not equipped with exhaust hoods. In such cases, emissions from the tank are fugitive and are exhausted t o the outside using wall

- mounted exhaust fans.

We estimate there are 145 5 facilities currently subject to the c hromium e lectroplating MACT standards. Of these, we estimate there are 699 hard chromium electroplating facilities

, 577 decorative chromium electroplating facilities , and 179 chromium anodizing facilities . Some facilities perform more than one type of chromium electroplating or anodizing. For purposes of our estimates, we classified facilities as hard chromium, decorativ e chromium, or chromium anodizing based on the primary type of electroplating operation performed at the facility. Some chromium electroplating facilities electroplate items that are used internally in the manufacturing process at the same facility or wit hin the same company. For example, some large printing facilities electroplate their printing rollers in house, and the chromium electroplating processes are located at the same site as the printing and publishing processes.Draft Risk Assessment for Chrome Plating Source Categories

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The data collected include information on 346 facilities and actual emissions data for approximately 270 facilities. After eliminating redundancies in the data and deleting data for facilities that were no longer in operation or no longer performing chromium electroplating, the da ta set included annual emissions for 197 facilities currently in operation. To assess nationwide residual risk, it was necessary to estimate emissions for much of the industry. We used a Monte Carlo procedure to simulate actual emissions for those facili ties for which actual emissions data were not available. The simulation model used the pool of available data on actual emissions concentrations, exhaust flow rates, and annual operating hours for each process type (hard chromium electroplating, decorativ e chromium electroplating, and chromium anodizing). Actual emissions data (lbs/yr) were fitted to a Weibull distribution and emissions were simulated using the actual data for each facility type. A total of 5,000 simulations were performed for each facil ity, and the average value for the simulated emissions was used to represent actual emissions for each facility.

In all the data sets, chromium compounds account for all the HAP emissions from the chromium electroplating and chromium anodizing source cate gories. I t was assumed that emissions from all chromium electroplating sources consisted of 98 percent hexavalent chromium and 2 percent trivalent chromium. The actual speciation of chromium in exhaust streams may vary slightly from source to source. Howe ver, historical data indicate that emissions from chromium electroplating sources are almost entirely comprised of hexavalent chromium, and the 98%/2% assumed speciation was believed to be representative of sources
on average.

The emissions for the hard c hromium electroplating source category are summarized in Table 3.1

- 1, t he emissions for the decorative chromium electroplating source category are summarized in Table 3.1

- 2, and t he emissions for the chromium anodizing source category are summarized in Tab le 3.1

- 3

.

Table 3.1

- 1 Summary of Emissions from the Hard Chromium Electroplating Source Category

HAP NPRM

Emissions (tpy) Number of

Facilities in the dataset Prioritized Inhalation Dose

- Response Value Identified by OAQPS a
PB

HAP ? Unit Risk Estimate for Cancer? Reference

Concentration for Chronic Non

- cancer ? Health

Benchmark Values for Acute Non

cancer ? Chromium III Compounds 0.008 699

Chromium VI Compounds 0.4 699 Y

a Specific dose

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

at http://www.epa.gov/ttn/atw/toxsource/summary.html and are availabl e in Appendix 5 of the Development of Preliminary Risk Estimates for Source Categories Previously Subjected to Technology

- based Standards document.Draft Risk Assessment for Chrome Plating Source Categories

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Table 3.1

- 2 Summary of Emissions from the Decorative Chromium Electroplating Source Category

HAP NPRM

Emissions (tpy) Number of

Facilities in the data set Prioritized Inhalation Dose

- Response Value Identified by OAQPS a
PB

HAP ? Unit Risk Estimate for Cancer? Reference

Concentration for Chronic Non

- cancer ? Health

Benchmark Values for Acute Non

cancer ? Chromium III Compounds 0.00 3 577

Chromium VI Compounds 0.1 577 Y

a Specific dose

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

at http://www.epa.gov/ttn/atw/toxsource/summary.html and are availabl e in Appendix 5 of the Development of Preliminary Risk Estimates for Source Categories Previously Subjected to Technology

- based Standards document.

Table 3 .1

- 3 Summary of Emissions from the Chromium Anodizing Source Category

HAP NPRM

Emissions (tpy) Number of

Facilities in the data set Prioritized Inhalation Dose

- Response Value Identified by OAQPS a
PB

HAP ? Unit Risk Estimate for Cancer? Reference

Concentration for Chronic Non

- cancer ? Health

Benchmark Values for Acute Non

cancer ? Chromium III Compounds 0.000 7 179

Chromium VI Compounds 0.03 179 Y

a Specific dose

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

at http://www.epa.gov/ttn/atw/toxsource/summary.html and are available in Appendix 5 of the Development of Preliminary Risk Estimates for Source Categories Previously Subjected to Technology

- based Standards document.



### 3.2 Risk Characterization

This section presents the results of the risk assessment for the source categor ies . The basic chronic inhalation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chronic haz ard index, and the cancer incidence. Also presented are the HAP ―drivers,‖ which are the HAPs that collectively contribute 90 percent of the maximum cancer risk or maximum hazard index at the highest exposure location, as well as a summary of the results of our facility

- wide assessments and our analysis of risks associated with the maximum allowed emissions under the current MACT standards. A detailed summary of the facility

- specific risk assessment results is available in Appendix 4

.

Table 3.2

- 1 summarize s the chronic inhalation risk results for th e hard chromium electroplating source category

. The results indicate that maximum lifetime individual cancer risks could be as high as 2 0 in a million, with chromium VI as the sole contributor to the risk. The total estimated cancer incidence from the source category is 0.0 5 excess cancer cases per year, or one case in every 2 0 years. Approximately 1

, 1 00 people are estimated to have cancer risks at or above 10 in a million, and ap proximately 1 3 0,000 people are estimated to haveDraft Risk Assessment for Chrome Plating Source Categories

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cancer risks at or above 1 in a million as a result of the emissions from 1 96 facilities

. The maximum chronic noncancer TOSHI value for the source category could be as high as 0. 02 from emissions of chromiu m VI.

Analysis of potential differences between actual emissions levels and the maximum emissions allowable under the MACT standards for hard chromium electroplating were also calculated. Risk results from the inhalation risk assessment using the MACT

- a llowable emissions (available in Appendix 4 ) indicate that the MIR could be as high as 50 in a million, and that the maximum chronic noncancer TOSHI value could be as high as 0.04

.

Table 3.2

- 1 Summary of Source Category Level Risks for Hard Chromium Electroplating Result HAP “Drivers” Facilities in Source Category Number of Facilities Estimated to be i n Source Category 699 n/a

Number of Facilities Identified Modeled in Preliminary Risk Assessment 699 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 20 chromium (VI) compounds
Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a Greater than or equal to 10 in 1 million 13 chromium (VI) compounds Greater than or equal to 1 in 1 million 196 chromium (VI) compounds Chronic Noncancer Risks Maximum Respiratory Hazard Index 0.02 chromium (VI) compounds Number of Facilities with Maximum Respiratory Hazard Index: Greater than 1 0 n/a Acute Noncancer Screening Results Maximum Acute Hazard Quotient a n/a Number of Facilities With Potential for Acute Effects 0 n/a
Population Exposure Number of People Living Within 50 Kilometers of Facilities Modeled 226

, 0 0 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 1,100 n/a Greater than or equal to 1 in 1 million 13 0 ,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 n/a
Contribution of HAP to Cancer Incidence chromium (VI) compounds 100% n/a

a Because there are no HAPs with an acute dose

- response benchmark value, no acute hazard quotients were calculated.Draft Risk Assessment for Chrome Plating Source Categories

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F acility

- wide MIR and TOSHI values ( available in Appendix 4) are based on actual emissions from all sources at the identified facilities. The results of the facility

- wide assessment for facilities with hard chromium electroplating operations are summarized in Table 3 .2

- 2 . The results indicate that 206 facilities have a facility

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

- wide MIR is 7 0 in a million, driven by emissions of nickel compounds from unspecified sources . The source category contributes approximately 20 percent to the facility

- wide MIR. The maximum facility

- w ide TOSHI value is 2, also driven by emissions of nickel compounds from unspecified sources . The source category contributes less than 1 percent to the facility

- wide TOSHI value.

Table 3.2

- 2 Source Category Contribution to F acility

- Wide Cancer Risks

– Hard Chromium Electroplating

Hard Chromium Electroplating Number of Facilities Binned by Facility

- Wide MIR (in 1 million) Source Category MIR Contribution to Facility

- Wide MIR < 1 1≤ MIR<10 10≤ MIR<100 > 100 Total

> 90% 468 180 12 0 660 50

- 90% 8 2 1 0 11 10

- 50% 9 3 1 0 13 < 10% 8 6 1 0 15 Total 493 191 15 0 699

Table 3.2

- 3 summarize s the chronic inhalation risk results for th e decorative chromium electroplating source category

. The results indicate that maximum lifetime individual cancer risks could be as high as 10 in a million, with chromium VI as the sole contributor to the risk. The total estimated cancer incidence from the source category is 0.02 excess cancer cases per
yea r, or one case in every 50 years. Approximately 100 people are estimated to have cancer risks at or above 10 in a million, and approximately 43,000 people are estimated to have cancer risks at or above 1 in a million as a result of the emissions from 100 facilities. The maximum chronic noncancer TOSHI value for the source category could be as high as 0. 008 from emissions of chromium VI.

Table 3.2

- 3 Summary of Source Category Level Risks for Decorative Chromium Electroplating Result HAP “Drivers” Facilities in Source Category Number of Facilities Estimated to be i n Source Category 577 n/a

Number of Facilities Identified Modeled in Preliminary Risk Assessment 577 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 10 chromium (VI) compounds
Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a Greater than or equal to 10 in 1 million 1 chromium (VI) compoundsDraft Risk Assessment for Chrome Plating Source Categories

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Table 3.2

- 3 Summary of Source Category Level Risks for Decorative Chromium Electroplating Result HAP “Drivers” Greater than or equal to 1 in 1 million 100 chromium (VI) compounds Chronic Noncancer Risks Maximum Respiratory Hazard Index 0.008 chromium (VI) compounds Number of Facilities with Maximum Respiratory Hazard Index: Greater than 1 0 n/a Acute Noncancer Screening Results Maximum Acute Hazard Quotient a n/a Number of Facilities With Potential for Acute Effects 0 n/a
Population Exposure Number of People Living Within 50 Kilometers of Facilities Modeled 21 9

, 000

, 0 00 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 140 n/a Greater than or equal to 1 in 1 million 43,000 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) 0.02 n/a
Contribution of HAP to Cancer Incidence chromium (VI) compounds 100% n/a

a Because there are no HAPs with an acute dose

- response benchmark value, no acute hazard quotients were calculated.

Analysis of potential differences between actual emissions levels and the maximum emissions allowable under the MACT standards for decorative chromium electroplating were also calculated. Risk results from the inhalation risk assessment using the MACT

- allowable emissions (available in Appendix 4 ) indicate that the MIR could be as high as 7 0 in a million, and that the maximum chronic noncancer TOSHI value could be as high as 0.0 6

.
The results of the facility

- wide assessment for facilities with decorative chromium electroplating operations are summarized in Table 3 .2

- 4 . The results indicate that 121 facilities have a facility

- wide cancer MIR g reater than or equal to 1 in a million. The maximum facility

- wide MIR is 8 0 in a million, driven by emissions of trichloroethylene from solvent degreasing . The source category contributes approximately 1 percent to the facility

wide MIR. The maximum facility

- wide TOSHI value for the source category is 7 , driven by emissions of nickel and manganese compounds from unspecified sources . The source category contributes less than 1 percent to the facility

- wide TOSHI value.Draft Risk Assessment for Chrome Plating Source Categories

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Table 3.2

- 4 Source Category Contribution to Facility

- Wide Cancer Risks

– Decorative Chromium Electroplating

Decorative Chromium Electroplating Number of Facilities Binned by Facility

- Wide MIR (in 1 million)

Source Category MIR Contribution to Facility

- Wide MIR < 1 1≤ MIR<10 10≤ MIR<100 > 100 Total

> 90% 400 96 1 0 497 50

- 90% 19 1 0 0 20 10

- 50% 8 5 3 0 16 < 10% 29 9 6 0 44 Total 456 111 10 0 577

Table 3.2

- 5 summarize s the chronic inhalation risk results for th e chromium anodizing source category

. The results indicate that maximum lifetime individual cancer risks could be as high as 5 in a million, with chromium VI as the sole contributor to the risk. The total estimated cancer incidence from the source category is 0.003 excess cancer cases per year, or one case in every 300 years. No people are estimated to have cancer risks at or above 10 in a million, and approximately 5,000 people are estimated to have cancer risks at or above 1 in a million as a result of the emissi ons from 32 facilities. The maximum chronic noncancer TOSHI value for the source category could be as high as 0. 004 from emissions of chromium VI.

Table 3.2

- 5 Summary of Source Category Level Risks for Chromium Anodizing

Result HAP “Drivers” Facilities in Source Category Number of Facilities Estimated to be i n Source Category 179 n/a

Number of Facilities Modeled in Preliminary Risk Assessment 179 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 5 chromium (VI) compounds
Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a Greater than or equal to 10 in 1 million 0 n/a Greater than or equal to 1 in 1 million 32 chromium (VI) compounds Chronic Noncancer Risks Maximum Respiratory Hazard Index 0.004 chromium (VI) compounds Number of Facilities with Maximum Respiratory Hazard Index: Greater than 1 0 n/a Acute Noncancer Screening Results Maximum Acute Hazard Quotient a n/a Number of Facilities With Potential for Acute Effects 0 n/a
Population ExposureDraft Risk Assessment for Chrome Plating Source Categories

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Table 3.2

- 5 Summary of Source Category Level Risks for Chromium Anodizing

Result HAP “Drivers” Number of People Living Within 50 Kilometers of Facilities Modeled 158

, 00 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 5,000 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) 0.003 n/a
Contribution of HAP to Cancer Incidence chromium (VI) compounds 100% n/a

a Because there are no HAPs with an acute dose

- response benchmark value, no acute hazard quotients were calculated.

Analy sis of potential differences between actual emissions levels and the maximum emissions allowable under the MACT standards for chromium anodizing were also calculated. Risk results from the inhalation risk assessment using the MACT

- allowable emissions (av ailable in Appendix 4 ) indicate that the MIR could be as high as 6 0 in a million, and that the maximum chronic noncancer TOSHI value could be as high as 0.0 5

.
The results of the facility

- wide assessment for facilities with chromium anodizing operations

ar e summarized in Table 3 .2

- 6 . The results indicate that 35 facilities have a facility

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

- wide MIR is 1 0 in a million, driven by emissions of trichloroethylene from solvent degreasi ng . The source category contributes approximately 1 percent to the facility

- wide MIR. The maximum facility

- wide TOSHI value for the source category is 0.1 . The source category contributes less than 1 percent to the facility

- wide TOSHI

.
As discussed above, there are no HAPs with an acute dose

- response benchmark value emitted from the sources in these source categories . Therefore, we did not perform a quantitative risk assessment for acute exposures to these pollutants. Also, no PB

- HAP e missions were identified from these s ource c ategories , indicating that exposures due to non

- inhalation routes of exposure are not significant.Draft Risk Assessment for Chrome Plating Source Categories

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Table 3.2

- 6 Source Category Contribution to Facility

- Wide Cancer Risks

– Chromium Anodizing

Chromium Anodizing Number of Facilities Binned by Facility

- Wide MIR (in 1 million) Source Category MIR Contribution to Facility

- Wide MIR < 1 1≤ MIR<10 10≤ MIR<100 > 100 Total

> 90% 137 31 0 0 168 50

- 90% 1 0 0 0 1 10

- 50% 3 2 0 0 5 < 10% 3 1 1 0 5 Total 144 34 1 0 179



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

While some of the preceding section s discuss ed speci fic uncertainties unique to the source categor ies , the following includes a general discussion of unce rtainties associated with RTR
assessments

.


### 4.1 Exposure Modeling Uncertainties

Although every effort has been made to identify all the relevant facilities and emission points, as well as to develop accurate estimates of the annual emission rates for all relevant HAPs , the uncertainties in our emission inventory likely dominate the un certainties in our exposure modeling estimates. The chronic exposure modeling uncertainties are considered relatively small in comparison, since we are using EPA’s refined local dispersion model with site

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

- or long

- term population mobility and by neglecting processes like deposition, plume depletion, and atmospheric degradation. Additionally, estimates o f the maximum individual risk (MIR) contain uncertainty, because they are derived at census block centroid locations rather than actual residences. This uncertainty is known to create potential underestimates and overestimates of the actual MIR values for individual facilities, but, overall, it is not thought to have a significant impact on the estimated MIR for a source category. Finally, we did not factor in the possibility of a source closure occurring during the 70

- year chronic exposure period, leadin g to a potential upward bias in both the MIR and population risk estimates; nor did we factor in the possibility of population growth during the 70

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

A sensitivity analysis performed for the 1999 NATA found that the selection of the meteorology dataset location could result in a range of chronic ambient concentrations which varied from as much as 17% below the estimated value to as much as 84% hi gher than the estimated value. This variability translates directly to the estimated exposures and risks in ourDraft Risk Assessment for Chrome Plating Source Categories

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assessment, indicating that the actual risks could vary from 17% lower to 84% higher than the estimated values.



### 4.2 Uncertainties in the Dose

- Resp onse Relationships

In the sections that follow, separate discussions are provided on uncertainty associated with cancer potency factors and noncancer reference values. Cancer potency values are derived for chronic (lifetime) exposures. Noncancer referen ce values are generally derived for chronic exposures (up to a lifetime), bu t may also be derived for acute ( <24 hours), short

- term (>24 hours up to 30 days), and subchronic (>30 days up to 10% of lifetime) exposure durations, all of which are derived bas ed on an assumption of continuous exposure throughout the duration specified. For the purposes of assessing all potential health risks associated wit h the emissions included in an assessment, we rely on both chronic (cancer and noncancer) and acute ( nonca ncer ) 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 HAPs have no peer

- reviewed cancer potency values o r reference values for chronic non

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

Additionally, chronic dose

- response values for certain compounds included in the assessment may be under EPA IRIS review, and revised assessments may determine that these pollutants are more or less potent than currently thought. We will re

- e valuate risks if, as a result of these reviews, a dose

- response metric changes enough to indicate that the risk assessment may significantly mischaracterize human health risk

Cancer assessment

The discussion of dose

- response uncertainties in the estimation of cancer risk below focuses on the uncertainties associated with the specific approach currently used by the EPA to develop cancer potency factors. In general, these same uncertainties atten d 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 Carcinog en Risk Assessment [ 25 ] (herein referred to as Cancer Guidelines ). ―The primary goal of EPA actions is protection of human health; accordingly, as an Agency policy, risk assessment procedures, including default options that are used in the absence of scien tific data to the contrary, should be health protective.‖ The approach adopted in this document is consistent with this approach as described in the Cancer Guidelines

.
For cancer endpoints EPA usually derives an oral slope factor for ingestion and a unit risk value for inhalation exposures. These values allow estimation of a lifetime probability of developing cancer given long

- term exposures to the pollutant. Depending on the pollutantDraft Risk Assessment for Chrome Plating Source Categories

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being evaluated, EPA relies on both animal bioassay and epidemiologi cal studies to characterize cancer risk. As a science policy approach, consistent with the Cancer Guidelines , EPA uses animal cancer bioassays as indicators of potential human health risk when other human cancer risk data are unavailable.

Extrapolatio n of study data to estimate potential risks to human populations is based upon EPA’s assessment of the scientific database for a pollutant using EPA’s guidance documents and other peer

- reviewed methodologies. The EPA Cancer Guidelines describes the Agency ’s recommendations for methodologies for cancer risk assessment. EPA believes that cancer risk estimates developed following the procedures described in the Cancer Guidelines and outlined below generally provide an upper bound estimate of risk. That is, EPA’s upper bound estimates represent a ―plausible upper limit to the true value of a quantity‖ (although this is usually not a true statistical confidence limit). 4 In some circumstances, the true risk could be as low as zero; however, in other circumstan ces the risk could also be greater. 5 When developing an upper bound estimate of risk and to provide risk values that do not underestimate risk, EPA generally relies on conservative default approaches. 6 EPA also uses the upper bound (rather than lower bo und or central) estimates in its assessments, although it is noted that this approach can have limitations for some uses (e.g. priority setting, expected benefits analysis).

Such health risk assessments have associated uncertainties, some which may be con sidered quantitatively, and others which generally are expressed qualitatively. Uncertainties may vary substantially among cancer risk assessments associated with exposures to different pollutants, since the assessments employ different databases with dif ferent strengths and limitations and the procedures employed may differ in how well they represent actual biological processes for the assessed substance. EPA’s Risk Characterization Handbook also recommends that risk characterizations present estimates d emonstrating the impact on the assessment of alternative choices, data, models and assumptions [ 26 ]. Some of the major sources of uncertainty and variability in deriving cancer risk values are described more fully below.

(1) The qualitative similarities or differences between tumor responses observed in experimental animal bioassays and those which would occur in humans are a source of uncertainty in cancer risk assessment. In general, EPA does not assume that tumor sites observed in an experimental ani mal bioassay are necessarily predictive of the sites at which

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

5 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 o n maximum likelihood estimates.

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

- assessment process when the correct scientific model is unknown or uncertain.‖ The 1983 NRC report Risk Assessment in the Federal Government: Managing the Process defined default option as ―the option chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to the contrary‖ (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the agency may depart from them in evaluating the risks posed by a specific substance w hen 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 overesti mate 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

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tumors would occur in humans. 7 However, unless scientific support is available to show otherwise, EPA assumes that tumors in animals are relevant in humans, regardless of target organ concorda nce. For a specific pollutant, qualitative differences in species responses can lead to either under

- estimation or over

- estimation of human cancer risks.

(2) Uncertainties regarding the most appropriate dose metric for an assessment can also lead to differences in risk estimates. For example, the measure of dose is commonly expressed in units of mg/kg/d ingested or the inhaled concentration of the pollutan t. However, data may support development of a pharmacokinetic model for the absorption, distribution, metabolism and excretion of an agent, which may result in improved dose metrics (e.g., average blood concentration of the pollutant or the quantity of ag ent metabolized in the body). Quantitative uncertainties result when the appropriate choice of a dose metric is uncertain or when dose metric estimates are themselves uncertain (e.g., as can occur when alternative pharmacokinetic models are available for a compound). Uncertainty in dose estimates may lead to either over or underestimation of risk.

(3) For the quantitative extrapolation of cancer risk estimates from experimental animals to humans, EPA uses scaling methodologies (relating expected response to differences in physical size of the species), which introduce another source of uncertainty. These methodologies are based on both biological data on differences in rates of process according to species size and empirical comparisons of toxicity betwe en experimental animals and humans. For a particular pollutant, the quantitative difference in cancer potency between experimental animals and humans may be either greater than or less than that estimated by baseline scientific scaling predictions due to uncertainties associated with limitations in the test data and the correctness of scaled estimates.

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

(5) Extrapolation from high to low doses is an important, and potentially large, source of uncertainty in cancer risk assessment. EPA uses different approaches to low dose risk assessment (i.e., developin g estimates of risk for exposures to environmental doses of an agent from observations in experimental or epidemiological studies at higher dose) depending on the available data and understanding of a pollutant’s mode of action (i.e., the manner in which a pollutant causes cancer). EPA’s Cancer Guidelines express a preference for the use of reliable, compound

- specific, biologically

- based risk models when feasible; however, such models are rarely available. The mode of action for a pollutant (i.e., the man ner in which a

7 Per the EPA Cancer Guidelines: ―The default option is that positive effects in animal can cer studies indicate that the agent under study can have carcinogenic potential in humans.‖ and ―Target organ concordance is not a prerequisite for evaluating the implications of animal study results for humans.‖Draft Risk Assessment for Chrome Plating Source Categories

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pollutant causes cancer) is a key consideration in determining how risks should be estimated for low

- dose exposure. A reference value is calculated when the available mode of action data show the response to be nonlinear (e.g., as in a thre shold response). A linear low

- dose (straight line from POD) approach is used when available mode of action data support a linear (e.g., nonthreshold response) or as the most common default approach when a compound’s mode of action is unknown. Linear extr apolation can be supported by both pollutant

- specific data and broader scientific considerations. For example, EPA’s Cancer Guidelines generally consider a linear dose

- response to be appropriate for pollutants that interact with DNA and induce mutations. Pollutants whose effects are additive to background biological processes in cancer development can also be predicted to have low

- dose linear responses, although the slope of this relationship may not be the same as the slope estimated by the straight line approach.

EPA most frequently utilizes a linear low

- dose extrapolation approach as a baseline science

policy choice (a ―default‖) when available data do not allow a compound

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

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

- dose nonlinear, non

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

- probit models) in representing d ose response relationships due to the variability in response within human populations. Another National Research Council (NRC) report [ 27 ] suggests that models based on distributions of individual thresholds are likely to lead to sigmoidal

- shaped dose

- res ponse functions for a population. This report notes sources of variability in the human population: ―One might expect these individual tolerances to vary extensively in humans depending on genetics, coincident exposures, nutritional status, and various o ther 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 oppos ed to responses in bioassays with genetically more uniform rodents). Note also that low dose linearity in risk can arise for reasons separate from population variability: due to the nature of a mode of action and additivity of a chemical’s effect on top o f background chemical exposures and biological
processes.

As noted above, EPA’s current approach to cancer risk assessment typically utilizes a straight line approach from the BMDL. This is equivalent to using an upper confidence limit on the slope of th e straight line extrapolation. The impact of the choice of the BMDL on bottom line risk estimates can be quantified by comparing risk estimates using the BMDL value to central estimate BMD values, although these differences are generally not a large contr ibutor to uncertainty in risk assessment (Subramaniam et. al., 2006) [ 28 ]. It is important to note that earlier EPA assessments, including the majority of those for which risk values exist today, were generally developed using the multistage model to extra polate down to environmental dose levels and did not involve the use of a POD. Subramaniam et. al. (2006) also provide comparisons indicating that slopes based on straight line extrapolation from a POD do notDraft Risk Assessment for Chrome Plating Source Categories

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show large differences from those based on the upper confidence limit of the multistage model.

(6) Cancer risk estimates do not generally make specific adjustments to reflect the variability in response within the human population

— resulting in another source of uncertainty in assessments. In the d iverse human population, some individuals are likely to be more sensitive to the action of a carcinogen than the typical individual, although compound

- specific data to evaluate this variability are generally not available. There may also be important life stage differences in the quantitative potency of carcinogens and, with the exception of the recommendations in EPA’s Supplemental Cancer Guidance for carcinogens with a mutagenic mode of action, risk assessments do not generally quantitatively address lif e stage differences. However, one approach used commonly in EPA assessments that may help address variability in response is to extrapolate human response from results observed in the most sensitive species and sex tested, resulting typically in the highe st URE which can be supported by reliable data, thus supporting estimates that are designed not to underestimate risk in the face of uncertainty and variability.

Chronic noncancer assessment

Chronic noncancer reference values represent chronic exposure l evels 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 ri sk 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 . Uncertai nty factors are commonly default values 8 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 assumpti ons are needed and more default factors are used. Thus there may be a greater tendency to overestimate risk

— in the sense that further study might support development of reference values that are higher (i.e., less potent) because fewer default assumptions are needed. However, for some pollutants it is possible that risks may be underestimated.

For non

- cancer endpoints related to chronic exposures, EPA derives a Reference Dose (RfD) for exposures via ingestion and a Reference Concentration (RfC) for inhal ation exposures.

8 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 o r uncertain.‖ The 1983 NRC report Risk Assessment in the Federal Government: Managing the Process defined default option as ―the option chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to the contrary ‖ (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the agency may depart from them in evaluating the risks posed by a specific substance when it believes this to be appropriate. In keeping with EPA’s goal of prot ecting 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 a nd Practices, EPA/100/B

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

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These values provide an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure (RfD) or a continuous inhalation exposure (RfC) to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. 9 To derive values that are intended to be ―without appreciable risk,‖ EPA’s methodology relies upon an uncertainty factor (UF) approach [ 29 ],[ 30 ] which includes consideration of both uncertainty and variability.

EPA begins by evaluating all of the available peer

- reviewed literature to determine non

cancer endpoints of concern, evaluating the quality, strengths and limitations of the available

s tudies. EPA typically chooses the relevant endpoint that occurs at the lowest dose, often using statistical modeling of the available data, and then determines the appropriate point of departure (POD) for derivation of the reference value. A POD is deter mined by (in order of preference): (1) a statistical estimation using the benchmark dose (BMD) approach; (2) use of the dose or concentration at which the toxic response was not significantly elevated (no observed adverse effect level

— NOAEL); or (3) use of the lowest observed adverse effect level (LOAEL).

A series of downward adjustments using default UFs is then applied to the POD to estimate the reference value [ 31 ] . While collectively termed ―UFs‖, these factors account for a number of different quant itative 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 vari ability); (2) uncertainty in extrapolating from experimental animal data to humans (i.e., interspecies differences); (3) uncertainty in extrapolating from data obtained in a study with less

- than

- lifetime exposure (i.e., extrapolating from subchronic to chr onic exposure); (4) uncertainty in extrapolating from a LOAEL in the absence of a NOAEL; and (5) uncertainty when the database is incomplete or there are problems with applicability of available studies

. When scientifically sound, peer

- reviewed assessment

- specific data are not available, default adjustment values are selected for the individual UFs. For each type of uncertainty (when relevant to the assessment) , EPA typically applies an UF value of 10 or 3 with the cumulative UF value leading to a downwar d 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 intersp ecies extrapolation is not required) the associated UF is not used. The major adjustment steps are described more fully below.

1) Heterogeneity among humans is a key source of variability as well as uncertainty. Uncertainty related to human variation is considered in extrapolating doses from a subset or smaller

- sized population, often of one sex or of a narrow range of life stages (typical of occupational epidemiologic studies), to a larger, more diverse population. In the absence of pollutant

- specifi c 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 sit uations, a smaller UF of 3 may be applied to reflect a known lack of significant variability among humans.

9 See IRIS glossaryDraft Risk Assessment for Chrome Plating Source Categories

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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 pot ential toxicity to humans , there are uncertainties in such extrapolations. In the absence of data to the contrary, the typical approach is to use the most relevant endpoint from the most sensitive species and the most sensitive sex in assessing risks to t he average human. Typically

, compound specific data to evaluate relative sensitivity in humans versus rodents are lacking, thus leading to uncertainty in this extrapolation. Size

- related differences (allometric relationships) indicate that typically huma ns are more sensitive than rodents when compared on a mg/kg/day basis. The default choice of 10 for the interspecies UF is consistent with these differences. For a s pecific chemical, differences in species responses may be greater or less than this value

.
Pharmacokinetic models are useful to examine species differences in pharmacokinetic processing and associated uncertainties; however, such dosimetric adjustments are not always possible. Information may not be available to quantitatively assess toxicok inetic or toxicodynamic differences between animals and humans, and in many cases a 10

- fold UF (with separate factors of 3 for toxicokinetic and toxicodynamic components) is used to account for expected species differences and associated uncertainty in ext rapolating 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 componen t.

3) In the case of reference values for chronic exposures where only data from shorter durations are available (e.g., 90

- day subchronic studies in rodents) or when such data are judged more appropriate for development of an RfC, an additional UF of 3 o r 10

- fold is typically applied unless the available scientific information supports use of a different value.

4) Toxicity data are typically limited as to the dose or exposure levels that have been tested in individual studies; in an animal study, for exa mple, treatment groups may differ in exposure by up to an order of magnitude. The preferred approach to arrive at a POD is to use BMD analysis; however, this approach requires adequate quantitative results for a meaningful analysis, which is not always po ssible. Use of a NOAEL is the next preferred approach after BMD analysis in determining a POD for deriving a health effect reference value. However, many studies lack a dose or exposure level at which an adverse effect is not observed (i.e., a NOAEL is n ot identified). When using data limited to a LOAEL, a UF of 10 or 3

- fold is often applied.

5) The database UF is intended to account for the potential for deriving an underprotective RfD/RfC due to a data gap preventing complete characterization of the chemical’s toxicity. In the absence of studies for a known or suspected endpoint of concern, a UF of 10 or 3

- fold is typically applied.Draft Risk Assessment for Chrome Plating Source Categories

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### 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 Manufac turing

. EPA

- 452/R

- 09

- 006. http://www.epa.gov/ttn/atw/rrisk/rtrpg.html.

3

. US EPA, 2010. SAB’s Response to EPA’s RTR Risk Assessment Methodologies. http://yosemite.epa.gov/sab/sabproduct.nsf/4AB3966E263D943A8525771F00668381/$File/E PA

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4 . US EPA, 2010. Memorandum from Dave Guinnup to RTR Wood Furniture Docket, entitled, ―EPA’s Actions in Response to Key Rec ommendations 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

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– AERMOD. EPA

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. http://www.epa.gov/scram001/7thconf/aermod/aermodugb.pdf

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8

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9 US EPA, 2005. Table 1. Priorit ized 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. 2005 National Air Toxics Risk Assessment. http://www.epa.gov/ttn/atw/nata 2005

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. US EPA, 2006. Integrated Risk Information System. http://www.epa.gov/iris/index.html

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.
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14

. NRC, 1994. National Research Council. Science and Judgment in Risk Assessment. Washington, DC: National Academy Press.

15

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.

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. CA Office of Environmental Health Hazard Assessment, 2005. Technical Support Document for Describing Available Cancer Potency Factors, May 2005

. http://www.oehha.ca.gov/air/hot_spots/may2005tsd.html

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. http://www.epa.gov/quality/informationguidelines/documents/EPA_InfoQualityGuidelines.pdf

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. US EPA, 2006. Performing risk assessments that include carcinogens described in the Supplemental Guidance as having a mutagenic mode of action. Science Policy Council Cancer Guidelines Implementation Workgroup Communication II: Memo from W.H. Farland dated 14 June 20 06. http://www.epa.gov/osa/spc/pdfs/CGIWGCommunication_II.pdf

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- life exposure to carcinogens. EPA/630/R

- 03003F. http://www.epa.gov/ttn/atw/childrens_supplement_final.pdf

.

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– 830.

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30

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