Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 1



## Draft Residual Risk Assessment fo r the Chromic Acid Anodizing, Decorative Chromium Electropl ating, and Hard Chromium Electroplating Source Categories

by EPA’s Office of Air Qualit y Planning and Standards Office of Air and Radiation July 2010Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 2



### Table of Contents

1 Introduction................................................................................................................. ....... 4 2 Methods...................................................................................................................... ........ 5 2.1 Emissions and source data ......................................................................................... 5 2.2 Dispersion modeling for inha lation exposure assessment ......................................... 5 2.3 Estimating human inhalation exposure ...................................................................... 8 2.4 Acute Risk Screening a nd Refined Assessments....................................................... 8 2.5 Multipathway and environm ental risk screening ....................................................... 9 2.6 Dose-Response Assessment....................................................................................... 9 2.6.1 Sources of chronic dose-response information .................................................. 9 2.7 Risk Characterization............................................................................................... 11 2.7.1 General ............................................................................................................. 11 2.7.2 Mixtures ........................................................................................................... 13 2.7.3 Facility-Wide Risk ........................................................................................... 14 3 Risk Results for the Chromic Acid Anodizi ng, Decorative Chromium Electroplating, and Hard Chromium Electroplating Source Categories.................................................................. 14 3.1 Source Category Descriptions and Results .............................................................. 14 3.2 Risk Characterization............................................................................................... 21 4 General Discussion of Uncertainties a nd How They Have Been Addressed................... 22 4.1 Exposure Modeling Uncertainties............................................................................ 22 4.2 Uncertainties in the Dose-Response Relationships.................................................. 23 5 References................................................................................................................... ..... 29

Index of Tables

Table 2.2-1 AERMOD version 09292 model options for RTR II modeling ............................ 6 Table 2.6-1 Dose-Response Values fo r Chronic Inhalation Exposures.................................. 11 Table 3.1-1 Summary of Emissions from the Hard Chromium Electroplating Source Category

............................................................................................................................... ................... 17 Table 3.1-2 Summary of Source Category Level Risks for Hard Chromium Electroplating. 17 Table 3.1-3 Summary of Emissions from the Decorative Chromium Electroplating Source Category ....................................................................................................................... ............ 18 Table 3.1- 4 Summary of Source Category Level Risks for Decorative Chromium Electroplating ................................................................................................................. .......... 19 Table 3.1-5 Summary of Emissions from th e Chromic Acid Anodizing Source Category.... 20 Table 3.1-6 Summary of Sour ce Category Level Risks for Chromic Acid Anodizing .......... 20

Appendices

Appendix 1 Emissions Inventory Support MemorandumDraft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 3

Appendix 2 Technical Support Docu ment for HEM-AERMOD Modeling Appendix 3 Meteorological Da ta for HEM-AERMOD Modeling Appendix 4 Analysis of Data on Short-Te rm Emission Rates Relative to Long-Term Emission Rates Appendix 5 Detailed Risk Modeling Results

Index of Acronyms

AERMOD American Meteorological Society/EPA Regulatory Model AEGL Acute exposure guideline level ASTDR US Agency for Toxic Substances and Disease Registry CalEPA California Environmental Agency ERPG Emergency Response Planning Guideline HAP Hazardous Air Pollutant HEM Human Exposure Model HI Hazard index HQ Hazard quotient IRIS Integrated Risk Information System MACT Maximum Achievable Control Technology MIR Maximum Individual Risk MOA Mode of action NAC National Advisory Committee NATA National Air Toxics Assessment NEI National Emissions Inventory NPRM Notice of Proposed Rulemaking PB-HAP Persistent and Bioaccumulative HAP POM Polycyclic organic matter REL Reference exposure level RfC Reference concentration RfD Reference dose RTR Risk and Technology TOSHI Target-organ-specific hazard index URE Unit risk estimateDraft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 4



### 1 Introduction

Section 112 of the Clean Air Act (CAA) establ ishes a two-stage regu latory process for addressing emissions of hazardous air pollutants ( HAPs) from stationary sources. In the first stage, section 112(d)(2) requires the Environmental Protectio n Agency (EPA, or the Agency) to develop technology-based standards for categ ories of industrial sources (e.g., petroleum refineries, pulp and paper mills, etc.) [ 1 ]. EPA has largely completed the initial Maximum Achievable Control Technology (MACT) standa rds as required under this provision. Under section 112(d)(6), EPA must review each of thes e technology-based standards at least every eight years and revise a sta ndard, as necessary, “taking in to account developments in practices, processes and control technologies.” In the second stage, EPA is required under section 112(f)(2) to assess th e health and environmental risks that remain after implementation of the MACT standards. If addi tional risk reductions ar e necessary to protect public health with an ample margin of safety or to prevent an adverse environmental effect, EPA must develop standards to address these remaining risks. This second stage of the regulatory process is known as the residual risk stage. For each source category for which EPA issued MACT standards, the residual risk st age must be completed within eight years of promulgation of the initial technology-based standard.

In December of 2006 we consulted with a panel from the EPA's Science Advisory Board (SAB) on the “Risk and Technology Review (R TR) Assessment Plan” and in June of 2007, we received a letter with the results of that c onsultation. Subsequent to the consultation, in July of 2009 a meeting was held with an SAB panel for a formal peer review of the “Risk and Technology Review (RTR) Risk Assessment Methodologies” [ 2 ]. We received the final SAB report on this review in May of 2010. Where appropriate, we have responded to the key messages from this review in developing our current risk assessments and we will be continuing our efforts to improve our assessm ents by incorporating updates based on the SAB recommendations as they are deve loped and become available.

This document contains the methods and result s of baseline risk assessments (i.e., after the implementation of the respective MACT st andards) performed for the chromic acid anodizing, decorative chromium electroplating, and hard chro mium electroplating source categories. The methods discus sion includes descriptions of the methods used to develop refined estimates of chronic inhalation exposur es and human health risks for cancer and noncancer endpoints, as well as de scriptions of the methods used to screen chronic non-inhalation health risks and adverse envir onmental effects. Since none of the screening assessments indicated any significant potential for chronic non-inha lation health effects or environmental impacts, including effects to threatened and endangered species, no further refinement of these assessments was performed. Because there are no HAP with an acute dose-response benchmark value, no acute hazard quotients were calculated for these source categories.Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 5



### 2 Methods

2.1 Emissions and source data

The 2005 National-Scale Air Toxics Assessmen t (NATA) National Emissions Inventory (NEI) served as the starting point for this assessment. The 2005 NEI purportedly contains information on actual emissions during the enti re 2005 base year. Using the process MACT codes 1 , we developed a subset of this inventory th at contains emissions and facility data for the source categories addressed. Next, we performed an engineering review of the information using EPA engineers who were dire ctly involved in the development of the MACT standards for the source category, and/ or who have extensive knowledge of the characteristics of this industry. NEI data were updated with available in dustry supplied data. The goal of the engineering review was to iden tify limitations and issues with the emissions data (particularly those that w ould greatly influence risk estima tes) and to make changes to the data where possible to address these issues and decrease the uncerta inties associated with the assessment.

A review of the NEI data indicated that not all chromium electroplating facilities were included in the data set. To address this situat ion, an additional data set was developed based on 1629 facilities with known addresses. Emissions for each type of plant were estimated based on the model plants developed for the MA CT standards, with hard chromium model plants having the highest emissions, followe d by decorative chromium electroplating, and then chromic acid anodizing.

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



### 2.2 Dispersion modeling for in halation exposure assessment Both long- and short-term inhalation exposure co ncentrations and associat ed health risks 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 dispersion modeling system (HEM-AERMOD). Th e approach used in applying this modeling system is outlined below, and further deta ils are provided in Appendix 2. HEM-AERMOD performs three main operations: atmospheric dispersion modeling, estimation of individual human exposures and health risks, and estimatio n of population risks. This section focuses on the dispersion modeling component. The expos ure and risk characterization components are discussed in other subsecti ons of Sections 2 and 3.

The dispersion model in the HEM-AERMOD sy stem, AERMOD version 09292, is a state-ofthe-science Gaussian plume di spersion model that is prefer red by EPA for modeling point,

1 The tagging of data with MACT codes allows EPA to de termine reductions attributable to the MACT program. The NEI associates MACT codes corresponding to MACT source categories with stationary major and area source data. MACT codes may be assigned either at the pro cess level or at the site level in the point source data (e.g., the MACT code for municipal waste combustors (M WCs) is assigned at the site level whereas the MACT code for petroleum refinery catalytic crack ing is assigned at the process level).Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 6

area, and volume sources of continuous ai r emissions from facility applications [ 3 ]. Further details on AERMOD can be found in the AERMOD Users Guide [ 4 ]. The model is used to develop annual average ambient concentra tions through the simulation of hour-by-hour dispersion from the emission sources into the su rrounding atmosphere. Hourly emission rates used for this simulation are generated by evenly dividing the total annual emission rate from the inventory into the 8,760 hours of the year.

The first step in the application of the HEM-AERMOD modeling system is to predict ambient concentrations at locations of interest. The AERMOD model options employed are summarized in Table 2.2-1 and are discussed further below.

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

Modeling Option Selected Parameter for chronic exposure

Type of calculations Hourly ambient concentration

Source type Point, area represented as pseudo point source

Receptor orientation Polar (13 rings and 16 radials) Discrete (census block centroids)
Terrain characterization Actual from USGS 1-degree DEM data

Building downwash Not Included

Plume deposition/depletion Not Included

Urban source option No

Meteorology 1 year representative NW S from nearest site (158 stations)

Meteorological data for HEM-AERMOD is sele cted from a list of 158 National Weather Service (NWS) surface observation stations ac ross the continental United States, Alaska, Hawaii, and Puerto Rico. In most cases, the neares t 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 em ploy up to five years of data to capture variability in weather patterns fr om year to year. However, because we had an insufficient number of appropriately forma tted model input files derived from available meteorological data, we modeled only a single y ear, typically 1991. While the se lection of a single year may result in underprediction of long- term ambient levels at some locations, likewise it may result in overprediction at others. For each facility identified by its characteristic latitude and longitude coordinates, the clos est meteorological station was us ed in the dispersion modeling. The average distance between a modeled facility and the applicable meteorological station was 40 miles (72 km). Appe ndix 3 (Meteorological Data Processing Using AERMET for HEM-AERMOD) provides a complete listing of stations and assumptions along with further details used in processing the data through AERM ET. The sensitivity of model results to the selection of the nearest weathe r station and the use of one y ear of meteorological data is discussed in “Risk and Technology Review (RTR) Risk Assessment Methodologies.”Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 7

The HEM-AERMOD model estimates ambient concen trations at the geog raphic centroids of census blocks (using the 2000 Census), and at othe r receptor locations that can be specified by the user. The model accounts for the effect s of multiple facili ties when estimating concentration impacts at each block centroid. Typically, we combined only the impacts of facilities within the same source category, and assessed chronic exposur e and risk only for census blocks with at least one resident (i .e., locations where people may reasonably be assumed to reside rather than receptor points at the fenceline of a facility). Chronic ambient concentrations were calculated as the annual average of all estimated short-term (one-hour) concentrations at each block centroid. Possible future residential use of currently uninhabited areas was not considered. Census blocks, the fi nest resolution availa ble in the census data, are typically comprised of approximately 40 people or about ten households.

In contrast to the developmen t of ambient concentrations fo r evaluating long-term exposures, which was performed only for occupied censu s blocks, worst-case short-term (one-hour) concentrations were estimated both at the censu s block centroids and at points nearer the facility that represent locations where people may be present for short periods, but generally no nearer than 100 meters from the center of the facility (note that for large facilities, this 100-meter ring could still contain locations inside the facility property). Since short-term emission rates were needed to screen for the potential for hazard via acute exposures, and since the NEI contains only annual emission tota ls, we applied the gene ral assumption to all source categories that the maxi mum one-hour emission rate from any source was ten times the average annual hourly emission rate for that sour ce. Average hourly emi ssions rate is defined as the total emissions for a year divided by the total number of operating hours in the year. This choice of a factor of ten for screening wa s originally based on engineering judgment. To develop a more robust peak-to-mean emissions factor, and in response to one of the key messages from the SAB consultation on our RTR Assessment Plan, we recently performed an analysis using a short-term emissions dataset from a number of sources located in Texas (originally reported on by Allen et al. 2004)[ 5 ]. In that report, the Texas Environmental Research Consortium Project compared hourly a nd annual emissions data for volatile organic compounds for all facilities in a heavily-industr ialized 4-county area (Harris, Galveston, Chambers, and Brazoria Counties, TX) over an eleven-month time period in 2001. We obtained the dataset and performe d our own analysis, focusing that analysis on sources which reported emitting high quantities of HAP over short periods of time (see Appendix 4, “Analysis of data on short-term emission rates relative to long-term emission rates”). Most peak emission events were less than twice the annual average, and the highest was a factor of 11 times the annual average. The factor of te n is intended to cover both routinely-variable emissions as well as startup, shutdown, and ma lfunction (SSM) emissions. While there are some documented emission excursions above this level, our analysis of the data from the Texas Environmental Research Consortium suggest s that this factor s hould cover more than 99% of the short-term peak gaseous or vol atile HAP emissions from typical industrial

sources.

Census block elevations for HEM-AERMOD modeling were determined nationally from the US Geological Service 1-degree digital elevation model (DEM ) data files, which have a spatial resolution of about 90 meters. Polar gr id elevations (used in estimating short- and long-term ambient concentrations) were evaluated at the highest elevation of any census blockDraft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 8

in that sector. If a sector does not contain a ny blocks, the model defaults to the elevation of the nearest block. If the eleva tion is not provided for the emi ssion source, the model takes the average elevation of all sectors of th e nearest model ring.

In addition to using receptor elevation to determine plume height, AERMOD adjusts the plume’s flow if nearby elevated hills are expected to influence the wind pa tterns. For details on how hill heights were estimated and used in the AERMOD modeling, see Appendix 2.



### 2.3 Estimating human inhalation exposure

For this assessment, we used the annual aver age 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 ce nsus block. That is, this risk analysis did not consider either the short-term or long-term behavior (mobility ) of the exposed populations and its potential influence on their exposure.

We did not address short-term human activity in this assessment for two reasons. First, our experience with the 1996, 1999, 2002 and 2005 NATA assessments [ 6 ] (which modeled daily activity using EPA’s HAPEM m odel) suggests that, given ou r current understanding of microenvironment concentrations and daily ac tivities, modeling short-term activity would, on average, reduce risk estimates about 25% for particulate HAP s; it will also reduce risk estimates for gaseous HAPs, but typically by much less. Second, basing exposure estimates on average ambient concentra tions at census block centr oids may underestimate or overestimate actual exposure conc entrations 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 in th is assessment nor populati on growth or decrease over 70 years, instead basing the assessment on the assumption that each person’s predicted exposure is constant over the cour se of their lifetime which is assumed to be 70 years. In assessing cancer risk, three metrics are gene rally estimated, the maximum individual risk (MIR) which is defined as the risk associated with a lifetime of exposure at the highest concentration, the population risk distribution, and the cancer inci dence. This assumption of not considering short or long- term population mobility does not bias the estimate of the theoretical MIR nor does it aff ect the estimate of cancer inci dence since the total population number remains the same. It does, however, a ffect the shape of the di stribution of individual risks across the affected populati on, shifting it toward higher estim ated individual risks at the upper end and reducing the number of people estima ted to be at lower risks, thereby biasing the risk estimates high.



### 2.4 Acute Risk Screening and Refined Assessments

In establishing a scientifically-defensible approa ch for the assessment of potential health risks due to acute exposures to HAP , we follow the same general approach that is used for developing chronic health risk assessments under the residual risk program. However, forDraft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 9

these source categories, there are no HAP with an acute dose-response benchmark value. Therefore, no acute hazard quotients we re calculated for th e source categories.



### 2.5 Multipathway and envi ronmental risk screening

The potential for significant hum an health risks due to expos ures via routes other than inhalation (i.e., multipathway exposures) was screened by first determining whether any sources emitted any hazardous air pollutants known to be persistent and bioaccumulative in the environment (PB-HAP). The PB-HAP co mpounds or compound classes are identified for the screening from the EPA’s Air Toxics Risk Assessment Library [ 7]. Examples of PB-HAP are cadmium compounds, chlordane, chlo rinated dibenzodioxins and furans, DDE, heptachlor, hexachlorobenzene, hexachlo rocyclohexane, lead compounds, mercury compounds, methoxychlor, polychlor inated biphenyls, polycyclic organic matter, toxaphene, and trifluralin. PB-HAP emissions were not identified from the chromic acid anodizing, decorative chromium electroplating, and hard chromium electroplati ng source categories, indicating that exposures due to non-inhalation routes of e xposure were not significant. The lack of PB-HAP emissions from these source categories indicates a ve ry low potential for adverse environmental effects due to exposures resulting from atmospheric deposition of PBHAPs. Thus, even if sensitive species are presen t in the areas surrounding these facilities with no PB-HAP emissions, it is still reasonable to assume that there are no adverse effects to populations in the areas su rrounding these facilities.

Additionally, we evaluated the potential for significan t ecological exposures to non PB-HAP from exceedances of chronic human health inhala tion thresholds in the ambient air near these facilities. Human health dose -response threshold values are generally derived from studies conducted on laboratory animals (such as rodent s) and developed with the inclusions of uncertainty factors that could be as high as 3000. As a result, these human threshold values are often significantly lower than the level expected to cause an adverse effect in an exposed rodent. It should be noted that there is a scarcity of data on th e direct atmospheric impact of these HAPs on other receptors, such as plants, birds, and wildlife. Thus, if the maximum inhalation hazard in an ecosystem is below the level of concern for humans, we have generally concluded that mammalian receptors shoul d be at no risk of adverse effects due to inhalation exposures from non PB-HAP, and have assurance that other ecological receptors are also not at any significant ri sk from direct atmospheric imp act. In some isolated cases where we have data indicating po tential adverse impacts on plants, birds, or other wildlife due to the direct atmospheric impacts of specific HAP s, we note that as an uncertainty and, where possible, refine our analysis by comparing our modeled impacts to available threshold values from the scientific literature.



### 2.6 Dose-Response Assessment

2.6.1 Sources of chronic dose-response information

Dose-response assessment information (car cinogenic and non-carcinogenic) for chronic exposure (either by inhalation or ingestion) for the HAPs reporte d in the emissions inventoryDraft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 10

is based on the EPA Office of Air Quality Planni ng and Standards’ existing recommendations for HAPs, also used for NATA 1999, 2002, and 2005 [ 8 ]. This information has been obtained from various sources and prioritized according to (1) conceptual consistency with EPA risk assessment guidelines and (2) level of peer re view received. The prioritization process was aimed at incorporating into our assessments th e best available science with respect to doseresponse information. The recommendations ar e based on the following sources, in order of priority:

1) US Environmental Protection Agency (EPA). EPA has developed dose-response assessments for chronic exposure for many of the pollutants in this study. These assessments typically provide a qualitative stat ement regarding the st rength of scientific data and specify a reference concentration (RfC, for inhalation) or reference dose (RfD, for ingestion) to protect against effects othe r than cancer and/or a unit risk estimate (URE, for inhalation) or slope factor (SF, for ingestion) to estimat e the probability of developing cancer. The RfC is defined as an “estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation e xposure to the human population (including sensitive subgroups) that is likely to be without an appreciabl e risk of deleterious effects during a lifetime.” The URE is defined as “the upper-bound excess ca ncer risk estimated to result from continuous lifet ime exposure to an agent at a concentration of 1 μg/m 3 in air.” The SF is “an upper bound, approximating a 95% confidence limit, on the increased cancer risk from a lifetime exposure to an agen t. This estimate, [is] usually expressed in units of proportion (of a populat ion) affected per mg/kg-da y...” EPA disseminates doseresponse assessment information in several fo rms, based on the level of review. The Integrated Risk Information System (IRIS) [ 9 ] is an EPA database that contains scientific health assessment information, including dose -response information. All IRIS assessments since 1996 have also undergone independent ex ternal peer review. The current IRIS process includes review by EPA scientists, interagency reviewers from other federal agencies, and the public, and peer review by in dependent scientists external to EPA. EPA’s science policy approach, under the current carcinogen gui delines, is to use linear low-dose extrapolation as a default option fo r carcinogens for which the mode of action (MOA) has not been identified. We expect future EPA dose-response assessments to identify nonlinear MOAs where appropriate, and we will use those analyses (once they are peer reviewed) in our risk assessments. At this time, however, there are no available carcinogen dose-response assessments for i nhalation exposure that are based on a nonlinear MOA

.
2) US Agency for Toxic Substances and Disease Registry (ATSDR). ATSDR, which is part of the US Department of Health and Huma n Services, develops and publishes Minimum Risk Levels (MRLs) [ 10 ] for inhalation and oral exposur e to many toxic substances. As stated on the ATSDR web site: “Following di scussions with scientists within the Department of Health and Human Services (HHS) and the EPA, ATSDR chose to adopt a practice similar to that of the EPA's Refere nce Dose (RfD) and Reference Concentration (RfC) for deriving substance specific health guidance levels for non neoplastic endpoints.” The MRL is defined as “an estimate of daily human exposure to a subs tance that is likely to be without an appreciable risk of advers e effects (other than cancer) over a specified duration of exposure.” ATSDR describes MRLs as substance-specific estimates to beDraft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 11

used by health assessors to select environm ental contaminants for further evaluation. Exposures above an MRL do not necessarily re present a threat, and MRLs are therefore not intended for use as predictors of adverse health effects or for setting cleanup levels.

3) California Environmental Protection Agency (CalEPA). The CalEPA Office of Environmental Health Hazard Assessment ha s developed dose-response assessments for many substances, based both on carcinogenicity a nd health effects other than cancer. The process for developing these assessments is si milar to that used by EPA to develop IRIS values and incorporates signifi cant external scientific peer review. As cited in the CalEPA Technical Support Document fo r developing their chronic assessments 2 : “The guidelines for developing chronic inhala tion exposure levels incorporate many recommendations of the U.S. EPA [ 11 ] and NAS [ 12 ].” The non-cancer information includes available inhalation hea lth risk guidance values expr essed as chronic inhalation reference exposure levels (RELs) [ 13 ]. CalEPA defines the R EL as “the concentration level at or below which no health effects are anticipated in the gene ral human population.” CalEPA's quantitative dose-response info rmation on carcinogenicity by inhalation exposure is expressed in terms of the URE [ 14 ], defined similarly to EPA's URE.

The emissions inventory for the source categor ies include emissions of three HAP with available quantitative inhalation dose-respon se values. These HAP, their dose-response values, and the source of the va lues are listed 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 III Compounds 16065831 Chromium VI Compounds 18540299 0.0001 0.012 IRIS -- L Chromium Trioxide (VI), chromic acid mist 11115745 0.000008 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 as sessment is the risk characteri zation, in which the information from the previous steps is integrated and an overa ll conclusion about risk is synthesized that is complete, informative, and useful for decision ma kers. In general, the nature of this risk characterization depends on the in formation available, the application of the risk information and the resources available. In all cases, majo r issues associated with determining the nature and extent of the risk are identified and disc ussed. Further, the EPA Administrator’s March 1995 Policy for Risk Characterization [ 15 ] specifies that a risk ch aracterization “be prepared

2 Air Toxics Hot Spots Program, Risk Assessment Guidelines, Part III - Technical Support Document for the Determination of Non-cancer Chronic Referen ce Exposure Levels. Air Toxicology and Epidemiology Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. February 2000 (http://www.oehha.ca.gov/ air/chronic_rels/pdf/relsP32k.pdf)Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 12

in a manner that is clear, transparent, r easonable, and consistent with other risk characterizations of similar scope prepared acro ss programs in the Agency.” These principles of transparency and consistency have been reinforced by the Agency’s Risk Characterization Handbook [ 16 ], in 2002 by the Agency’s information quality guidelines [ 17], and in the OMB/OSTP September 2007 Memorandum on U pdated Principles for Risk Analysis 3 , and are incorporated in these assessments.

Estimates of health risk are pres ented in the context of uncertainties and limitations in the data and methodology. Through our tiered, iterative an alytical approach, we have attempted to reduce both uncertainty and bias to the greatest degree possible in these assessments. In our assessments we provide summaries of risk metrics (including maxi mum individual cancer risks and non-cancer hazards, as well as cancer incidence estimates) along with a discussion of the major uncertainties associated with thei r 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 approp riate URE. This calculated cancer risk is defined as the upper-bound probability of de veloping cancer over a 70- yr 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 le vel may be lower than predicted, and could be

zero.

For EPA’s list of carcinogenic HAPs th at act by a mutagenic mode-of-action [ 18 ], we apply EPA’s Supplemental Guidance for Asse ssing Susceptibility from Early-Life Exposure to Carcinogens [ 19 ]. 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 th is 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 term s 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 implementation policy [ 20 ] recommends applying the Supplemental Guidance to all carcinogenic PAHs for which risk estimates are based on relative potency. Acco rdingly, we apply the Supplemental Guidance to all unspeciated POM mixtures.

Increased cancer incidence for the entire receptor population with in the area of analysis is estimated by multiplying the estimated lifetime cancer risk for each census block by the number of people residing in that block, then summing the results for the entire modeled domain. This lifetime populati on incidence estimate is divide d by 70 years to obtain an estimate of the number of cancer cases per year.

3 Memorandum for the Heads of Executive Departments and Agencies - Updated Principles for Risk Analysis (September 19, 2007), From Susan E. Dudley, Administrator, Office of Information and Regulatory Affairs, Office of Management and Budget; and Sharon L. Hays, Associate Director and Depu ty Director for Science, Office of Science and Technology Policy (http://www.whitehouse.gov/omb/memoranda/fy2007/m07-24.pdf)Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 13

In the case of benzene, the high end of th e reported cancer URE range is used in our assessments to provide a conservative estimate of potential cancer risks. Use of the high end of the range provides risk estimates that are approximately 3.5 times higher than use of the equally-plausible low end value. If the esti mated benzene–associated risks exceed 1 in a million, we evaluate the impact of using the low end of the URE range on our risk results.

Unlike linear dose-response assessments for can cer, noncancer health hazards generally are not expressed as a probability of an adverse occurrence. Inst ead, “risk” for noncancer effects is expressed by comparing an exposure to a refe rence level as a ratio. The “hazard quotient” (HQ) is the estimated exposure divided by a re ference 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 in cludes the degree of confidence ascribed to the RfC values for the compound(s) of concern (i.e., high, medium, or lo w confidence) and discusses the impact of this on possible hea lth interpretations.

The risk characterization for chronic effects othe r than cancer is expressed in terms of the HQ for inhalation, calculated for each HAP at each census block centroid. As discussed above, RfCs incorporate generally conservative uncer tainty 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 adve rse effects will occur, and is unlikely to be proportional to adve rse 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 a ssociated with all the exposures from a particular source category combined.

To combine risks across multiple carcinogens, ou r assessments use the mixtures guidelines’ [ 21

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

In assessing non-cancer hazard from chronic expo sures, in cases where different pollutants cause adverse health effects via completely different modes of action, it may be inappropriate to aggregate HQs. In consideration of th ese mode-of-action differences, the mixtures guidelines support aggregating effects of different substances in specif ic and limited ways. To conform to these guidelines, we aggregated non-cancer HQs of HAPs that act by similar toxic modes of action, or (where this information is absent) that affect the same target organ. This process creates, for each target organ, a target-organ-specific hazard index (TOSHI), defined as the sum of hazard quotients for indi vidual HAPs that affect the same organ or organ system. All TOSHI calcu lations presented here were based exclusively on effectsDraft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 14

occurring at the “critica l dose” (i.e., the lowest dose that pr oduces adverse health effects). Although HQs associated with some pollutants ha ve been aggregated into more than one TOSHI, this is done only in cases where the criti cal dose affects more than one target organ. Because impacts on organs or systems that o ccur above the critical dose have not been 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 e ffects, or as strict delineation of “safe” and “unsafe” levels. Rather, the TO SHI is another measur e of the potential for adverse health outcomes associated with pollu tant exposure, and needs to be interpreted carefully by health scientists and risk managers.

2.7.3 Facility-Wide Risks

To help place the source category risks in cont ext, we examined “facility-wide” risks using the results of the 2005 NATA. For the faciliti es in these source categories, we extracted (based on facility ID) the NAT A estimates of inhalation cancer and chronic non-cancer risks associated with all HAP emissions sources at the facilities, including emissions sources that are not part of the source cat egories but that are located wi thin a contiguous area and are under common control. We analyzed risks due to the inhalation of HAP for the populations residing within 50 kilometers of each facility. The results of this “facility-wide” assessment are provided 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 5.



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

3.1 Source Category Descriptions and Results

The hard chromium electroplating source category consists of fac ilities that plate base metals with a relatively thick layer of chromium using an electrolyt ic process. Hard chromium electroplating provides a finish that is resist ant to wear, abrasion, heat, and corrosion. These facilities plate large cylinders and industrial ro lls used in construction equipment and printing presses, hydraulic cylinders and rods, zinc di e castings, plastic molds, engine components, and marine hardware.

The decorative chromium electropl ating source category consists of facilities that plate base materials such as brass, steel, aluminum, or plastic with laye rs of copper and nickel, followed by a relatively thin layer of chro mium to provide a bright, tarnis h- and wear-resistant surface. Decorative chromium electroplating is used for items such as automotive trim, metal furniture, bicycles, hand t ools, and plumbing fixtures.

The chromic acid anodizing source category consis ts of facilities that use chromic acid to form an oxide layer on aluminum to provide resistance to corrosion. The chromic acid anodizing process is used to coat aircraft parts (suc h as wings and landin g gears) as well as architectural structures th at are subject to high stress and corrosive conditions.Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 15

The only HAP emission sources at chromium elect roplating facilities are the tanks in which the chromium deposition takes place. For hard chromium and decorative chromium electroplating facilities, the emission sources are electropl ating tanks. For the chromic acid anodizing source category, the emissi on sources are anodizing tanks.

The emission controls used by th e facilities in these source categories include packed bed scrubbers, mesh pad mist eliminators, com posite mesh pad systems, high efficiency particulate air (HEPA) filters, and wetting agent/fume suppressant s (WAFS). Most decorative chromium electroplating plants comply with the MACT standards by us ing WAFS in the tank bath to control surface tension, which in turn reduces emissions. Some plants use a combination of WAFS and add-on control to meet the 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 exhaust emissions through the contro l device and out the stack. However, when WAFS are used as the only means of emission c ontrol, the tanks often are not equipped with exhaust hoods. In such cases, emissions from the tank are fugitive and are exhausted to the outside using wall-mounted exhaust fans.

There are an estimated 1,795 plants currently subject to the MACT standards. Of these, there are an estimated 800 hard chromium electr oplating plants, 750 decorative chromium electroplating plants, and 245 chromic acid anodiz ing plants. Some facilities perform more than one type of chromium electroplating or anodi zing; in those cases, the facility is classified as hard chromium, decorativ e chromium, or chromic acid anodizing based on the primary type of electroplating operation performed at the facility. In addition, many chromium electroplating plants also perform other types of electropla ting, such as nickel or cadmium electroplating. Some chromium electroplating facilities elec troplate items that are used internally in the manufacturing pr ocess at the same facility or within the same company. For example, some large printing facilities electrop late their printing rollers in house, and the chromium electroplating processe s are co-located with the pr inting and publishing processes.

For those facilities for whic h the source category is unknown, we assigned them to the hard chromium electroplating source category for the purposes of assessment because those sources have the highest estimated emissions. Consequently, we modeled more sources as hard chromium electroplating sources than the 800 we estimate are in the source category, and we modeled fewer than the 750 and 245 sources in the decorative chromium and chromic acid anodizing source categor ies, respectively.

For the chromium electroplating source categorie s, we compiled preliminary data using the 2005 NEI, which identified 122 chromium electr oplating facilities. We reviewed the emissions data in the NEI and made revisions based on our knowledge of the facilities, the processes involved, typical emissi on rates, and information cont ained in facility permits or permit applications. We revised emission estim ates for eight hard chromium electroplating plants and six decorative chromium electropl ating plants. Data were available for 44 additional facilities through re sponses to a CAA section 114 info rmation request that was sent to facilities for the Plating and Polishing Area Source rule. The data for these facilities were added to the NEI data set, resulting in a data set for 166 facilities, which are approximately 9 percent of the total estimated facilitie s covered by the MACT standards.Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 16

To address the possibility that the 166 facili ties may not be representative of the source categories, an additional data set was developed based on faci lities with known addresses (excluding the 166 facilities) using model plant emi ssions data. This data set includes a total of 1,629 facilities, and data on emissions and release characteristics were based on model plants used in the MACT standards. The annual emissions for each type of plant were estimated based on the emission rates for uncontrolled model plants. Post-MACT emissions were then estimated by applying the control effi ciencies developed for the MACT standards. Using this approach, the resulting emissions rese mble allowable emissions. More information about the development of the model plants can be found in “Model Plant Data Used to Estimate Risk from Chromium Electroplating Sources” [ 23 ]

In both the NEI-based and the model plant data sets, chromium compounds account for all the HAP emissions. For the hard chromium electro plating source category, in the NEI-based data set, chromium VI compounds account for 98 perc ent of the emissions, with chromium III and chromium trioxide compounds comprising the rema ining HAP. In the model plant data set, we made the conservative assumption that 100 percent of the emissions are chromium VI compounds. For the decorative chromium elect roplating source category, in the NEI-based data set, chromium VI compounds account for 94 percent of the emissions, with chromium III and chromium trioxide compounds comprising the remaining HAP. In the model plant data set, we made the conservative assumption that 100 percent of the emissi ons are chromium VI compounds. For the chromic acid anodizing sour ce category, in the NEI-based data set, chromium VI compounds account for 99 percen t of the emissions with chromium III compounds comprising the remaining HAP. In the model plant data set, we made the conservative assumption that 100 percent of the emissions are chromium VI compounds.

The emissions estimates in the model plant data set are considered to be allowable emissions because they are based on the MACT level of control. The emissions included in the NEIbased data set represent actual emissions levels. Most of these faciliti es have low emissions, which are generally less than 2 pounds per year . For hard chromium electroplating and decorative chromium electroplating, stack emissi on test data indicate that, for the control systems in use, there is considerable variability in actual emission rates. Even for the best controls used to comply with the MACT st andards, there is significant variability in emissions; some sources with properly operating controls have emissions near the emission limit, while other sources with the same type of control device operate well below the emission limit. These variations are characteristic of the indu stry and the types of emission controls used. There is little emissions data available for de corative chromium electroplating facilities and chromic acid anodizing facilities. We conclude th ese facilities op erate near the surface tension limit so that the actual emissions would essentially be equal to the allowable emissions. Details about the test data and ratio s of allowable to actual emissions can be found in “Actual vs. Allowable Emissions for Chromi um Electroplating Plants - Emission Standards Technical Support and Post Promulgation Activities” [ 24 ]Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 17

Tables 3.1-1 through 3.1-6 summarize the estimat ed emissions and health risks for each source category.

Table 3.1-1 Summary of Emissions from th e Hard Chromium Electroplating Source Category a Prioritized Inhalation Dose-Response Value Identified by OAQPS b

HAP NPRM Emissions (tpy) Number of Facilities in the dataset Unit Risk Estimate for Cancer? Reference Concentrati on for Chronic Non-cancer? Health Benchmark Values forAcute Noncancer? PBHAP

?

Chromium III Compounds 0.0008 48

Chromium VI Compounds 5.7 1,282 Y Υ

Chromium Trioxide (VI), chromic acid mist 0.0003 1 Y

a This summary combines emissions data based on site-specific data and model plant data.

b Specific dose-response values fo r each chemical are id entified 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 Previ ously Subjected to T echnology-based Standards document.

Table 3.1-2 Summary of Source Categor y Level Risks for Hard Chromium Electroplating a
Result HAP “Drivers” Facilities in Source Category Number of Major Facilities Estimated to be Subject to MACT in Source Category 800 n/a

Number of Facilities Identified Modeled in NPRM Risk Assessment 1,282 b n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) from any Facility in the Category 70 Chromium 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 342 Chromium compounds
Greater than or equal to 1 in 1 million 1175 Chromium compounds

Chronic Non-cancer Risks Maximum Respiratory Hazard Index 0.06 Chromium compounds Number of Facilities with Maximu m Respiratory Hazard Index: Greater than 1 0 n/aDraft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 18

Table 3.1-2 Summary of Source Categor y Level Risks for Hard Chromium Electroplating a
Result HAP “Drivers” Acute Non-cancer Screening Results Maximum Acute Hazard Quotient c n/a
Number of Facilities With Potential for Acute Effects c n/a

Population Exposure Number of People Living Within 50 Kilometers of Facilities Modeled 224,000,000 n/a

Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a
Greater than or equal to 10 in 1 million 71,000 Chromium compounds
Greater than or equal to 1 in 1 million 14,200,000 Chromium compounds

Number of People Exposed to Non-c ancer Respiratory Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.8 Chromium compounds

Contribution of HAP to Cancer Incidence Chromium compounds 100%

a This summary combines the results of the assessments based on site-specific da ta and model plant data.
b For those facilities for which the source category is unknown, we assigned them to the hard chromium electroplating source category for the purposes of assessment because those sources have the highest estimated emissions. Consequently, we modeled more hard chromium electroplating sources than the 800 we estimate are in the source category.

c Because there are no HAP with an acute dose-response benc hmark value, no acute hazard quotients were calculated.

Table 3.1-3 Summary of Emissions from the Decorative Chromium Electroplating Source Category a Prioritized Inhalation Dose-Response Value Identified by OAQPS b

HAP NPRM Emissions (tpy) Number of Facilities in the data set Unit Risk Estimate for Cancer? Reference Concentrati on for Chronic Non-cancer? Health Benchmark Values forAcute Noncancer? PBHAP

?

Chromium III Compounds 0.002 38

Chromium VI Compounds 0.43 433 Y Υ

Chromium Trioxide (VI), chromic acid mist 0.00002 1 Y

a This summary combines emissions data based on site-specific data and model plant data.

b Specific dose-response values fo r each chemical are id entified 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 Previ ously Subjected to T echnology-based Standards document.Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 19

Table 3.1-4 Summary of Source Category Le vel Risks for Decorative Chromium Electroplating a
Result HAP “Drivers” Facilities in Source Category Number of Major Facilities Estimated to be Subject to MACT in Source Category 750 n/a

Number of Facilities Identified Modeled in NPRM Risk Assessment 433 b n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) from any Facility in the Category 70 Chromium 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 58 Chromium compounds
Greater than or equal to 1 in 1 million 301 Chromium compounds

Chronic Non-cancer Risks Maximum Respiratory Hazard Index 0.06 Chromium compounds Number of Facilities with Maximu m Respiratory Hazard Index: Greater than 1 0 n/a Acute Non-cancer Screening Results Maximum Acute Hazard Quotient c n/a
Number of Facilities With Potential for Acute Effects c n/a

Population Exposure Number of People Living Within 50 Kilometers of Facilities Modeled 166,000,000 n/a

Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a
Greater than or equal to 10 in 1 million 4,300 Chromium compounds
Greater than or equal to 1 in 1 million 390,000 Chromium compounds

Number of People Exposed to Non-c ancer Respiratory Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.08 Chromium compounds

Contribution of HAP to Cancer Incidence Chromium compounds 100%

a This summary combines the results of the assessments based on site-specific da ta and model plant data.
b For those facilities for which the source category is unknown, we assigned them to the hard chromium electroplating source category for the purposes of assessment because those sources have the highest estimated emissions. Consequently, we modeled fewer than the 750 sources estimated to be in the decorative chromium electroplating source category.

c Because there are no HAP with an acute dose-response benc hmark value, no acute hazard quotients were calculated.Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 20

Table 3.1-5 Summary of Emissions from th e Chromic Acid Anodizing Source Category a Prioritized Inhalation Dose-Response Value Identified by OAQPS b

HAP NPRM Emissions (tpy) Number of Facilities in the data set Unit Risk Estimate for Cancer? Reference Concentrati on for Chronic Non-cancer? Health Benchmark Values forAcute Noncancer? PBHAP

?

Chromium III Compounds 0.0002 4

Chromium VI Compounds 0.04 80 Y Υ

a This summary combines emissions data based on site-specific data and model plant data.

b Specific dose-response values fo r each chemical are id entified 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 Previ ously Subjected to T echnology-based Standards document.

Table 3.1-6 Summary of Source Category Le vel Risks for Chromic Acid Anodizing a

Result HAP “Drivers” Facilities in Source Category Number of Major Facilities Estimated to be Subject to MACT in Source Category 245 n/a

Number of Facilities Identified Modeled in NPRM Risk Assessment 80 b n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) from any Facility in the Category 5 Chromium 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 Chromium compounds
Greater than or equal to 1 in 1 million 28 Chromium compounds

Chronic Non-cancer Risks Maximum Respiratory Hazard Index 0.004 Chromium compounds Number of Facilities with Maximu m Respiratory Hazard Index: Greater than 1 0 n/a Acute Non-cancer Screening Results Maximum Acute Hazard Quotient c n/a
Number of Facilities With Potential for Acute Effects c n/a

Population Exposure Number of People Living Within 50 Kilometers of Facilities Modeled 108,000,000 n/a

Number of People Exposed to Cancer Risk:Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 21

Table 3.1-6 Summary of Source Category Le vel Risks for Chromic Acid Anodizing a

Result HAP “Drivers” Greater than or equal to 100 in 1 million 0 n/a
Greater than or equal to 10 in 1 million 0 Chromium compounds
Greater than or equal to 1 in 1 million 2,800 Chromium compounds

Number of People Exposed to Non-c ancer Respiratory Hazard Index: Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.003 Chromium compounds

Contribution of HAP to Cancer Incidence Chromium compounds 100%

a This summary combines the results of the assessments based on site-specific da ta and model plant data.
b For those facilities for which the source category is unknown, we assigned them to the hard chromium electroplating source category for the purposes of assessment because those sources have the highest estimated emissions. Consequently, we modeled fewer than the 245 sources estimated to be in the chromic acid anodizing source category.

c Because there are no HAP with an acute dose-response benc hmark value, no acute hazard quotients were calculated.



### 3.2 Risk Characterization

The modeling results for the hard chromi um electroplating, decorative chromium electroplating, and chromic acid anodizing source categories indicate that maximum lifetime individual cancer risks could be as high as 70-in-1 million, 70-in-1 million, and 5-in-1 million, respectively. Also, the maximum chronic non-cancer TOSHI values for the hard chromium electroplating, deco rative chromium electroplati ng, and chromic acid anodizing source categories could be as high as 0.06, 0.06, and 0.004, respectively. The total estimated cancer incidence from hard chromium electropl ating facilities is 0.8 ex cess cancer cases per year, or one case in every 1.25 y ears. The total estimated can cer incidence from decorative chromium electroplating facilitie s is 0.08 excess cancer cases pe r year, or one case in every 12.5 years. The total estimated cancer incidence from chromic acid anodizing facilities is 0.003 excess cancer cases per year, or one case in every 333 years.

As discussed above, there are no HAPs with an acute dose-response benchmark value, so no acute hazard quotients were calculated, and the po tential for any acute impacts of concern is considered negligible. Also, no PB-HAP em issions were identified from these source categories, indicating that e xposures due to non-inhalation routes of exposure are not significant. Regarding the “facility-wide” asse ssment, there are no faci lities in any of the source categories with a source category TOSHI value greater than one, and there is only one facility in the three source categories with a facility-wide TOSHI value greater than 1. This facility has a facility-wide TO SHI value of 2 (nervous system ), and the source category does not contribute to it at all becau se the respiratory system is th e target organ for the chromium compounds. The highest source category MIR for the hard chromium el ectroplating source category is 70-in-1 million, which is also the facility-wide MIR for the same facility. The highest facility-wide MIR for the hard chromi um electroplating sour ce category is 90-in-1Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 22

million, for which the source category contributes 1 percent. The highest source category MIR for the decorative chromium electroplating source category is 70-in-1 million, but we do not have a facility-wide MIR estimate for the same facility. The highest facility-wide MIR for the decorative chromium electroplating so urce category is 90-in-1 million, for which the source category contributes 7 percent. The hi ghest source category MIR for the chromic acid anodizing source category is 5-in-1 million, which occurs at the same facility that has the highest facility-wide MIR of 20-in-1 million.

Our analyses of potential differences between ac tual emission levels and emissions allowable under the MACT standards are based on emissions test data from specific facilities. A comparison of these test results to allowable em issions at these faciliti es indicates that the ratio of MACT-allowable to actual emissions varies considerably from faci lity to facility. As a result, a uniform factor was not available to apply to all faci lities. However, for the hard chromium electroplating source category, we did evaluate the facility that was modeled as having the highest maximum individual lifetime cancer risk (70-in-1 million) based on actual emissions. Our analysis indicate s that this facilit y, if operated at the allowable emissions limit, could have a maximum individual lifetim e cancer risk as high as 90-in-1 million. Furthermore, we have concluded that no other hard chromium electropl ating facility would have a cancer risk that high if opera ted at the allowable emissions limit.

For the decorative chromium electroplating sour ce category, we performed a similar analysis of the available data and concluded that th e maximum individual life time cancer risk would not exceed 70-in-1 million for any facility that operated at the allowable emissions limit. As stated earlier, because most chromic acid anod izing facilities use WAFS, we believe actual emissions are essentially the same as allowabl e emissions. Thus, we believe that the MIR based on allowable emissions would be the same as that based on actual emissions, i.e., 5-ina-million.



### 4 General Discussion of Uncertaint ies and How They Have Been Addressed

While each of the preceding sections discussed specific uncertainties unique to the source categories, the following includes a general disc ussion of uncertainties associated with RTR

assessments.



### 4.1 Exposure Modeling Uncertainties

Emission inventory uncertainties were previously discussed in sections 2.1 and 3.1. We have used model plant emissions for most of the sour ces in the categories because of the lack of site-specific emissions data, a nd we have purposely biased the emission estimates high in all of the model plants in order to ensure that we do not underestimate potenti al cancer risks. The chronic exposure modeling uncertainties are cons idered relatively small since we are using EPA’s refined local dispersion model with reas onably representative meteorology. It is possible that population exposure estimates are al so biased slightly higher by not accounting for short- or long-term popul ation mobility, and by neglec ting processes like deposition, plume depletion, and atmo spheric degradation.Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 23



### 4.2 Uncertainties in the Do se-Response Relationships

In the sections that follow, se parate discussions are provided on uncertainty associated with cancer potency factors and for non-cancer refe rence values. Cancer potency values are derived for chronic (lifetime) exposures. Non- cancer reference values are generally derived for chronic exposures (up to a lifetime), but may also be derived for acute (

 <24 hours), shortterm (>24 hours up to 30 days), and subchronic (>30 days up to 10% of lifetime) exposure durations, all of which are derived based on an assumption of con tinuous exposure throughout the duration specified. For the purposes of assess ing all potential health risks associated with the emissions included in an assessment, we rely on both chronic (cancer and non-cancer) and acute (non-cancer) benchmarks, which are described in more detail below.

Although every effort is made to identify p eer-reviewed dose-respons e values for all HAPs emitted by the sources included in an assessment, some HAP have no peer-reviewed cancer potency values or reference values for chroni c non-cancer or acute e ffects (inhalation or ingestion). Since exposures to these pollutants cannot be incl uded in a quantitative risk estimate, an understatement of risk for these po llutants at environmental exposure levels is possible. As discussed above, there are no HAPs with an acute dose-response benchmark value in these source categories. Therefore, no acute hazard quotie nts were calculated.

Additionally, chronic dose -response values for certain compo unds included in an assessment may be under EPA IRIS review and revised asse ssments may determine that these pollutants are more or less potent than currently thought. We will re-evaluate risks if, as a result of these reviews, a dose-response metric changes enough to indicate that the risk assessment may significantly mischaracterize human health risk.

Cancer assessment

The discussion of dose-response uncertainties in the estimation of cancer risk below focuses on the uncertainties associated with the specifi c approach currently used by the EPA to develop cancer potency factors. In general, these same uncertainties attend the development of cancer potency factors by CalEPA, the sour ce of peer-reviewed cancer potency factors used where EPA-developed values are not yet ava ilable. To place this discussion in context, we provide a quote from the EPA’s Guidelines for Carcinogen Risk Assessment [ 25 ] (herein referred to as Cancer Guidelines ). “The primary goal of EPA actions is prot ection of human health; accordingly, as an Agency policy, ri sk assessment procedures, including default options that are used in the absence of scien tific data to the cont rary, should be health protective.” The approach adopt ed in this document is consis tent with this approach as described in the Cancer Guidelines

.
For cancer endpoints EPA usually derives an oral slope factor for inge stion and a unit risk value for inhalation exposures. These values allow estimation of a lifetime probability of developing cancer given long-term exposures to the pollutant. Depending on the pollutant being evaluated, EPA relies on both animal bioassay and epidemiological studies toDraft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 24

characterize cancer risk. As a science policy approach, consistent with the Cancer Guidelines , EPA uses animal cancer bioassays as i ndicators of potential human health risk when other human cancer risk data are unavailable.

Extrapolation of study data to estimate poten tial 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 ri sk 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; howev er, in other circumstances 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 lowe r bound or central) estimates in its assessments, although it is noted that this approach can have limitations for some uses (e.g. prio rity setting, expected benefits analysis).

Such health risk assessments have associated uncertainties, some wh ich may be considered quantitatively, and others which generally are ex pressed qualitatively. Uncertainties may vary substantially among cancer risk a ssessments associated with expos ures to different pollutants, since the assessments employ different database s with different strengt hs 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 estimat es demonstrating 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 valu es are described more fully below.

(1) The qualitative similarities or differen ces between tumor responses observed in experimental animal bioassays and those wh ich would occur in humans is a source of uncertainty in cancer risk assessment. In ge neral, EPA does not assume that tumor sites observed in an experimental an imal 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, an d which is based on 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 knowle dge and policy judgment, that are applied to various elements of the risk-assessment process when the correct scientific model is unknown or uncertain.” The 1983 NRC report Risk Assessment in the Federal Government: Managing the Process defined default option as “the option chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to the contrary” (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the agency may depart from them in evaluating the risks posed by a specific substance when it believes this to be appropriate. In keeping with EPA’s goal of protecting public health and the environment, default assumptions are used to ensure that risk to chemicals is not under estimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An Examination of EPA Risk Asse ssment Principles and Practices, EPA/100/B-04/001 available at: http://w ww.epa.gov/osa/pdfs/ratf-final.pdf.Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 25

tumors would occur in humans. 7 However, unless scientific support is ava ilable to show otherwise, EPA assumes that tumors in animals are relevant in humans, regardless of target organ concordance. For a specific pollutant, qua litative differences in species responses can lead to either under-estimation or over-e stimation of human cancer risks.

(2) Uncertainties regarding the most appropriate dose metric for an assessment can also lead to differences in risk predictions. For exam ple, the measure of dose is commonly expressed in units of mg/kg/d ingested or the inhaled con centration of the pollutant. However, data may support development of a pharmacokinetic mode l for the absorption, distribution, metabolism and excretion of an agent, which may resu lt in improved dose metrics (e.g., average blood concentration of the pollutant or the quantity of agent metabolized in the body). Quantitative uncertainties result when the appropriate choice of a dose metric is uncertain or when dose metric estimates are themselves uncerta in (e.g., as can occur when alternative pharmacokinetic models are available for a co mpound). 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 met hodologies (relating expected response to differences in physical size of the species), which introdu ce another source of uncertainty. These methodologies are based on both biol ogical data on differences in rates of process according to species size and empirical comparisons of toxicity between expe rimental animals and humans. For a particular pollutant, the quant itative difference in cancer potency between experimental animals and humans may be either greater than or less than that estimated by baseline scientific scaling predictions due to uncertainties associated with limitations in the test data and the correctness of scaled estimates.

(4) EPA cancer risk estimates, whether based on epidemiological or experimental animal data, are generally developed using a benchmark dose (BMD) analysis to estimate a dose at which there is a specified excess risk of cancer (a PO D). Statistical uncertain ty in developing a POD using a benchmark dose (BMD) approach is ge nerally addressed though use of the 95% lower confidence limit on the dose at which the sp ecified excess risk occurs (the BMDL), decreasing the likelihood of understating risk. EPA has generally utilized the multistage model for estimation of the BMDL using cancer bioassay data (see further discussion below).

(5) Extrapolation from high to low doses is an important, and potential ly large, source of uncertainty in cancer risk assessment. EPA uses different approaches to low dose risk assessment (i.e., developing estimates of risk for exposures to environmental doses of an agent from observations in experimental or ep idemiological studies at higher dose) depending on the available data and understa nding 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, bi ologically-based risk models when feasible; however, such models are rarely available. The mode of action for a pollutant (i.e., the manner in which a pollutant causes cancer) is a key considerati on in determining how ri sks should be estimated

7 Per the EPA Cancer Guidelines: “The default option is that positive effects in animal cancer studies indicate that the agent under study can have carcinogenic potential in humans.” and “Target organ concordance is not a prerequisite for evaluating the implications of animal study results for humans.”Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 26

for low-dose exposure. A reference value is calculated when the available mode of action (MOA) data show the response to be nonlinear (e.g., as in a threshol d response). A linear low-dose (straight line from POD) approach is used when available mode of action data support a linear (e.g., nonthreshold response) or as the most common default approach when a compound’s mode of action is unknown. Linear extrapolation can be supported by both pollutant-specific data and broader scientif ic 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. Pollu tants whose effects ar e additive to background biological processes in cancer development can also be predicted to have low-dose linear responses, although the slope of th is relationship may not be the same as the slope estimated by the straight line approach.

EPA most frequently utilizes a linear low-dose extrapolation appr oach as a baseline sciencepolicy choice (a “default”) when available data do not allow a compound-specific determination. This approach is designed to not underestimate risk in the face of uncertainty and variability. EPA believes that linear dose-response models , when appropriately applied as part of EPA’s cancer risk assessment proce ss, provide an upper bound estimate of risk and generally provide a health protec tive approach. Note that anothe r source of uncertainty is the characterization of low-dose non linear, non-threshold relationships. The National Academy of Sciences has encouraged the exploration of sigmoidal type functions (e.g., log-probit models) in representing dose res ponse relationships due to the variability in response within human populations. A recent National Research Council (NRC) report [ 27] suggests that models based on distributions of individual thresholds are likely to lead to sigmoidal-shaped dose-response functions for a population. This report notes sources of variability in the human population: “One might expect these in dividual tolerances to vary extensively in humans depending on genetics, co incident exposures, nutritional status, and various other susceptibility factors...” Thus , if a distribution of thresholds approach is considered for a carcinogen risk assessment, application would depend on ability of modeling to reflect the degree of variability in respons e in human populations (as opposed to responses in bioassays with genetically more uniform rodents). Note al so that low dose linearity in risk can arise for reasons separate from population variability: du e to the nature of a mode of action and additivity of a chemical’s effect on top of background chemical exposures and biological

processes.

As noted above, EPA’s current approach to cancer risk assessment typically utilizes a straight line approach from the BMDL. This is equiva lent to using an upper confidence limit on the slope of the straight line extr apolation. The impact of the choice of the BMDL on bottom line risk estimates can be quantified by comparing ri sk estimates using the BMDL value to central estimate BMD values, although these differences are generally not a large contributor to uncertainty in risk assessment (Subramaniam et. al., 2006) [ 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 extrapolate down to environmental dose levels and did not involve the use of a POD. Subramaniam et. al. (2006) also provide comparisons indicating that slopes based on st raight line extrapolation from a POD do not show large differences from those based on the upper confidence limit of the multistage model.Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 27

(6) Cancer risk estimates do not generally make specific adjustments to reflect the variability in response within the human population — resu lting in another source of uncertainty in assessments. In the diverse human population, some individuals are likely to be more sensitive to the action of a carcinogen than the typical individual , although compound-specific data to evaluate this variability are generally not available. There may also be important life stage differences in the quantitative potency of carcinogens and, with the exception of the recommendations in EPA’s Supplemental Cancer Guidance for carcinogens with a mutagenic mode of action, risk assessments do not generally quantitatively address life stage differences. However, one approach used commonly in EPA assessments that may help address variability in response is to extrapolate human response fr om results observed in the most sensitive species and sex tested, resulting typically in the highest URE which can be supported by reliable data, thus supporting estimates that ar e designed not to underestimate risk in the face of uncertainty and variability.

Chronic non-cancer assessment

Chronic non-cancer reference values represent chronic exposure leve ls that are intended to be health-protective. That is, EPA and other orga nizations which develop non-cancer reference values (e.g., the Agency for Toxic Substances and Disease Registry – ATSDR) utilize an approach that is intended not to underestimate risk in the face of uncertainty and variability. When there are gaps in the available informa tion, uncertainty factors (UFs) are applied to derive reference values that are intended to be protective against appreciable risk of deleterious effects. Uncertainty factors are commonly default values 8 e.g., factors of 10 or 3, used in the absence of compound-specific data; wh ere data are available, uncertainty factors may also be developed using compound-specific information. When data are limited, more assumptions are needed and more default fact ors are used. Thus there may be a greater tendency to overestimate risk—in the sense th at further study might support development of reference values that are higher (i.e., less pot ent) because fewer default assumptions are needed. However, for some pollutants it is possible that risks ma y be underestimated.

For non-cancer endpoints related to chronic exposures, EPA derives a Reference Dose (RfD) for exposures via ingestion, and a Reference C oncentration (RfC) for inhalation exposures. These values provide an estimate (with uncerta inty spanning perhaps an order of magnitude) of daily oral exposure (RfD) or of a conti nuous inhalation exposure (RfC) to the human

8 According to the NRC report Science and Judgment in Risk Assessment (NRC, 1994) “[Default] options are generic approaches, based on general scientific knowle dge and policy judgment, that are applied to various elements of the risk-assessment process when the correct scientific model is unknown or uncertain.” The 1983 NRC report Risk Assessment in the Federal Government: Managing the Process defined default option as “the option chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to the contrary” (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the agency may depart from them in evaluating the risks posed by a specific substance when it believes this to be appropriate. In keeping with EPA’s goal of protecting public health and the environment, default assumptions are used to ensure that risk to chemicals is not under estimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An examination of EPA Risk Assess ment Principles and Practices, EPA/100/B-04/001 available at: http://w ww.epa.gov/osa/pdfs/ratf-final.pdf.Draft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 28

population (including sensitive subgroups) that is lik ely 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 met hodology relies upon an uncertain ty factor (UF) approach [ 29 ],[ 30 ]which includes consideration of both uncertainty and variability.

EPA begins by evaluating all of the availabl e peer-reviewed literature to determine noncancer endpoints of concern, eval uating the quality, strengths and limitations of the available studies. EPA typically chooses th e relevant endpoint that occu rs at the lowest dose, often using statistical modeling of the available data, and then determines th e appropriate point of departure (POD) for derivation of the reference value. A POD is determined by (in order of preference): (1) a statistical estimation using the benchmark dos e (BMD) approach; (2) use of the dose or concentration at which the toxic response was not signi ficantly elevated (no observed adverse effect level— NOAEL); or (3) use of the lowest observed adverse effect level (LOAEL).

A series of downward adjustments using defau lt 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 quantitative consid erations when utilizing observe d animal (usually rodent) or human toxicity data in a risk assessment. The UFs are intende d to account for: (1) variation in susceptibility among the members of the human population (i .e., inter-individual variability); (2) uncertainty in extrapolating fr om experimental animal data to humans (i.e., interspecies differences); (3) uncertainty in ex trapolating from data obtained in a study with less-than-lifetime exposure (i.e., extrapolati ng from subchronic to chronic exposure); (4) uncertainty in extrapolating from a LOAEL in the absence of a NOAEL; and (5) uncertainty when the database is incomplete or there are pr oblems with applicability of available studies. When scientifically sound, peer-reviewed assess ment-specific data are not available, default adjustment values are selected for the indivi dual UFs. For each type of uncertainty (when relevant to the assessment), EPA typically applie s an UF value of 10 or 3 with the cumulative UF value leading to a downward adjustment of 10-3000 fold from the selected POD. An UF of 3 is used when the data do not support the use of a 10-fold factor. If an extrapolation step or adjustment is not relevant to an assessment (e.g., if applying human toxicity data and an interspecies extrapolation is not required) the associated UF is not used. The major adjustment steps are described more fully below.

1) Heterogeneity among humans is a key sour ce of variability as well as uncertainty. Uncertainty related to human variation is consid ered in extrapolating doses from a subset or smaller-sized population, often of one sex or of a narrow range of life stages (typical of occupational epidemiologic studies), to a larger , more diverse population. In the absence of pollutant-specific data on human variation, a 10 -fold UF is used to account for uncertainty associated with human variation. Human variatio n may be larger or smaller; however, data to examine the potential magnitude of human va riability are often una vailable. In some situations, a smaller UF of 3 ma y be applied to reflect a known l ack of significant variability among humans.

9 See IRIS glossaryDraft Risk Assessment for Chrome Plat ing Source Categories -- FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 29

2) Extrapolation from results of studie s in experimental animals to humans is a necessary step for the majority of chemical ri sk assessments. When interpreting animal data, the concentration at the POD (e.g. NOAEL, BM DL) in an animal model (e.g. rodents) is extrapolated to estimate the human response. While there is long-sta nding scientific support for the use of animal studies as indicators of potential toxicity to humans, there are uncertainties in such extrapolat ions. In the absence of data to the contrary, the typical approach is to use the most relevant endpoint from the most sensitive species and the most sensitive sex in assessing risks to the aver age human. Typically, compound specific data to evaluate relative sensitivity in humans versus rodents are lacki ng, thus leading to uncertainty in this extrapolation. Size-related differences (allometric relationships) indicate that typically humans are more sensitive than rodents when compared on a mg/kg/day basis. The default choice of 10 for the interspecies UF is consis tent with these differences. For a specific chemical, differences in species responses may be greater or less than this value.

Pharmacokinetic models are useful to examine species differences in pharmacokinetic processing and associated uncertainties; however , such dosimetric adjustments are not always possible. Information may not be available to quantitatively a ssess toxicokinetic or toxicodynamic differences between animals a nd humans, and in many cases a 10-fold UF (with separate factors of 3 for toxicokinetic and toxicodyna mic components) is used to account for expected species differences and as sociated uncertainty in extrapolating from laboratory animals to humans in the derivation of a reference value. If information on one or the other of these components is availabl e and accounted for in the cross-species extrapolation, a UF of 3 may be used for the remaining component.

3) In the case of reference values for ch ronic exposures where only data from shorter durations are available (e.g., 90-da y subchronic studies in rodent s) or when such data are judged more appropriate for development of an RfC, an additional UF of 3 or 10-fold is typically applied unless th e available scientific information supports use of a different value.

4) Toxicity data are typically limited as to the dose or exposure levels that have been tested in individual studies; in an animal study, for example, treatment groups may differ in exposure by up to an order of magnitude. The pref erred approach to arrive at a POD is to use BMD analysis; however, this approach requires ad equate quantitative results for a meaningful analysis, which is not always possible. Use of a NOAEL is the next preferred approach after BMD analysis in determining a POD for deriving a health effect reference value. However, many studies lack a dose or exposure level at wh ich an adverse effect is not observed (i.e., a NOAEL is not identified). When using data lim ited to a LOAEL, a UF of 10 or 3-fold is often applied.

5) The database UF is intended to a ccount for the potential for deriving an underprotective RfD/RfC due to a data gap pr eventing complete char acterization of the chemical’s toxicity. In the absence of studies for a known or suspecte d endpoint of concern, a UF of 10 or 3-fold is typically applied.



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23 RTI International, 2010 . Memorandum from R. Marinshaw, RT I Internatio nal, to P. Mulrine, US EPA. Model Plant Data Used to Estimate Risk from Chromium Electroplating Sources Emission Standards Techni cal Support and Post Pr omulgation Activities.

24 RTI International, 2010. Memorandum from R. Marinshaw, RT I Internatio nal, to P. Mulrine, US EPA. Actual vs. Allowable Emissions fo r Chromium Electroplati ng Plants - Emission Standards Technical Support and Post Promulgati on Activities.

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http://www.epa.gov/iris/rfd.htm.

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