Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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## Draft Residual Risk Assessment for
PHOSPHATE FERTILIZER PRODUCTION

and
PHOSPHORIC ACID MANUFACTURING

by EPA’s Office of Air Quality Planning and Standards

Office of Air and Radiation
October 2014Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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2 

### Table of Contents

1. Introduction

................................ ................................ ................................ ............................. 5

2. Methods

................................ ................................ ................................ ................................ ... 6
2.1. Emissions and source data

................................ ................................ ............................ 6
2.2. Dispersion modeling for inhalation exposure assessment

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

................................ ........................... 8
2.4. Screening for potential acute impacts of concern

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

................................ . 12 Multipathway Human Health Screening

................................ ................................ ........... 12
2.6. Dose

- response assessment

................................ ................................ .......................... 16
2.6.1. Sources of chronic dose

- response i nformation

................................ ................... 16
2.6.2. Sources of acute dose

- response information

................................ ....................... 24
2.7. Risk characterization

................................ ................................ ................................ .. 28
2.7.1. General

................................ ................................ ................................ ................ 28
2.7.2. Mixtures

................................ ................................ ................................ .............. 29
2.7.3. Facility

- wide risks

................................ ................................ ............................... 30
2.7.4. MACT

- allowable risks

................................ ................................ ........................ 30
3. Risk Results for Phosphate Fertilizer Production

................................ ................................ . 31
3.1 So urce category description and results

................................ ................................ ..... 31
3.2 Baseline risk characterization

................................ ................................ ..................... 33
4. Risk Results for the Phosphoric Acid Manufactu ring Source Category

............................... 38
4.1 Source category description and results

................................ ................................ ..... 38
4.2 Risk characterization

................................ ................................ ................................ .. 42
5. General Discussion of Uncertainties and How They Have Been Addressed

....................... 48 5.1 Exposure modeling uncertainties

................................ ................................ .................. 48
5.2 Uncertainties in the dose

- response relationships

................................ ........................... 49
6 References

................................ ................................ ................................ ................................ . 58Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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3 Index of Tables

Table 2.2

- 1 AERMOD version 11103 model options for RTR modeling

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

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcinogens

..... 21
Table 2.6

- 1(b) Dose

- Response Values for Chronic Oral Exposure to Carcinogens

................ 22
Table 2.6

- 2 (a) Dose

- Response Values for Chroni c Inhalation Exposure to Noncarcinogens 22
Table 2.6

- 2 (b) Dose

- Response Values for Chronic Oral Exposure to Noncarcinogens

......... 24
Table 2.6

- 3 Dose

- Response Values for Acute Exposure

................................ .......................... 27
Table 3.1

- 1 Summary of Emissions from the Phosphate Fertilizer Production Source Category and Availability of Dose

- Response Values

................................ ............................... 32
Table 3.2

- 1 Summary of Source Category Level Inhalation Risks for Phosphate Fertilizer
Production

................................ ................................ ................................ ................................ . 34
Table 3.2

- 2 Summary of the “T ier 1 and 2” Multipathway Screening Analysis for the Phosphate Fertilizer Production Source Category

................................ ................................ .... 36
Table 3.2

- 3 Summary of the “Tier 2 and 3” Multipathway Screening Analysis for Phosphate Fertilizer Production for Mississippi Phosphates (NEIMS059305)

................................ ......... 37
Table 3.2

- 4 Summary of Environmental Risk Screening Results for the Phosphate Fertilizer Production Source Category

................................ ................................ ................................ ..... 38
Table 4.1

- 1 Summary of Emissions from the Phosphoric Acid Manufacturing Source Category and Availability of Dose

- Response Values

................................ ............................... 40

Ta ble 4.2

- 1 Summary of Source Category Level Inhalation Risks for Phosphoric Acid Manufacturing

................................ ................................ ................................ ........................... 44
Table 4.2

- 2 Summary of Acute Refined Results for Phosphoric Acid Manufacturing

............ 45
Table 4.2

- 3 Summary of the “Tier 1 and 2” Multipathway Screening Analysis for the Phosphoric Acid Manufacturing Source Category

................................ ................................ ... 47
Table 4.2

- 4 Summary of Environmental Risk Screening Results for the Phosphoric Acid Manufacturing Source Category

................................ ................................ ............................... 48

Appendices

Appendix 1 Technical Support Document for HEM3 Modeling Appendix 2 Meteorological Data for HEM3 Modelin g Appendix 3 Analysis of data on short

- term emission rates relative to long

- term emission

rates Appendix 4 Draft Detailed Risk Modeling Results Appendix 5 Technical Support Document for TRIM

- Based Multipathway Tiered Screening

Scenario for RTR: Summar y of Approach and Evaluation Appendix 6 Dispersion Model Receptor Revisions and Additions Appendix 7 Environmental Risk Screen ing Appendix 8 Acute Noncancer Risk Analysis for Phosphate Fertilizer and Phosphoric Acid

Manufacturi ng Appendix 9 Technical Support Document : Human Health Multipathway Residual Risk

Screening Assessment for the Phosphate Fertilizer Production and Phosphoric Acid Manufacturing Source CategoriesDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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4 In dex 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

H AP Hazardous Air Pollutant

HEM Human Exposure Model

HI Hazard index HQ Hazard quotient

IRIS Integrated Risk Information System
LOAEL Lowest Observed Adverse Effect Level

MACT Maximum Achievable Control Technology

MIR Maximum Individual Ris k

MOA Mode of action

NAC National Advisory Committee NAAQS National Ambient Air Quality Standard

NATA National Air Toxics Assessment

NEI National Emissions Inventory
NOAEL No Observed Adverse Effect Level

NPRM Notice of Proposed Ru lemaking

PB

- HAP Persistent and Bioaccumulative

- HAP
POM Polycyclic organic matter

REL Reference exposure level
RfC Reference concentration

RfD Reference dose

RTR Risk and Technology Review

TOSHI Target

- organ

- specific hazard index

URE Unit risk esti mateDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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5 

### 1. Introduction

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

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

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

- based standards at least every eight years and revise a standard, as necessary, “taking into account developments in practices,

processe s and control technolog ies.” In the second stage, EPA is required under section 112(f)(2) to assess the health and environmental risks that remain after implementation of the MACT standards. If additional risk reductions are necessary to protect public health with an ample mar gin of safety or to prevent an adverse environmental effect, EPA must develop standards to address these remaining risks. This second stage of the regulatory process is known as the residual risk stage. For each source category for which EPA issued MACT standards, the residual risk stage must be completed within eight years of promulgation of the initial technology

- based standard.

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

t o Key Recom mendations from the SAB Review of RTR R isk Assessment Methodologies” [ 4 ].

This document contains the methods and the results of baseline risk assessments (i.e., after the implementation of the MACT standard) performed for the phosp hate fertilizer produ ction an d phosphoric acid manufacturing source categories. The methods discussion includes descriptions of the methods used to develop refined estimates of chronic inhalation exposures and human health risks for cancer and noncancer endpoints, as well as descriptions of the
methods used to screen for acute health risks, chronic non

- inhalation health risks, and adverse
environmental effects.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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6 

### 2. Methods

2.1. Emissions and source data

Data from a CAA section 114 information collection request (ICR) were used for this

assessment. In April 20 10

, we issued the ICRs to all U.S. phosphate fertilizer and phosphoric acid manufacturers to gather information needed to conduct the technology review and residual risk requirements of the CAA. The ICRs requested available i nformation regarding process equipment, control devices, phosphate and acid production, inventory data for all point and fugitive emissions, practices used to control fugitive emissions, and other aspects of facility operations, including stack parameters and locations. Additional survey information from this source category was collected in January 2014 and used in the assessment, namely new mercury and hydrofluoric acid (HF) emissions collected from plants that utilize calciners. Next, EPA engineers who have extensive knowledge of the characteristics of this industry performed an engineering and quality assurance/quality control review of the data to identify limitations and issues. Finally, EPA engineers contacted facility and industry representatives to clarify details and resolve issues with their data submissions.

The 2005 National

- Scale Air Toxics Assessment (NATA) National Emissions Inventory (NEI) was updated for these source categor ies with data obtained from industry thr o u gh the

ICR process

. The emissions data and corrections are described in more detail in the memo entitled “ Emissions Data Used in Residual Risk Modeling: Phosphoric Acid and P hosphate Fertilizer Production Source Categories ” available in the docket for this action

.



### 2.2. Dispers ion modeling for inhalation exposure assessment
Both long

- and short

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

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

. The

HEM

- 3 performs three main oper ations: atmospheric dispersion modeling, estimation of individual human exposures and health risks, and estimation of population risks. This section focuses on the dispersion modeling component. The exposure and risk characterization components are discu ssed in other subsections of Sections 2 and 3.

The dispersion model in the HEM

- 3 system, utilizing EPA’s AERMOD version 11103 The version available at the time of the analysis) , Gaussian plume dispersion model for modeling point, area, and volume sources of continuous air emissions from facility applications [ 5 ]. Further details on AERMOD can be found in the AERMOD Users Guide [ 6 ]. The model is used to develop annual average ambient concentrations through the simulation of hour

- by

hour dispersion from th e emission sources into the surrounding atmosphere. Hourly emission rates used for this simulation are generated by evenly dividing the total annual emission rate from the inventory into the 8,760 hours of the year.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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7 The first step in the application of the HEM3 modeling system is to estimate 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 11103 mo del options for RTR modeling

Modeling Option Selected Parameter for chronic exposure

Type of calculations Hourly Ambient Concentration

Source type Point, area represented as pseudo point source

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

- supplied receptors

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 re presentative NWS from nearest site ( over 200 stations)

In HEM

- 3 , meteorological data are ordinarily selected from a list of over 200 National Weather Service (NWS) surface observation stations across the continental United States, Alaska, Hawaii, and Pue rto Rico (the number of stations available at the time of the analysis)

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

- site meteorological data

, most site

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

estimation of long

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

estimation at others. For each facility identified b y its characteristic latitude and longitude coordinates, the closest meteorological station was used in the dispersion modeling. Appendix 2 ( Meteorological Data Processing Using AERMET for HEM

- 3 ) provides a complete listing of stations and assumptions a long with further details used in processing the data through AERMET. The sensitivity of model results to the selection of the nearest weather station and the use of one year of meteorological data is discussed in “ Risk and Technology Review (RTR) Risk As sessment Methodologies ” [ 2 ].

The HEM

- 3 system estimates ambient concentrations at the geographic centroids of census blocks (using the 2010 Census), and at other receptor locations that can be specified by the

user. See Appendix 6 to this document ( Dispe r sion Model Receptor Revisions and Additions ) for a discussion of user receptors and centroid location changes specific to these source categories. The model accounts for the effects of multiple facilities when estimating concentration impacts at each blo ck centroid. Typically we combined only the impacts ofDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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8 facilities within the same source category, and assessed chronic exposure and risk only for census blocks with at least one resident (i.e., locations where people may reasonably be
assumed to reside r ather 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 un inhabited areas was not considered. Census blocks, the finest resolution available in the census data, are typically comprised of approximately 40 people or about ten households.

In contrast to the development of ambient concentrations for evaluating l ong

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

- case short

- term (one

- hour) concentrations were estimated both at the census block centroids and at points nearer the facility that represent locations where people may be presen t 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 s creen for the potential for hazard via acute exposures, and
since the ICR contains only annual emission totals, we generally apply the assumption to all source categories that the maximum one

- hour emission rate from any source is ten times the

average annu al hourly emission rate for that source. 1 More description of our short

- term
assessment can be found in section 2.4 of this document

, Acute Risk Screening and Refined

Assessment

.

Census block elevations for HEM

- 3 modeling were determined nationally fro m the US Geological Service 1/3 Arc Second National Elevation Dataset, which have a spatial resolution of about 10 meters. Elevations of polar grid points used in estimating short

- and long

- term ambient concentrations were assumed to be equal to the highe st elevation of any census block falling within the polar grid sector corresponding to the grid point. If a sector does not contain any blocks, the model defaults the elevation to that of the nearest block. If an elevation is not provided for the emissio n source, the model uses the average elevation of all sectors within the innermost model ring. AERMOD adjusts the plume’s flow if nearby elevated hills are expected to influence the wind patterns. For details on how hill heights
were estimated and used in the AERMOD modeling see Appendix 2 of this document, Technical Support Document for HEM3 Modeling

.



### 2.3. Estimating chronic human inhalation exposure

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

- term or long

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

We did not address short

- term human activity for two reasons. First, our experience with NATA assessments (which modeled daily activity using EPA’s HAPEM model) suggests that, given our current understanding of m icro environment concentrations and daily activities, modeling short

- term activity would, on average, reduce risk estimates about 25 percent for

1 In situations where we have in formation on hourly emissions, we will adjust the multiplier when evaluating
acute risks.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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9 particulate HAPs; it w ould also reduce risk estimates for gaseous HAPs, but typically by much less. Second, bas ing exposure estimates on average ambient concentrations at census block centroids may underestimate or overestimate actual exposure concentrations at some residences. Further reducing exposure estimates for the most highly exposed residents by modeling t heir short

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

We did not address long

- term migration nor population growth or decrease over 70 years, instead basing the assessment on the assumption that each person’s predicted exposure is

con stant over the course of their lifetime which is assumed to be 70 years. In assessing cancer risk, we generally estimated three metrics: the maximum individual risk (MIR), which is defined as the risk associated with a lifetime of exposure at the highest concentration (note that the MIR can be estimated for each source as well as for the entire source category); the population risk distribution; and the cancer incidence. The assumption of not considering short or long

- term population mobility does not bia s the estimate of the MIR nor does it affect the estimate of cancer incidence since the total population number remains the same. It does, however, affect the shape of the distribution of individual risks across the affected population, shifting it toward higher estimated individual risks at the upper end and reducing the number of people estimated to be at lower risks, thereby increasing the estimated number of people at specific risk levels.



### 2.4. S creening for potential acute impacts of concern

In establishin g a scientifically defensible approach for the assessment of potential health risks due to acute exposures to HAP, we f ollowed the same general approach that has been used for developing chronic health risk assessments under the residual risk program. Tha t is, we developed a tiered, iterative approach. This approach to risk assessment was endorsed by the National Academy of Sciences in its 1993 publication “Science and Judgment in Risk Assessment” and subsequently was adopted in the EPA’s “Residual Risk R eport to Congress”
in 1999.

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

- case

exposure . The result of this sc reening process is that either the facility being assessed poses

no potential acute health risks (i.e., it “screens out”), or that it requires further , more refined
assessment. A refined assessment could u s e industry

- or site

- specific data on the temporal pattern of emissions, the layout of emission points at the facility, the boundaries of the facility, and /or the local meteorology. In some cases, all of these site

- specific data would be needed to refine the assessment; in others, lesser amount s of site

- specific data c an be used to determine that acute exposures are not a concern, and significant additional data collection is
not necessary.

Acute health risk screening was performed for each facility as the first step. When we identify acute impacts wh ich exceed their relevant benchmarks, we pursue refining our acute screening estimates to the extent possible using available data . In some cases, this mayDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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10 include the use of a facility

- specific emissions multiplier to estimate the peak hourly emission

ra tes from the average rates (rather than the default factor of 10). In other cases, this may entail determining the actual physical layout and boundaries of a facility and surrounding
communities to more accurately gauge where people might reasonably be ex posed for an
hour.

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

- site location as the surrogate for the maximum potential acute exposure concentration for any individ ual. These hourly concentrations are based on hourly emissions, as described above. Since information is not usually available on
short

- term emission rates, we generally apply the assumption that the maximum one

- hour emission rate from any source is ten times the average annual hourly emission rate for that source. (The average hourly emissions rate is defined as the total emissions for a year divided by the total number of operating hours in the year.) This choice of a factor of ten for acute screening was originally based on engineering judgment

.

To develop a more robust peak

- to

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

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

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

- industrialized 4

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

- month time period in 2001 . We obtained the dataset and performed our own analysis, focusing on sources which reported emitting high quanti ties of HAP over short periods of time (see Appendix 3 of this document, 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 o f 74 times the annual average , and the 99 th percentile ratio of peak hourly emission rate to the annual hourly emission rate was 9. Based on these results, we generally chose the factor of ten for all initial screening. This factor is intended to cover a ll possible hourly peaks associated with routinely

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

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

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

- specific data, we use this same default approach for particulate emissions as well. For phosphate fertilizer production facilities an acute multiplier of 10 (x) the average 1

- hr emission rates was applied to all sources.

For phosphoric acid manufacturing facilities a m ultiplier of 10 (x) was applied for point sources based on the ICR data and engineering knowledge of the source category processes and for emissions from fugitive sources (gypsum ponds and cooling ponds) an acute multiplier of 1 was applied.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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11 As mentio ned above, when we identify acute impacts which exceed their relevant benchmarks, we pursue refining our acute screening estimates to the extent possible. For the phosphate fertilizer production source category, all facilities screened out for acute risks from
the initial HEM run , refer to Appendix 8 to this document ( Acute Noncancer Risk Analysis for Phosphate Fertilizer and Phosphoric Acid Manufacturing) , Table 1 to view initial acute
screen risk values

.

The hydrogen fluoride emissions from the phosphor ic acid manufacturing gypsum ponds drove the acute risks. This emission source was considered stable and homogeneous and not subject to major fluctuations in hourly emissions over the year and therefore an acute multiplier of 1 was applied. This was appli ed to all area sources in the entire source category except for one facility that had site

- specific data for their gypsum ponds, an acute multiplier of 2 was applied for this facility. This data was considered unique to the facility and not applicable for any other site. For further information on the acute multipliers applied for these source categories refer to the memo entitled “ Emissions Data Used in Residual Risk Modeling: Phosphoric Acid and Phosphate Fertilizer Production Source Categories ”
availa ble in the docket for this action.

In summary, we used conservative assumptions for emission rates, meteorology, and exposure location, and refined data where available. We used the following assumptions in our acute assessment approach:

 Peak 1

- hour e missions were based upon specific emission process groups varying
from 1 to 1 0 times the average 1

- hour emission rates except for area source emissions
from phosphoric acid manufacturing facilities , an acute hourly multiplier of 1 was
used except for 1 sit e we had site

- specific data to calculate an hourly multiplier

.

 For facilities with multiple emission points, peak 1

- hour emissions were assumed to occur at all emission points at the same time.

 For facilities with multiple emission points, 1

- hour concentra tions at each receptor
were assumed to be the sum of the maximum concentrations due to each emission point, regardless of whether those maximum concentrations occurred during the same
hour.

 Worst

- case meteorology (from one year of local meteorology) was a ssumed to occur at the same time the peak emission rates occur. The recommended EPA local

- scale dispersion model, AERMOD, is used for simulating atmospheric dispersion.

 A person was assumed to be located downwind at the point of maximum impact during this same 1

- hour period, but no nearer to the source than 100 meters.

 The maximum impact was compared to multiple short

- term health benchmarks for the chemical being assessed to determine if a possible acute health risk might exist. These
benchmarks are descr ibed in section 2.6 of this report.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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### 2.5. Multipathway human health and environmental risk screening

Multipathway H uman H ealth S creening

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

- HAP) 2 . The PB

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

PB

- HAP are cadmium compounds, chlordane, chlorinated dibenzodioxins and furans, DDE, heptachlor, hexachlorobenzene, hexachlorocyclohexane, lead compounds, mercury compounds, methoxychlor, polychl orinated biphenyls (PCB) , polycyclic organic matter (POM) , toxaphene, and triflurali n. There were PB

- HAP emissions identified for both of the source categories addressed in this risk document. For the phosphorate fertilizer production
source category, we identified emissions of cadmium compounds, lead compounds , and mercury compounds. For the phosphoric acid manufacturing source category, we identified emissions of cadmium compounds, lead compounds , mercury compounds, POM, and dioxin.

With respect to PB

- HAP emissions other than lead, emissions were evaluated for potential

non

- inhalation risks using a tiered screening approach which was developed for use with the EPA’s peer

- reviewed Total Risk Integrated Methodology

– Fate, Transport, and Ecological

Ex posure (TRIM.FaTE 3 ) model. With this approach, we first determine whether the facility

specific emission rates of each of the emitted PB

- HAP are large enough to create the potential for significant non

- inhalation human health risks under reasonable worst

- case conditions. To facilitate this step, we developed emission rate levels for each PB

- HAP using a hypothetical

upper

- end screening exposure scenario developed for use in conjunction with TRIM.FaTE. The exposure scenario includes a generic farming/fishi ng exposure scenario that simulates a subsistence environment. We conducted a sensitivity analysis on the screening scenario to ensure that its key design parameters would represent the upper end of the range of possible values, such that it would represe nt a conservative but not impossible scenario. The PB

- HAP emissions from each facility in the source category were compared to the emission rate levels
for each of the PB

- HAP identified to assess the potential for significant human health risks via

non

- in halation pathways. For the purpose of developing emission rates for the multipathway screen, we derived emission levels for each PB

- HAP (other than lead) at which the maximum human health risk would be 1 in a million for lifetime cancer risk or a hazard q uotient of 1.0 for noncancer impacts. We call this application of the TRIM.FaTE model the Tier 1 Screen.

Se e Appendix 5 of this document, ( Technical Support Document for TRIM

- Based Multipathway Screening Scenario for RTR: Summary of Approach and Evaluat ion ) for a complete discussion of the development and testing of the screening scenario, as well as for the values of facility

- level emission rates developed for screening potentially significant

2 Although the two

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

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

- letter chemical symbol for lead is not used in this document).

3 EPA’s Total Risk Integrated Methodology (General Information) http://www2.epa.gov/fera/total

- risk

integrated

- methodology

- trim

- generalDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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13 multipathway impacts.

If the PB

- HAP emissions for a facil ity exceed the Tier screening emission rate, we conduct a Tier 2 multipathway screen. In the Tier 2 screen, the location of each facility that exceeded the Tier 1 emission level is used to refine some of the assumptions associated with the
environmental s cenario while maintaining the exposure scenario assumptions. We then adjust
the risk

- based Tier 1 screening level for each PB

- HAP for each facility based on an understanding of how exposure concentrations estimated for the screening scenario change
with m eteorology and environmental assumptions. The screening scenario s developed include 2 separate receptors; 1) subsistence fisher and 2) subsistence farmer. This step creates a facility

- specific emission level for each PB

- HAP ( i.e., the level for cadmium c ould be different for every facility), unlike the Tier 1 emission level which was constant for the same

PB

- HAP at different facilities (i.e., the level for cadmium was the same for every facil ity).

The subsistence fisher scenario assumes a high

- end fish consumption rate of 373 grams/day

. 4
Also, the assessment uses the assumption that the biological productivity limitation of each lake is 1 gram of fish per acre of water Thus, in order to fulfill the adult ingestion rate, we may need to model more than on e lake , refer to Appendix 5 of this document ( Technical Support Document for TRIM

- Based Multipathway Screening Scenario for RTR: Summary of Approach and Evaluation ) for a complete discussion of the bioassay studies used to support this assumption.

If we need to include more than one lake to achieve the 373 g/day ingestion rate, we begin with the lake with highest chemical concentration of a given PB

- HAP group, and “fish” up to the lake’s biological productivity. We then systematically proceed to other lakes based on concentration, until the 373 g/day limit is met. A maximum travel radius of 50 km relative to the facility is used to maintain a realistic scenario. The final Tier 2 screening result for the fisher can be expressed as the sum of the risk fr om each lake that is fished (which is based on the amount of fish ingested for each lake multiplied by the fish concentration). If the highest

concentration lake is at least 373 acres, the ingestion rate is not altered (i.e., remains 373 g/d for adults). I f the cumulative size of multiple visited lakes exceeds 373 acres, the model includes from the final lake only the amount of fish necessary to satisfy the ingestion rate (i.e., to reach the 373 g/d). If there are not 373 acres of lake, the risk reflects a reduced ingestion rate based on the lake acreage. The farmer scenario (same approach for all Tiers) involves an individual living for a 70

- year lifetime on a farm homestead in the vicinity of the source and consuming produce grown on, and meat and animal p roducts raised on, the farm. The ingestion rate used for these food groups are set at the 90 th percentile of EPA’s “Exposure Factors Handbook: 2011 Edition”, and is considered an upper

- bound level. [ 9 ]

Facility emissions of PB

- HAP that do not exceed th ese new Tier 2 screening levels are considered to pose no significant risks. When facilities exceed the Tier 2 screening levels, it does not mean that multipathway impacts are significant, only that we cannot rule out that possibility based on the results of the screen. Se e Appendix 5 of this document ( Technical

4 Burger, J. 2002. Daily consumption of wild fish and game: Exposures of high end
recreationalists. Enviro nmental Health Research. 12(4):343

– 354Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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14 Support Document for TRIM

- Based Multipathway Screening Scenario for RTR: Summary of Approach and Evaluation ) for a complete discussion of the Tier 2 screen.

If the PB

- HAP emissions for a faci lity exceed the Tier 2 screening emissions rate, and data are available, we may decide to conduct a more refined multipathway assessment. This next iteration of assessment could be an extensive refined assessment that replaces as many of the assumptions m ade in the Tier 2 screen with site

- specific data as possible or it could be focused on a few parameters such as adequacy of the lake, and/or the effective plume height
and the use of time

- series meteorology in conjunction with hourly effective release heig hts

. We refer to the latter as the Tier 3 screen. In the Tier 3 screen, the lakes included in the screen are scrutinized for accessibility (i.e., private or public) and appropriateness (i.e., fishable lake v. industrial waste pond). In addition, a Tier 3 screen may include an
examination of the site

- specific meteorological mixing height relative to the effective plume rise. As with the Tier 2 screen, the Tier 3 step creates a facility

- specific emission rate level
for each PB

- HAP (i.e., the level for cad mium could be different for every facility). Also as with the Tier 2 screen, if facilities exceed the Tier 3 screening levels, it does not mean that multipathway impacts are significant, only that we cannot rule out that possibility based on
the results o f the screen. See Appendix 5 of this document ( Technical Support Document for

TRIM

- Based Multipathway Screening Scenario for RTR: Summary of Approach and
Evaluation ) for a complete discussion of the Tier 3 screen. For the phosphate fertilizer production s ource category, we did conduct a Tier 3 screening assessment for Mississippi Phosphates Corporation in Pascagoula , Mississippi. In evaluating the potential multipathway risks from emissions of lead compounds, rather than developing a screening emission rate for
them , we compared maximum estimated chronic atmospheric concentrations with the current National Ambient Air Quality Standard (NAAQS) for lead. Values below the NAAQS were considered to have a low potential for multipathway risks.

The NAAQS val ue, a public health policy judgment, incorporated the Agency’s most recent health evaluation of air effects of lead exposure for the purposes of setting a national ambient air quality standard. In setting this value, the Administrator promulgated a standa rd that was requisite to protect public health with an adequate margin of safety. We consider values below the level of the primary NAAQS to protect against multipathway risks because as mentioned above, the primary NAAQS is set as to protect public healt h with an adequate margin of safety. However, ambient air lead concentrations above the NAAQS are considered to pose the potential for increased risk to public health. We consider this NAAQS assessment to be a refined analysis given: 1) the numerous heal th studies, detailed risk and exposure analyses, and level of external peer and public review that went into the development of the primary NAAQS for lead, combined with: 2) the site

- specific dispersion modeling used in this assessment to estimated ambient lead concentrations due to primary
aluminum emissions. It should be noted, however, that this comparison does not account for possible population exposures to lead from sources other than the one being modeled; for example, via consumption of water from untreated local sources or ingestion of locally grown food. Nevertheless, the Administrator judged that such a standard would protect, with an adequate margin of safety, the health of children and other at

- risk populations against an array
of adverse heal th effects, most notably including neurological effects, particularly neurobehavioral and neurocognitive effects, in children (73 FR 67007). The Administrator, inDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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15 setting the standard, also recognized that no evidence

- or risk based bright line indicated a single appropriate level. Instead a collection of scientific evidence and other information was used to select the standard from a range of reasonable values (73 FR 67006).

We further note that comparing ambient lead concentrations to the NAAQS for lead

, considering the level, averaging time, form and indicator, also informs whether there is the potential for adverse environmental effects. This is because the primary lead NAAQS, set to protect against adverse welfare effects (including adverse environme ntal effects), has the same averaging time, form, and level as the primary standard. Thus, ambient lead concentrations above the NAAQS for lead also indicate the potential for adverse
environmental effects.

Environmental Risk Screening

The EPA has deve loped a screening approach to examine the potential for adverse environmental effects as required under section 112(f)(2)(A) of the CAA. The environmental screen focuses on the following seven environmental HAP:

 Five persistent bioaccumulative HAP (PB

- HA P)

– cadmium, dioxins/furans, POM, mercury (both inorganic mercury and methyl mercury), and lead,

 Two acid gases

– hydrogen chloride (HCl) and hydrogen fluoride (HF).

HAP that persist and bioaccumulate are of particular environmental concern because they accumulate in the soil, sediment, and water. The acid gases

– HCl and HF

– were included
due to their well

- documented potential to cause direct damage to terrestrial plants.

For the environmental risk screening analysis, EPA first determined whether any facilities in the source category emitted any of the seven environmental HAP. If one or more of the seven environmental HAP evaluated are emitted by at least one facility in the source categor ies we proceed to the second step of the evaluation.

For cadmi um, mercury, POM, and dioxins/furans, the environmental screening analysis consists of two tiers. In the first tier, TRIM.FaTE modeling was conducted under worst

- case environmental conditions to determine whether the facility

- specific off

- site emission ra tes of each of the emitted environmental HAP exceeded ecological benchmarks represented as
emissions levels. If off

- site emissions from a facility do not exceed the Tier 1 levels the facility “passes” the screen, and therefore, is not evaluated further un der the screening approach. If off

- site emissions from a facility exceed the Tier 1 levels, we evaluate the facility further in Tier 2.

In Tier 2 of the environmental screening analysis, the screening emission levels are adjusted
to account for local met eorology and the actual location of lakes in the vicinity of facilities that did not pass the Tier 1 screen. If off

- site emissions from a facility do not exceed the Tier 2 levels, the facility passes the screen, and is typically not evaluated further. If off

- site emissions from a facility exceed the Tier 2 levels, the facility does not pass the screen, and, therefore, may have the potential to cause adverse environmental effects. Such facilities areDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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16 evaluated further to investigate factors such as the ma gnitude and characteristics of the area of
exceedance.

For acid gases, the environmental screening analysis evaluates the potential phytotoxicity and reduced productivity of plants due to chronic exposure to acid gases. The environmental risk screening m ethodology for acid gases is a single

- tier screen that compares the average off

- site ambient air concentration over the modeling domain to ecological benchmarks for each of the acid gases. For purposes of ecological risk screening, EPA identifies a potent ial for adverse environmental effects to plant communities from exposure to acid gases when the average concentration of the HAP around a facility exceeds the LOAEL ecological benchmark. In such cases, we further investigate factors such as the magnitude and characteristics of the area of exceedance (e.g., land use of exceedance area, size of exceedance area) to determine if
there is an adverse environmental effect.

For lead compounds, we currently do not have the ability to calculate media concentrations using the TRIM.FaTE model. However, air concentrations of lead are already calculated as part of the human health exposure and risk analysis using the HEM3

- AERMOD air dispersion model. To evaluate the potential for adverse environmental effects from lea d, we compare the average modeled air emission concentrations of lead from each facility in the source category emissions to the level of the secondary National Ambient Air Quality Standard (NAAQS) for lead. The secondary lead NAAQS is a reasonable means of evaluating environmental risk because it is set to provide substantial protection against adverse welfare effects which can include “effects on soils, water, crops, vegetation, man

- made materials, animals, wildlife, weather, visibility and climate, dama ge to and deterioration of property, and hazards to transportation, as well as effects on economic values and on personal comfort and well

being.” 5



### 2.6. Dose

- r esponse a ssessment

2.6.1. Sources of chronic dose

- response information

Dose

- response assessment (carcinog enic and non

- carcinogenic) for chronic exposure (either by inhalation or ingestion) for the HAP reported in the emissions inventories for the source categories in this document were based on the EPA Office of Air Quality Planning and Standards’ existing r ecommendations for HAPs [ 10 ], which were also used for NATA [ 11 ]. This information has been obtained from various sources and prioritized according to (1) conceptual consistency with EPA risk assessment guidelines and (2) level of peer review
received. The prioritization process was aimed at incorporating into our assessments the best

5 A secondary standard, as defined in Section 109(b)(2), must “specify a level of air quality the attainment and maintenance of which, in the judgment of the Administrator, based on criteria, is requisite to protect the public welfare from any known or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.” Welfare effects as defined in section 302(h) (42 U.S.C. 7602(h)) include, but are not limited to, “effects on soils, wate r, crops, vegetation, man

- made materials, animals, wildlife, weather, visibility and climate, damage to and deterioration of property, and hazards to transportation, as well as effects on economic values and on personal comfort and
well

- being.”Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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17 available science with respect to dose

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

1) EPA has developed dose

- response a ssessments for chronic exposure for many of the pollutants in this study. These assessments typically provide a qualitative statement regarding the strength of scientific data and specify a reference concentration (RfC, for inhalation) or reference dose ( RfD, for ingestion) to protect against effects other than cancer and/or a unit risk estimate (URE, for inhalation) or slope factor (SF, for ingestion) to estimate the probability of developing cancer. The RfC is defined as an “ estimate (with uncertainty s panning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. ” Similarly, the RfD is “a n estima te (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. ” The URE is defined

as “ the upper

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

- day ...” EPA disseminates dose

- response assessment information in several forms, based on the level of review. The Integrated Risk

Inf ormation System (IRIS) [ 12 ] is an EPA database that contains scientific health assessment information, including dose

- response information. All IRIS assessments since 1996 have also undergone independent external peer review. The current IRIS process
inclu des review by EPA scientists, interagency reviewers from other federal agencies, and the public, and peer review by independent scientists external to EPA. New IRIS values are developed and old IRIS values are updated as new health effects data become

ava ilable. Refer to the “IRIS Track” website for detailed information on status and scheduling of current individual IRIS assessments and updates ( http://cfpub.epa.gov/ncea/iristrac/index.cfm )

. EPA’ s science policy approach , under the current carcinogen guidelines, is to use linear low

- dose extrapolation as a default option for carcinogens for which the mode of action (MOA) has not been identified. We expect
future EPA dose

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

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

.

2) US Agency for Toxic Substances and Disease Registry (ATSDR). ATSDR, which is part of the US Department of Health and Human Services, develops and publishes Minimum Risk Levels (MRLs) [ 13 ] for inhalation and oral exposure to many toxic subst ances. As
stated on the ATSDR web site: “ Following discussions with scientists within the Department of Health and Human Services (HHS) and the EPA, ATSDR chose to adopt a practice similar to that of the EPA's Reference Dose (RfD) and Reference Concentrat ion (RfC) for deriving substance specific health guidance levels for non neoplastic endpoints .” The MRL is defined as “an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse effects (other than cance r) over a specifiedDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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18 duration of exposure.” ATSDR describes MRLs as substance

- specific estimates to be used by health assessors to select environmental contaminants for further evaluation. Exposures above an MRL do not necessarily represent a threat, and MRLs are therefore not intended for use as predictors of adverse health effects or for setting cleanup levels.

3) California Environmental Protection Agency (CalEPA). The CalEPA Office of Environmental Health Hazard Assessment has developed dose

- response as sessments for many substances, based both on carcinogenicity and health effects other than cancer. The process for developing these assessments is similar to that used by EPA to develop IRIS values and incorporates significant external scientific peer rev iew. As cited in the CalEPA Technical Support Document for developing their chronic assessments 6 : “The guidelines for developing chronic inhalation exposure levels incorporate many recommendations of the U.S. EPA [ 14 ] and NAS [ 15 ].” The non

- cancer informat ion includes available inhalation health risk guidance values expressed as chronic inhalation reference exposure levels (RELs) [ 16 ]. CalEPA defines the REL as “the concentration level at or below which no health effects are anticipated in the general human population.” CalEPA's quantitative dose

- response information on carcinogenicity by inhalation exposure is expressed in terms of the URE [ 17 ], defined similarly to EPA's URE.

As mentioned above, in order to characterize non

- cancer chronic effects, and in response to key recommendations from the SAB, the EPA selects dose

- response values that reflect the best
available science for all HAP included in RTR risk assessments 7 . More specifically, for a given HAP, EPA examines the availability of inhalation re ference values from the sources included in our tiered approach (e.g., IRIS first, ATSDR second, Cal EPA third) and determines which inhalation reference value represents the best available science. Thus, as new inhalation reference
values become available , EPA will typically evaluate them and determine whether they should be given preference over those currently being used in RTR risk assessments. In developing chronic risk estimates, we adjusted dose

- response values for some HAPs based on professional ju dgment, as follows:

1) There is an existing IRIS RfC for manganese (Mn) published in 1993 8 . This value was in the RTR risk assessment supporting the 2011 Ferroalloys Notice of Proposed Rulemaking. However, since the 2011 proposal ATSDR has published an as sessment of Mn toxicity (2012) which includes a chronic inhalation reference value (i.e., an ATSDR Minimal Risk Level or MRL) 9 . Both the 1993 IRIS RfC and the 2012 ATSDR MRL were based on the same study (Roels et al., 1993). In developing their assessmen t, ATSDR used updated dose

- response modeling methodology (benchmark dose approach) and considered recent pharmacokinetic

6 Air Toxi cs Hot Spots Program, Risk Assessment Guidelines, Part III

- Technical Support Document
For the Determination of Non

- cancer Chronic Reference Exposure Levels. Air Toxicology and Epidemiology Section, Office of Environmental Health Hazard Assessment, Calif ornia Environmental Protection Agency. February 2000 ( http://www.oehha.ca.gov/air/chronic_rels/pdf/relsP32k.pdf )

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

- SAB

- 10

- 007

- unsigned.pdf

. 8 USEPA I ntegrated Risk Information System Review of Manganese (1993) available at http://www.epa.gov/iris/subst/0373.htm

. 9 Agency for Toxic Substances & Disease Registry Toxicological Profile for Manganese ( 2012) available at http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=102&tid=23

.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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19 findings to support their MRL derivation. In the interest of using the best available science, the EPA has chosen to rely on the ATSDR MRL for Mn in the current secondary aluminum proposal.

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

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

- containing emissions. Nickel speciation information for

some o f the largest nickel

- emitting sources (including oil combustion, coal combustion, and others) suggested that at least 35 percent of total nickel emissions may be soluble compounds and that the URE for the mixture of inhaled nickel compounds (based on
nicke l subsulfide, and representative of pure insoluble crystalline nickel) could be derived to reflect the assumption that 65 percent of the total mass of nickel may be carcinogenic.

Based on consistent views of major scientific bodies (i.e., National Toxic ology Program (NTP) in their 12 th Report of the Carcinogens (ROC) 10 , International Agency for Research on Cancer (IARC) 11 , and other international agencies) 12 that consider all nickel compounds to be carcinogenic, we currently consider all nickel compounds to have the potential of being carcinogenic to humans. The 12th Report of the Carcinogens states that the “combined results of epidemiological studies, mechanistic studies, and carcinogenic studies in rodents support the concept that nickel compounds genera te nickel ions in target cells at sites critical for carcinogenesis, thus allowing consideration and evaluation of these compounds as a single group.” Although the precise nickel compound (or compounds) responsible for the carcinogenic effects in humans i s not always clear, studies
indicate that nickel sulfate and the combinations of nickel sulfides and oxides encountered in the nickel refining industries cause cancer in humans (these studies are summarized in a review by Grimsrud et al., 2010 13 ). The majo r scientific bodies mentioned above have also recognized that there are differences in toxicity and/or carcinogenic potential across the different nickel compounds.

Therefore, in the inhalation risk assessment for this supplemental proposal, to take a

c onservative approach, we considered all nickel compounds to be as carcinogenic as nickel subsulfide and applied the IRIS URE for nickel subsulfide without a factor to reflect the assumption that 100 percent of the total mass of nickel may be as carcinogeni c as pure nickel subsulfide. However, given that there are two additional URE values 14

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

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

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

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

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

- 7. Availa ble online at http://www.occup

- med.com/content/5/1/7

. 14 Two UREs (other than the current IRIS values) have been derived for nickel compounds as a group : one developed by the California Department of Health ServicesDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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20 derived for exposure to mixtures of nickel compounds, as a group, that are 2

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

.

3) Where possible for emissions of unspecified mi xtures of HAP categories such as metal compounds and POM, we apply category

- specific chemical speciation profiles appropriate to the source category to develop a composite dose

- response value for the category.

4) Where POM emissions were not speciated into individual compounds, we applied the same simplifying a ssumptions to assessments that are used in NATA [ 18 ]. The NATA approach partitions POM into eight different non

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

The emissions inventory for the phosphate fertilizer production and phosphoric acid manufacturing source categories includes emissions of HAP with available chronic quantita tive inhalat ion dose

- response values. Of these

, 2 2 are classified as known, probable, or possible carcinogens, with quantitative cancer dose

- response values available. These 2 2 HAPs, their quantitative inhalation chronic cancer dose

- response values, and the source of
each value are listed in Table 2.6

- 1(a). The POM compounds and dioxin with chronic oral
cancer dose

- response values available (for which multipathway screening assessments were performed) are listed in Table 2.6

- 1(b). Fifty HAP have quanti tative inhalation chronic noncancer threshold values available, four of these HAP (mercury , lead, dioxin, and
cadmium ), for which a multipathway assessment was performed, also have quantitative oral
chronic noncancer threshold values available. These 50 H AP, their threshold values, and the
source of the value are listed in Table 2.6

- 2(a) and Table 2.6

- 2(b).

( http://www.arb.ca.gov/toxics/id/summary/nickel_tech_b.pdf ) and the other by the Texas Commission on Environmental Quality ( http://www.epa.gov/ttn/atw/nata1999/99pdfs/healtheffectsinfo.pdf ).Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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21 Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhalation Exposure to Carcinogens

URE (unit risk estimate for cancer) 15 = cancer risk per μg/m 3 of average lifetime exposure. Sources: IRIS = EPA Integrated Risk Information System, EPA OAQPS = interim value recommended by the EPA Office of Air Quality Planning & Standards, CAL = California
EPA Office of Environmental Health Hazard Assessment

, Conv. Oral = Oral unit risk
converted to inhalation.

Pollutant CAS

Number 16 URE 7

(1/μg/m 3 ) Source

1,2,3,6,7,8

- hexachlorodibenzo

- p

- dioxin 57653857 3.3 EPA

- ORD 2,4

- dinitrotoluene 121142 0.000089 CAL Acetaldehyde 75070 0.0000022 IRIS Arsenic compounds 7 440382 0.0043 IRIS

Benzene 17 71432 0.0000078 IRIS Benzyl c hloride 100447 0.000049 CAL Beryllium compounds 7440417 0.0024 IRIS

Bromoform 75252 0.0000011 IRIS Cadmium compounds 7440439 0.0018 IRIS Chromium (VI) compounds 18540299 0.012 IRIS Ethyl b enze ne 100414 0.0000025 CAL Ethylene dibromide 106934 0.0006 IRIS Ethylene d ichloride 107062 0.000026 IRIS Ethylene o xide 75218 0.000088 CAL Formaldehyde 18 50000 0.000013 IRIS Methyl tert

- butyl e ther 1634044 0.00000026 CAL Methylene c hloride 75092 0.00 0 00 00 1 6 IRIS Naphthalene 91203 0.000034 CAL Nickel compounds 7440020 0.00048 EPA OAQPS Polycyclic Organic Matter 19 (POM)
Benzo[a]pyrene 50328 0.00176 CAL

Tetrachloroeth ene 127184 0.00000026 IRIS

15 The URE is the upper

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

16 Chemical Abstract Services identification number. For groups of compounds that lack a CAS number we have used a surrogate 3

- digi t identifier corresponding to the group’s position on the CAA list of HAPs.

17 The EPA IRIS assessment for benzene provides a range of plausible UREs. This assessment used the highest value in that range, 7.8E

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

- 06 per ug/m 3

. 18 The EPA has used the CIIT URE value, 5.5X10

- 9 per mg/m 3 , to characterize formaldehyde cancer risk in some
instances.

19 Assigned the URE associated with a mixture of POM compounds having a similar potency. Details of this method, also use d in the National Air Toxics Assessments, are available at http://www.epa.gov/nata2002/methods.html#pomDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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22 Table 2 .6

- 1(b) Dose

- Response Values for Chronic Oral Exposure to Carcinogens

SF (oral slope factor for cancer) = cancer risk per mg/kg/d of average lifetime exposure. Sources : IRIS = EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Health
Hazar d Assessment, EPA/OAQPS = interim value recommended by the EPA Office of Air Quality Planning and Standards, EPA ORD = EPA Office of Research and Development, HEAST = EPA Health
Effects Assessment Tables

Pollutant CAS
Number SF

(1/mg/kg/d) Source
Dioxin/ Furans
Hexachlorodibenzo

- p

- dioxin 19408743 6200 IRIS 2,3,7,8

- Tetrachlorodibenzo

- p

- dioxin 1746016 150000 EPA ORD Methylene chloride 75092 0.00 2 IRIS Polycyclic organic matter (POM) Benzo(a)pyrene 50328 7.3 IRIS

T able 2.6

- 2 ( a ) D ose
- Response Values for Chronic In halation Exposure to Noncarcinogens

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including

s ensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRIS = EPA Integrated Risk Information System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency

f or Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables, EPA OAQPS = EPA Office of Air Quality Planning & Standards

Pollutant CAS

Number 8 RfC

(mg/m 3 ) Source 20

2,4

- dinitrotoluene 121142 0.007 CAL

2

- chloroacetophenone 532274 0.0 0003 IRIS

– L/ M Acetaldehyde 75070 0.009 IRIS

- L

Acrolein 107028 0.00002 IRIS

- M Antimony compounds 7440360 0.0002 IRIS

- L Arsenic compounds 7440382 0.000015 CAL

Benzene 71432 0.03 IRIS

- M Beryllium compounds 7440417 0.00002 IRIS

- M

Cadmium com

pounds 7440439 0.00001 ATSDR

Carbon disulfide 75150 0.7 IRIS

- M

Chlorobenzene 108907 1 CAL

Chloroform 67663 0.098 ATSDR Chromium (VI) compounds 18540299 0.0001 IRIS

- M Cobalt compounds 7440484 0.0001 ATSDR

Cumene 98828 0.4 IRIS

- M Cyanide & Cyani de c pds Cyanide compounds 21 57125 0.00 08 IRIS

– L /M

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

21 The value for hydrogen cyanide was used as a surrogate for all cyanide compounds without an RfC.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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23 Diethanolamine 111422 0.003 CAL Ethyl benzene 100414 1 IRIS

- L Ethyl chloride 75003 10 IRIS

- M Ethylene dibromide 106934 0.009 IRIS

- M Ethylene dichloride 107062 2.4 ATSDR Formaldehyde 5 0000 0.0098 ATSDR Hydrochloric acid 7647010 0.02 IRIS

- L Hydrofluoric acid 7664393 0.014 CAL Isophorone 78591 2 CAL Lead compounds 7439921 0.00015 EPA OAQPS Manganese compounds 7439965 0.000 3 ATSDR Mercury c ompounds Elemental gaseous mercury 7 439976 0.0003 IRIS

- M Gaseous divalent mercury 201 0.0003 IRIS

- M Particulate divalent mercury 202 0.0003 IRIS

- M Methyl bromide 74839 0.005 IRIS

- H Methyl chloride 74873 0.09 IRIS

- M Methyl isobutyl ketone 108101 3 IRIS

- L/M Methyl methacr ylate 80626 0.7 IRIS

- M/H Methyl tert

- butyl ether 1634044 3 IRIS

- M Methylene chloride 75092 0.6 IRIS

– M/H Naphthalene 91203 0.003 IRIS

- M

n

- hexane 110543 0.7 IRIS

- M Nickel compounds 7440020 0.00009 ATSDR

Phenol 108952 0.2 CAL Propionaldehyde 123386 0.008 IRIS

– L/M Selenium compounds 7782492 0.02 CAL Styrene 100425 1 IRIS

- M

Tetrachloroethene 127184 0.04 IRIS

- M

Toluene 108883 5 IRIS

- H Vinyl acetate 108054 0.2 IRIS

- H Xylenes (mixed) 1330207 0.1 IRIS

- M

m

- Xylene 22 108383 0.1 I RIS

- M

o

- Xylene 22 95476 0.1 IRIS

- M

p

- Xylene 22 106423 0.1 IRIS

- M

22 The RfC for mixed xylene was used as a surrogate.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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24 Table 2.6

- 2 (b) Dose

- Response Values for Chronic Oral Exposure to Noncarcinogens

RfD (reference dose) = an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous oral exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime.
Sources: IRIS = EPA Integrated Risk Information System, A TSDR = US Agency for Toxic Substances and Disease Registry, HEAST = EPA Health Effects Assessment Tables

Pollutant CAS Number RfD (mg/kg/d) Source Cadmium compounds 7440439 0.0005 IRIS

- H Mercury and Mercury Compounds 23

Mercuric chloride 7439 976 0.0003 IRIS

- H Methyl mercury 22967926 0.0001 IRIS

- H Phenylmercuric acetate 62384 0.00008 IRIS

- L
2,3,7,8

- Tetrachlorodibenzo

- p

- dioxin 1746016 0.0000000007 IRIS

- H

Tetrachloroethene 127184 0.006 IRIS

- M Tetraethyl lead 78002 0.00000 01 IRIS

- M

2.6.2. Sources of acute dose

- response information

Hazard identification and dose

- response assessment information for preliminary acute
inhalation exposure assessments is based on the existing recommendations of OAQPS for HAPs [ 19 ]

. Depending on ava ilability, the results from screening acute assessments are compared to both “no effects” reference levels for the general public, such as the California Reference Exposure Levels (RELs), as well as emergency response levels, such as Acute Exposure Guideli ne Levels (AEGLs) and Emergency Response Planning Guidelines (ERPGs), with the recognition that the ultimate interpretation of any potential risks associated with an estimated exceedance of a particular reference level depends on the definition of that
lev el and any limitations expressed therein. Comparisons among different available inhalation health effect reference values (both acute and chronic) for selected HAPs can be found in an EPA document of graphical arrays. 24

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

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

The acute REL ( http://www.oehha.ca.gov/air/pdf/acuterel.pdf ) is defined by CalEPA
as “ t he concentration level at or below which no adverse health effects are anticipated for a specified exposure duration . [ 20 ]

. RELs are based on the most sensitive, relevant, adverse health effect reported in the medical and toxicological literature. RELs are designed to protect the most sensitive individuals in the population by the
inclusion of margins of safety. Since margins of safety are incorporated to address

23 The multipathway e xposure assessment for mercury included fate and transport analysis, that included separate oral exposure estimates for divalent mercury and methylmercury.

24 See : U.S. EPA. Graphical Arrays of Chemical

- Specific Health Effect Reference Values for Inhalatio n Exposures [Final Report]. (U.S. Environmental Protection Agency, Washington, D.C., EPA/600/R

- 09/061,
2009. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003 .)Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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25 data gaps and uncertainties, exceeding the REL does not automatically indicate an adverse health impact. ” Acute RELs are developed for 1

- hour (and 8

- hour) exposures. The values incorporate uncertainty factors similar to those used in deriving EPA’s Inhalation Reference Concentrations (RfCs) for chronic exposures (and, in fact, California also has developed chronic RELs).

Acute Exposure Guideline Levels (AEGLs ). AEGLs are developed by the National Advisory Committee (NAC) on Acute Exposure Guideline Levels (NAC/AEGL) f or Hazardous Substances , and then reviewed and published by the National Research
Council. A s described in the Committee’s “Standing Operating Procedures (SOP) ” ( http://www.epa.gov/opptintr/aegl/pubs/sop.pdf ), AEGLs “represent threshold exposure limits for the general public and are applicable to emergency exposures ranging from 10
min to 8 h.” Their intended application is “for conducting risk assessments to aid in the development of emergency preparedness and prevention plans, as well as real time emergency response actions, for accidental chemical releases at fixed facilities and from transport carriers.” The document states: “the primary purpose of the AE GL program and the NAC/AEGL Committee is to develop guideline levels for once

- in

- a

- lifetime , short

term exposures to airborne concentrations of acutely toxic, high

- priority chemicals.” In detailing the intended application of AEGL values, the document sta tes that

, “ It is anticipated that the AEGL values will be used for regulatory and nonregulatory purposes by U.S. Federal and State agencies, and possibly the international community in conjunction with chemical emergency response, planning, and prevention programs. More specifically, the AEGL values will be used for conducting various risk assessments to aid in the development of emergency preparedness and prevention plans, as well as
real

- time emergency response actions, for accidental chemical releases a t fixed facilities and from transport carriers.” The NAC/AEGL defines AEGL

- 1 and AEGL

- 2 as:

“ AEGL

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

exposure. ”

“ AEGL

- 2 is the airborne concentration (expressed as ppm or mg/m 3 ) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long

- lasting adverse health effects or an impaired ability to escape. ”

“ Airborne co ncentrations below AEGL

- 1 represent exposure levels that can produce mild and progressively increasing but transient and nondisabling odor, taste, and sensory irritation or certain asymptomatic, nonsensory effects. With increasing airborne
concentrations above each AEGL, there is a progressive increase in the likelihood of occurrence and the severity of effects described for each corresponding AEGL. Although the AEGL values represent threshold levels for the general public, including susceptible subpopula tions, such as infants, children, the elderly, persons with asthma, and those with other illnesses, it is recognized that individuals, subject to unique or idiosyncraticDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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26 responses, could experience the effects described at concentration s below the

correspo nding AEGL.”

Emergency Response Planning Guidelines (ERPGs). The American Industrial Hygiene Association (AIHA) has developed Emergency Response Planning Guidelines (ERPGs) [ 21 ] for acute exposures at three different levels of severity. These guidelines represent concentrations for exposure of the general population (but not particularly sensitive persons) for up to 1 hour associated with effects expected to be mild or transient (ERPG

- 1), irreversible or serious (ERPG

- 2), and potentially life

- threatening (ERPG

- 3).

ERPG values https://www.aiha.org/get

involved/AIHAGuidelineFoundation/EmergencyResponsePlanningGuidelines/Pages/def ault.a

spx ) are described in their supporting documentation as follows: “ Emergency Response Planning Guidelines (ERPGs) were developed for emergency planning and are intended as health based guideline concentrations for single exposures to chemicals. Thes e guidelines (i.e., the ERPG Documents and ERPG values) are intended for use as planning tools for assessing the adequacy of accident prevention and emergency response plans, including transportation emergency planning and for developing comm unity emergenc y response plans. The emphasis is on ERPGs as planning values: When an actual chemical emergency occurs
there is seldom time to measure airborne concentrations and then to take action. ” ERPG

- 1
and ERPG

- 2 values are defined by AIHA as follows:

“ ERPG

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

“ ERPG

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

In assessing the potential risks associated with acute exposures to HAP, we do not follow a prioritization scheme and therefore we consider available dose

- response values from multiple
authoritative sources.

The emissions inventory for the phosphate fertilizer production and phosphoric acid manufacturing source categories includes emissions of 3 5 HAP with relevant and available quantitative acute dose

- response threshold values. These HAPs, their acute thresh old values,
and the source of the value are listed below in Table 2.6

- 3.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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27 Table 2.6

- 3 Dose

- Response Values for Acute Exposure

Pollutant CAS

Number AEGL

- 1

(1

- hr) (mg/m 3 ) AEGL

- 2

(1

- hr) (mg/m 3 ) ERPG

1 (mg/m 3 ) ERPG

- 2

(mg/m 3 ) REL

Acetal dehyde 75070 81 490 18 360 0.47

Acrolein 107028 0.069 0.23 0. 11 0. 34 0.0025 Arsenic and Arsenic Compounds Arsenic compounds 744038 2 0.0002

Benzene 71432 170 2600 16 0 48 0 1.3 Benzyl chloride 10044 7 5.2 52 0.24 Beryllium c ompounds 7440 417 0.025

Carbon d isulfide 75150 40 500 3.1 160 6.2

Chlorobenzene 108907 46 690

Chloroform 67663 310 24 0 0.15

Cumene 98828 250 1500 Dimethyl sulfate 7778 1 0.12 0.62 Ethyl b enzene 100414 140 4800 Ethylene d ibromide 106934 130 180 Ethylene d ichloride 107062 200 810 Formaldehyde 50000 1.1 17 1. 2 1 2 0.055

n

- Hexane 110543 12000 Hydrochloric a cid 7647010 2.7 33 4.5 3 0 2.1 Hydrofluoric acid 7664393 0.82 20 1.6 16 0.24 Mercury (elemental) 743997 6 1.7 2 0.0006 Methyl b ro mide 74839 820 19 0 3.9 Methyl c hloride 74873 1900 83 0 Methyl hydrazine 6034 4 3.2 Methyl m ethacrylate 80626 70 490 Methyl tert

- butyl e ther 1634044 180 2100 Methylene c hloride 75092 690 1900 100 0 26 00 14

Phenol 108952 58 89 3 8 190 5.8

P ropionaldehyde 123386 110 620 Styrene 100425 85 550 210 110 0 21

Tetrachloroethene 127184 240 1600 68 0 14 00 20

Toluene 108883 750 4500 190 110 0 37 Vinyl a cetate 108054 24 630 18 260 Xylenes (mixed) 1330207 560 4000 22

m

- Xylene 22 108383 22

o

- Xylene 2 2 95476 22

p

- Xylene 2 2 106423 22Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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28 

### 2.7. Risk c haracterization

2.7.1. General
The final product of the risk assessment is the risk characterization, in which the information from the previous steps is integrated and an overall conclusio n about risk is synthesized that is complete, informative, and useful for decision makers. In general, the nature of this risk characterization depends on the information available, the application of the risk information
and the resources available. In all cases, major issues associated with determining the nature and extent of the risk are identified and discussed. Further, the EPA Administrator’s March

1995 Policy for Risk Characterization [ 22 ] specifies that a risk characterization “be prepared

in a m anner that is clear, transparent, reasonable, and consistent with other risk characterizations of similar scope prepared across programs in the Agency.” These principles of transparency and consistency have been reinforced by the Agency’s Risk Characteriz ation
Handbook [ 23 ], in 2002 by the Agency’s information quality guidelines [ 24 ], and in the OMB/OSTP September 2007 Memorandum on Updated Principles for Risk Analysis 25 , and are incorporated in these assessments.

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

For each carcinogenic HAP included in an assessment that has a potency estimate available,
individu al and population cancer risks we re calculated by multiplying the corresponding lifetime average exposure estimate by the appropriate URE. This calculated cancer risk is defined as the upper

- bound probability of developing cancer over a 70

- y r period (i.e., the assumed human lifespan) at that exposure. Because UREs for most HAPs are upper

- bound estimates, actual risks at a given exposure level may be lower than estimated , and could be

zero.

For EPA’s list of carcinogenic HAPs that act by a mutagenic mode

- of

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

- Life Exposure to Carcinogens [ 26 ]

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

- 1), 3 (for children aged 2

- 15), or 1.6 (for 70 years of exposure beginning at birth), as needed in ri sk assessments . In this case, this has the effect of increasing the estimated life time risks for these pollutants by a factor of 1.6. In addition, although only a
small fraction of the total POM emissions may be reported as individual compounds, EPA

25 Memorand um f

or t he Heads o f Executive Departments a nd Agencies

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

- 24.pdf )Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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29 exp resses carcinogenic potency for compounds in this group in terms of benzo[a]pyrene equivalence, based on evidence that carcinogenic POM have the same mutagenic mechanism
of action as does benzo[a]pyrene. For this reason

, EPA implem entation policy [ 27 ]

reco mmends applyi ng the Supplemental Guidance to all carcinogenic PAHs for which risk estimates are based on relative potency. Accordingly, we applied the Supplemental Guidance to all unspeciated POM mixtures.

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

Unlike linear dose

- response assessments for cancer, noncancer health hazards generally are not expressed as a probability of an adverse occurrence. Instead, “risk” for noncancer effects is expressed by comparing an exposure to a reference level as a ratio. The “hazard quotient” (HQ) is the estimated exposure divided by a reference level (e.g., the RfC). For a given HAP, exposures at or below the re ference 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 estimated to be above the RfC, the
risk c haracterization includes the degree of confidence ascribed to the RfC values for the compound(s) of concern (i.e., high, medium, or low confidence) and discusses the impact of this on possible health interpretations.

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

.

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

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

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

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

, 29 ] default assumption of additivity of effects, and combine risks by summing them using the independence formula in the mixtures guidelines.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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30 In assessi ng noncancer hazard from chronic exposures, in cases where different pollutants cause adverse health effects via completely different modes of action, it may be inappropriate to aggregate HQs. In consideration of these mode

- of

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

- cancer HQs of HAP that act by similar toxic modes of action, or (where this information is absent) that aff ect the same target organ. This process creates, for each target organ, a target

- organ

- specific hazard index (TOSHI), defined as the sum of hazard quotients for individual HAP that affect the same organ or organ system. A ll TOSHI calculations presented h ere were based exclusively on effects occurring
at the “ critical dose” (i.e., the lowest dose that produces adverse health effects). Although HQs associated with some pollutants have been aggregated into more than one TOSHI, this has been done only in cas es where the critical dose affects more than one target organ

. Because impacts on organs or systems that occur above the critical dose have not been included in the TOSHI calculations, some TOSHIs may have been underestimated. As with the HQ, the TOSHI s hould not be interpreted as a probability of adverse effects, or as strict delineation of “safe” and “unsafe” levels. Rather, the TOSHI is another measure of the potential for adverse health outcomes associated with pollutant exposure, and needs to be
int erpreted carefully by health scientists and risk managers.

Because of the conservative nature of the acute inhalation screening and the variable nature of emissions and potential exposures, acute impacts were screened on an individual pollutant basis, not using the TOSHI approach.

2.7.3. Facility

- wide r isks
To help place the source category risks in context, we examined “facility

- wide” risks using 2005 NEI data and modeling as described in Section 2.2. For the facilities in these source categories, we estimated the maximum inhalation cancer and chronic noncancer risks associated with all HAP emissions sources at the facility, including emissions sources that are not part of the source categories but are located within a contiguous area and are under

co mmon control. We analyzed risks due to the inhalation of HAP for the populations residing within 50 kilometers of each facility. The results of these facility

- wide assessments are
summarized below in the Risk Characterization sections of this document. The complete results of the facility

- wide assessments are provided in Appendix 4

.

2.7.4. MACT

- a llowable r isks
The emissions data in the data sets for these seven source categories are estimates of actual
emissions on an annual basis. The risk results presented in the following sections are based
on these actual emissions. For these two source categories, the MACT

- allowable emissions are estimated to be equivalent to the actual emissions except for certain emission sources

. See
the memo randum titled “Emissions Data Used in Residual Risk Modeling: Phosphoric Acid and Phosphate Fertilizer Production Source Categories ” available in the docket for this action. Therefore, except for certain sources, the risks based on MACT

- allowable emissions would be equivalent to the actual risks presented below. See the source category risk
characterization sections for details on the MACT

- allowable risk.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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31 

### 3. Risk Results for P hosphate Fertilizer Production

3.1 Source c ategory d escription and r esults
Phosphate fertilizer production facilities use beneficiated phosphate rock with acids and/or nitrates to produce different types and grades of fertilizers. Phosphate fertilizers are used in agricultural applications as a plant nutrient. Phosphoric A cid M anufacturing (40 CFR part 63 subp art AA) and P hosphate F ertilizers P roduction (40 CFR part 63 subpart BB) were established as separate source categories by EPA. However, these operations are generally collocated, as phosphoric acid manufacturing facilities provide feedstock for phosphate fertilizer production facilities and much of the phosphoric acid produced in the U.S. is
consumed in the manufacture of fertilizers.

Phosphate fertilizers are classified according to the concentration of phosphorus pentoxide in the final product. Normal superphosphate is made by reacting phosphate rock with sulfuric acid. Granular triple superphosphate (GTSP) is made by reacting phosphoric acid (produced at a phosphoric acid facility) with beneficiated phosphate rock. Ammonium phosphates, of
which diammo nium phosphate (DAP) is the most common, are made by reacting phosphoric acid, sulfuric acid, and anhydrous ammonia. Emission point s along the phosphate fertilizer production process include reactors, granulators, dryers, screens, and grinding and drying

p rocesses.

Emissions data

, collected via ICRs sent to all U.S. phosphate fertilizer, were used to conduct this assessment. The data include information regarding process equipment, control devices, phosphate and acid production, inventory data for all point and fugitive emissions, practices used to control fugitive emissions, and other aspects of facility operations, including stack parameters and locations.

We currently estimate that there are eleven phosphate fertilizer production facilities operatin g in the U nited S tates . Ten of these eleven facilities are co

- located with phosphoric acid manufacturing facilities. The 2005 National

- Scale Air Toxics Assessment (NATA) National Emissions Inventory (NEI) was updated for this category with data from indus try and enhanced quality assurance of facility and emission locations. All eleven of these facilities are identified as major sources in the NEI.

The emissions for the phosphate fertilizer production source category ICR data set ( eleven facilities) a re summarized in Table 3.1

- 1. The total HAP emissions for the source category are approximately 105 tons per year. Based on these data, the HAP emitted in the largest quantities across these eleven facilities is hydrofluoric acid . Th is chemical account s fo r 9 6
percent of the total emissions by mass. Persistent and bioaccumulative HAP (PB HA P) 26 reported as emissions from these facilities include mercury, lead, and cadmium compounds. The following environmental HAP are emitted from the p hosphate f ertilizer p roduction source

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

EPA

- 453K

- 04

- 001A, and provided on the EPA’s Technology Transfer Network website for Fate, Exposure, and

Risk Assessment at http://www2.epa.gov/fera/risk

- assessment

- and

- modeling

- air

- toxics

- risk

- assessment

reference

- libraryDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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32 category and are included in the environmental risk screen: mercury compounds, cadmium, lead, and hydrofluoric acid.

Table 3. 1

- 1 Summary of Emissions from the Phosphate Fertilizer Production Source Category and
Availab ility of Dose

- Response Values

HAP a Emissions (tpy) Number of

Facilities Reporting HAP (1 1 facilities in
ICR data set) Prioritized I nhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit Risk
Estimate for
Cancer? Reference

Concentration
for Ch ronic
Noncancer? Health

Benchmark
Values for
Acute
Noncancer? Hydrofluoric Acid 101 11   Manganese Compounds 0.5 11 

  Nickel Compounds 0.3 11  

 Mercury Compounds

   Elemental Gaseous Mercury 0. 01 11 

 

 

 Gaseous Divalent Mercury 0.0 04 11 

  

 Particulate Divalent Mercury 0.0 04 11 

 

 Lead Compounds 0.10 11 c

 

 Chromium Compounds

  Chromium (III) Compounds 0.09 11
Chromium (VI) Compounds 0.04 11   Cadmium Compounds 0.03 11 

 

  Arsenic Compounds 0.03 11 

 

 

 Selenium Compounds 0.02 11

 

 Cobalt Compounds 0.02 11 

 Antimony Compounds 0.01 11 

 Beryllium Compounds 0.005 11  

 

a Notes for how HAP were speciated for risk assessment:

 For most metals, e missions reported as the elemental metal are combined with metal compound emissions (e.g., “cadmium” emissions modeled as “cadmium & compounds”). In the absence of speciation information, we assume the reported mass is 100 percent metal.

 For emissions rep orted generically as “chromium” or “chromium & compound,” emissions are speciated 75% “chromium (III) compounds” and 25% “chromium (VI) compounds” for this source category. Chromium speciation profiles can be found on the EPA’s Technology Transfer Network website for emissions inventories at http://www.epa.gov/ttn/chief/net/2005inventory.html

.

 For emissions reported generically as “mercury” or “mercury & compounds,” emissions are speciated f or this category as 80% elemental gaseous mercury, 10% gaseous divalent mercury, and 10% particulate divalent

mercury. Mercury speciation profiles can be found on the EPA’s Technology Transfer Network website for

emissions inventories at http://www.epa.gov/ttn/chief/net/2005inventory.html

.

b Specific dose

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

toxics at http://www2.epa.gov/fera/dose

- response

- assessment

- assessing

- health

- risks

- associated

- exposure

- hazardous

- air

pollutants

c There is no reference concen tration for lead. In considering noncancer hazards for lead in this assessment, we compared maximum annual ambient exposure estimates to the National Ambient Air Quality Standards (NAAQS) for lead (0.15 μg/m 3 ). These NAAQS for lead were reviewed with revis ions adopted in October 2008 ( http://www.epa.gov/air/lead/actions.html ). The primary (health

- based) standard is a maximum or not

- to

- be

- exceeded, rolling
three

- month average, measured as total suspended particles (TSP). The secondary (welfare

- based) standard is identical to the primary standard.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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33 

### 3.2 Baseline r isk c haracterization
This section presents the results of the risk assessment for the phosphate fertilizer production source category. The basic chroni c inhalation risk estimates presented here are the maximum individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotie nts, as well as the results of our preliminary screen for potential non

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

- specific risk assessment results is available in Appendix 4 of this document, Draft Detailed Risk Modeling Results

.

Baseline Inhalation Risk Assessment Results Based on Actual Emissions

Tabl e 3 .2

- 1 summarizes the preliminary inhalation risk results for this source category. The
results indicate that maximum lifetime individual cancer risks are less than 1 in a million. The total estimated cancer incidence from this source category is 0.001 excess cancer cases

per year

. The maximum chronic non cancer target organ specific hazard index ( TOS HI) value for the source category could be up to 0. 003 associated with emissions of hydrogen fluoride

, indicating no significant potential for chronic nonca ncer impacts.

Worst

- case a cute hazard quotients (HQs) were calculated for every HAP shown in Table 2.6

- 3 that has an acute benchmark . Based on maximum hourly emission estimates an emissions multiplier of 10 was used to estimate the peak hourly emission rates for this source category. See the memorandum entitled, “Emissions Data Used in Residual Risk Modeling: Phosphoric Acid and Phosphate Fertilizer Production Source Categories ” for detailed description of how the maximum hourly emissions were develope d for this source category (found in the docket for this rule making ). No HAP in this source category had an acute HQ of greater than 1 for any benchmark.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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34 Table 3. 2

- 1 Summary of Source Category Level Inhalation Risk s for Phosphate
Fertilizer Production

Result HAP “Drivers” Facilities in Source Category

Number of Facilities Estimated to be i n Source Category 11 n/a

Number of Facilities Modeled in Risk

Assessment 11 n/a

Cancer Risks

Maximum Individual Lifetime Ca ncer Risk (in 1 million) 0.5 chromium (VI) compounds, nickel 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

Greater than or e qual to 1 in 1 million 0

Chronic Noncancer Risks

Maximum Skeletal Hazard Index 0. 003 Hydrogen fluoride Number of Facilities with Maximum Skeletal l Hazard Index:

Greater than 1 0 n/a Acute Noncancer Screening Results

Maximum Acute Hazard Quotient 0. 4
0. 09
0.0 4
0.0 03
0.0 04 elemental gaseous mercury (REL)

hydrofluoric acid (AEGL

- 1) hydrofluoric acid (ERPG

- 1) hydrofluoric acid (AEGL

- 2) hydrofluoric acid (ERPG

- 2)

Number of Facilities With Potential for Acute
Effects 0 n/a

Population Exposure

Number of People Living Within 50
Kilometers of Facilities Modeled 5,000,000 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 0 n/a Greater than or equal to 1 in 1 million 0 n/a Number of People Exposed to Noncancer Skeleta l Hazard Index:

Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.001 n/a

Contribution of HAP to Cancer Incidence chromium (VI) compounds 65% n/a nickel compounds 19% n/a arsenic compounds 11% n/aDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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35 Baseline Inhalation Assessment Results Based on Allowable Emissions

Analysis of potential differences between actual emissions levels and the maximum emissions
allowable under the MACT standards were also calculated for this source category. Based upon the above analysis we multiplied the modeled actual risks for the MIR facility with process site

- specific multipliers to estimate allowable risks under the MACT. This approach was deemed sufficient due to the low act ual modeled risks for the source category.
The maximum lifetime individual cancer risks based upon allowable are still less than 1 in a
million

. The maximum chronic noncancer TOSHI value for allowable emissions was estimated with an estimated HI = 0.003, the same as the actuals.

Baseline Multipathway Assessment Results Based on Actual Emissions

To identify potential multipathway health risks from PB

- HAP other than lead, we first performed a screening analysis (Tier 1 ) that compared emissions of PB

- HAP em itted from the phosphate fertilizer production s ource category (based on actual emissions) to screening emission rates ( see section 2.5) see Appendix 5 for a more detailed discussion of the screening emission rates

. The PB

- HAP emitted by facilities in thi s category include mercury compounds (11 facilities), lead compounds (11 facilities), and cadmium compounds (11 facilities. We compared reported emissions of PB

- HAP to the Tier 1 screening emission thresholds established by the EPA for the purposes of the RTR risk assessments. One facility (NEIMS059305) emitted divalent mercury (Hg 2+ ) above the Tier 1 screening threshold level, exceeding the screening threshold by a factor of 20 , and we found it necessary to conduct a
Tier 2 screening assessment.

W e refine d our Tier 2 screen with some additional site

- specific information (See Appendix 5
of this document, Technical Support Document for TRIM

- Based Multipathway Screening Scenario for RTR: Summary of Approach and Evaluation , for more information about the
Tier 2 screen.)

. The additional site

- specific information included the location of fishable

l akes and local wind direction and speed. The result of this analysis was the development of
site

- specific emission screening levels for each of the four PB

- HAP for t he farmer and fisher
scenarios.

Similar to the results from the Tier 1 screen, an exceedance of a screening level in Tier 2 cannot be equated with a risk value or a hazard quotient (or hazard index). Rather, it represents a high

- end estimate of what t he risk or hazard may be. For example, an
exceedance of 2 for a non

- carcinogen can be interpreted to mean that we have high confidence that the hazard would be lower than 2. Similarly, an exceedance of 30 for a carcinogen means that we have high confiden ce that the risk is lower than 30 in a million. Our confidence comes from the conservative, or health

- protective, assumptions that are in the screens: we choose inputs from the upper end of the range of possible values for the influential parameters used in the screens; and we assume that the exposed individual exhibits ingestion behavior that would lead to a high total exposure.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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36 Based on this Tier 2 screening analysis, mercury emissions exceed ed the non

- cancer screening thresholds by a factor of 3 for the subsistence fisher . A review of the 3 lakes the
fisher needed to fish to support his fish ingestion intake of 373 grams/day indicated the lakes
were fishable. Due to the theoretical construct of the screening model, these factors are not directly translatable into estimates of risk or hazard quotients for these facilities. Table 3.2

- 2
summarizes the results of the Tier 1 and Tier 2 screens. We further note that these results are biased high for purposes of screening and are therefore subject to significant uncertainties.

Table 3.2

- 2 Summary of the “Tier 1 and 2 ” Multipathway Screening Analysis for the Phosphate Fertilizer Production Source Category

To refine our mercury Tier 2 s creen for Mississippi Phosphates, we proceeded to a Tier 3

scre en; a ) we examined the set of lakes from which the fisher ingested fish. Any lakes that appeared to not be fishable or not publicly accessible were removed from the assessment, and the screening assessment was repeated. After we made the determination the 3 critical lakes were fishable, we analyzed b ) plume rise data, a review of the hourly data indicated about a 33 percent decrease in the Tier 2 screening value resulting in a value of 2; we than proceeded
to step c ) assessment of time

- series meteorology an d effective stack release heights. Using

TRIM

- FaTE for the Tier 2 screening scenario for Mississippi Phosphates we used time

- series meteorology to calculate the cumulative loss of chemical being released above the mixing height as well as fate and transp ort effects for each lake body . This refined screen reduce d the
media concentration and exposure s for each of the lakes and decrease d the non

- cancer screening value to 1, refer to Table 3.2

- 3

.

For this source category our analysis indicates the multipa thway risks are at levels that are acceptable and below a level of concern. For further discussion on the methods and results
for each of the three Tier screen s , s ee Appendix 9 of this document, Technical Support Document: Human Health Multipathway Residu al Risk Screening Assessment for the Phosphate Fertilizer Production and Phosphoric Acid Manufacturing Source Categories

.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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37 Table 3.2

- 3 Summary of the “Tier 2 and 3 ” Multipathway Screening Analysis for Phosphate Fertilizer Production for Mississippi Phosp hates (NEIMS059305)

The multipathway s creen s includes some hypothetical elements, namely the hypothetical
farmer and fisher scenarios. We also included children in different age ranges and adults. It is important to note that even though the multipa thway assessment has been conducted, no data exist to verify the existence of either the farmer or fisher scenario outlined above. The farmer scenario involves an individual living for a 70

- year lifetime on a farm homestead in the vicinity of the source a nd consuming produce grown on, and meat and animal products raised on, the farm. The individual also incidentally ingests surface soil at the location of the
farm homestead. The fisher scenario involves an individual who regularly consumes fish caught in freshwater lakes in the vicinity of the source of interest over the course of a 70

- year lifetime. In addition, exposure estimates and risks for infants consuming contaminated breast milk were evaluated in the case of dioxins, with the assumption that the nursing mother was exposed to chemicals via one of the two scenarios described above.

I n evaluating the potential for multipathway effects from emissions of lead, modeled maximum annual lead concentrations were compared to the secondary NAAQS for lead (0.15 μg/m 3 ) . Results of this analysis estimate that the NAAQS for lead w ould not be
exceeded at any off

- site locations.

Baseline Environmental Risk Screening Based on Actual Emissions

We conducted a screening

- level evaluation of the potential fo r adverse environmental risks associated with emissions of the following environmental HAP from the p hosphate f ertilizer

p roduction source category: mercury, cadmium, lead compounds, and hydrofluoric acid. The results of the environmental screening analy sis are summarized in Table 3.2

- 4 . In our Tier 1 analysis, emissions of mercury and cadmium did not exceed the threshold emission rates for any of the ecological benchmarks (either the LOAEL or NOAEL) for any facility in the
source category . Therefore, w e did not conduct a Tier 2 environmental screening analysis. For lead, estimate s of air concentrations did not exceed the secondary lead NAAQS for any individually modeled point for any facility

. For hydrofluoric acid, the average modeled
concentration a round each facility (i.e., the a verage concentration of all off site data points inDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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38 the modeling domain) did not exceed any ecological benchmark (either the LOAEL or NOAEL). In addition , each individual modeled concentration of hydrofluoric acid (i.e., eac h
off site data point in the modeling domain) was below the ecological benchmarks for all
facilities.

Table 3.2

- 4 Summary of Environmental Risk Screen ing Results for the Phosphate

Fertilizer Production Source Category

Environmental
HAP Number of Facil ities In Category Exceeding Percent of Modeled Area in Category Exceeding 2

Tier 1 Screen Tier 2 Screen 1 NOAEL LOAEL NOAEL LOAEL NOAEL LOAEL

PB

HAP Hg None None

- - 0% 0%

Cd N one N one

- - 0% 0%

Pb N one N one

- - 0% 0%

Acid

Gases 3 HF NA N one

- - NA 0%

NA

– Not applicable.

1

- Tier 2 screen is only performed for PB

- HAP (other than lead) when there are exceedances of the Tier 1

screen. The acid gas and lead screen s are a single

- tier.

2

- A value of 0% indicates that none of the modeled data poi nts exceeded the benchmark. For PB

- HAP the percent area is based on the Tier 2 results, if a Tier 2 analysis is performed. Otherwise, the percent area is based
on the Tier 1 results.

3

– For HF, we evaluated two benchmarks, one from Canada and the other from the State of Washington. Although, they are both considered to be LOELs

- the level between a NOAEL and a LOAEL, we have listed the
results under the LOAEL column.

Facility

- wide Inhalation Assessment Results

The facility

- wide M IR and TOSHI, avail able in Appendix 4 , are based on actual emissions, as

c ollected in the 114 request, from all emissions sources at the identified facilities. The results
indicate that 11 facilities with phosphate fertilizer production processes have facility

- wide

cancer M IR less than or equal to 1 in a million. The maximum facility

- wide TOSHI is less
than 1.



### 4. Risk Results for the Phosphoric Acid Manufacturing Source Category

4.1 Source c ategory d escription and r esults

Phosphoric acid manufacturing facilities produce phosph oric acid from beneficiated phosphate rock. Phosphoric acid is used as a food additive, chemical feedstock, and as a raw material for certain types of fertilizers and animal feed supplements. Phosphoric A cid

M anufacturing (40 CFR part 63 subpart AA) and P h osphate F ertilizers P roduction (40 CFR part 63 subpart BB) were established as separate source categories by EPA. However, these operations are generally collocated, as phosphoric acid manufacturing facilities provideDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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39 feedstock for phosphate fertilizer pro duction facilities and much of the phosphoric acid produced in the U.S. is consumed in the manufacture of fertilizers.

Phosphate rock is the starting material for the production of all phosphate products. All phosphate rock deposits contain mercury, fluo rides, carbonates, and radionuclides along with the phosphate nodules of the ore. Once the ore reaches the phosphoric acid production facility, phosphoric acid is produced using the wet method, in which beneficiated ground phosphate rock is reacted with su lfuric acid and weak phosphoric acid to produce phosphoric acid and phosphogypsum, a waste product. The phosphogypsum is disposed of on

- site in waste piles known as “gypsum stacks.” Emission point s along the phosphoric acid manufacturing process include wet process phosphoric acid process lines, superphosphoric acid process lines (including vacuum evaporation processes and submerged combustion processes), phosphate rock dryers, phosphate rock calciners, dryers, cooling ponds, and gypsum stacks

.

Emission s data, collected via ICRs sent to all U.S. phosphoric acid manufacturers, were used to conduct this assessment. The data include information regarding process equipment, control devices, phosphate and acid production, inventory data for all point and fug itive emissions, practices used to control fugitive emissions, and other aspects of facility operations, including stack parameters and locations. We currently estimate that there are twelve phosphoric acid manufacturing facilities operating
in the U nited S tates . Ten of these twelve facilities are co

- located with phosph ate fertilizer production facilities. The 2005 National

- Scale Air Toxics Assessment (NATA) National Emissions Inventory (NEI) was updated for this category with data from industry and
enhanc ed quality assurance of facility and emission locations. Eleven of these twelve facilities are identified as major sources in the NEI, and one facility is identified as an area source.

The emissions for the phosphoric acid manufacturing source categor y ICR data set (of twelve facilities) are summarized in Table 4.1

- 1 . The total HAP emissions for the source category are approximately 2,200 tons per year. Based on these data, the HAP emitted in the largest quantities across these twelve facilities are hy drofluoric acid and hydrochloric acid . These two
chemicals account for 99 percent of the total emissions by mass. Persistent and bioaccumulative HAP (PB HA P) 27 reported as emissions from these facilities include cadmium compounds, c hlorinated d ibenzodioxins and f urans (analyzed as 2,3,7,8

- t etrachlorodibenzo

- p

- dioxin ), lead, mercury, and p olycyclic o rganic ma tter (analyzed as b enzo(a) p yrene ). The following environmental HAP are emitted from the p hosphoric a cid

m anufacturing source category and are included i n the environmental risk screen: mercury compounds, cadmium, POM, dioxins/furans, lead, hydrochloric acid and hydrofluoric acid.

27 Persistent and bioaccumulative HAP are defined in the EPA’s Air Toxics Risk Assessment Library , Volume 1,

EPA

- 453K

- 04

- 001A, and provided on the EPA’s T echnology Transfer Network website for Fate, Exposure, and
Risk Assessment at http://www2.epa.gov/fera/risk

- assessment

- and

- modeling

- air

- toxics

- risk

- assessment

reference

- libraryDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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40 Table 4.1

- 1 Summary of Emissions from the Phosphoric Acid Manufacturing Source Category and Availability of Dose

- Response V alues

HAP a Emissions (tpy) Number of
Facilities Reporting HAP (1 2 facilities in
ICR data set) Prioritized I nhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit Risk
Estimate
for
Cancer? Reference

Concentration
for Chronic
Noncancer? Health

Benchmark
Values for
Acute
Noncancer? Hydrofluoric Acid 2194 12 

 

 Hydrochloric Acid 27 1 

 

 Methyl Isobutyl Ketone 9 1 

 Mercury Compounds
Elemental Gaseous Mercury 0. 1 12 

 

 

 Gaseous Divalent Mercury 0.00 1 12 

  

 Particulate Divalent Mercury 0.00 1 12 

 

 Nickel Compound s 0.2 12  

  Manganese Compounds 0.08 12

 

 

 Chromium Compounds

  Chromium (III) Compounds 0.06 11
Chromium (VI) Compounds 0.01 12   Cyanide Compounds 0.06 1

 

 Selenium Compounds 0.05 12 

 Formaldehyde 0.04 1  

 

Benzene 0.03 1 

 

 

 Cadmium Compounds 0.02 12 

 

   Lead Compounds 0.02 12

 c

 

 Benzyl Chloride 0.02 1 

 

 Isophorone 0.01 1 

 

 Acetaldehyde 0.01 1 

 

  Methyl Chloride 0.01 1

 

 

 Toluene 0.01 1 

 

 Arsenic Compoun ds 0.009 12  

 

 Propionaldehyde 0.008 1

 

 

Acrolein 0.006 1 

 

 Methylene Chloride 0.006 1  

 

 Cobalt Compounds 0.005 12

 

  Methyl Hydrazine 0.004 1

  Methyl Bromide 0.004 1  

 Carbon Disulfide 0.003 1 

 

 Antimony Comp ounds 0.003 12 

  Ethyl Benzene 0.002 1  

  Polycyclic Organic Matter

   Polycyclic Organic Matter 0.002 1 

 

 Benzo[a]pyrene 0.0000009 1 

 

 N

- hexane 0.001 1

  

Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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41 Table 4.1

- 1 Summary of Emissions from the Phosphoric Acid Manufacturing Source Category and Availability of Dose

- Response V alues

HAP a Emissions (tpy) Number of
Facilities Reporting HAP (1 2 facilities in
ICR data set) Prioritized I nhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit Risk
Estimate
for
Cancer? Reference

Concentration
for Chronic
Noncancer? Health

Benchmark
Values for
Acute
Noncancer? Naphthalene 0.001 1  

  Chloroform 0.001 1

 

 

Dimet hyl Sulfate 0.001 1

 

 Ethyl Chloride 0.0009 1 

 Ethylene Dichloride 0.0009 1  

 

Bromoform 0.0009 1 

   Xylenes (mixed) 0.0008 1

   Methyl Tert

- butyl Ether 0.0008 1  

 

 Beryllium Compounds 0.0008 12 

 

 

 Tetrachloroethene 0. 0007 1 

 

 

 Styrene 0.0006 1

 

 

 Chlorobenzene 0.0005 1 

 

 Methyl Methacrylate 0.0004 1 

 

 Phenol 0.0004 1 

 

 Acetophenone 0.0003 1

  Vinyl Acetate 0.0002 1  
1,1,2,2

- tetrachloroethane 0.0002 1

  2,4

- dinitrotoluene 0.00 02 1 

 

Cumene 0.0001 1

 

 

O

- xylene 0.0001 1 

 

 Ethylene Dibromide 0.00003 1  

 

 2

- chloroacetophenone 0.000006 1

 

  Dioxins and Furans

 1,2,3,6,7,8

- hexachlorodibenzo

- p

- dioxin 0.000000006 1 

  



a Notes for how HAP were speciated for risk assessment:

 For most metals, emissions reported as the elemental metal are combined with metal compound emissions (e.g., “cadmium” emissions modeled as “cadmium & compounds”). In the absence of speciation information, we assume the rep orted mass is 100 percent metal.

 For emissions reported generically as “chromium” or “chromium & compound,” emissions are speciated 75% “chromium (III) compounds” and 25% “chromium (VI) compounds” for this source category. Chromium speciation profiles can be found on the EPA’s Technology Transfer Network website for emissions inventories at http://www.epa.gov/ttn/chief/net/2005inventory.html

.

 For emissions reported generically as “mercury” o r “mercury & compounds,” emissions are speciated for this category as 80% elemental gaseous mercury, 10% gaseous divalent mercury, and 10% particulate divalent

mercury. Mercury speciation profiles can be found on the EPA’s Technology Transfer Network websi te for
emissions inventories at http://www.epa.gov/ttn/chief/net/2005inventory.html

.

b Specific dose

- response values for each chemical are identified on EPA’s Technology Transfer Network we bsite for air
toxics at http://www2.epa.gov/fera/dose

- response

- assessment

- assessing

- health

- risks

- associated

- exposure

- hazardous

- air

pollutantsDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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42 c There is no reference concentration for lead. In considering noncancer hazards for lead in this assessment, we compared maximum annual ambient exposure estimates to the National Ambient Air Quality Standards (NAAQS) for lead (0.15 μg/m 3 ). These NAAQS for lead were reviewed with revisions adopted in October 2008 ( http://www.epa.gov/air/lead/actions.html ). The primary (health

- based) standard is a maximum or not

- to

- be

- exceeded, rolling
three

- month average, measured as total suspended particles (TSP). The secondary (welfare

- based) standard is identic al to the primary standard.



### 4.2 Risk c haracterization
This section presents the results of the risk assessment for the phosphoric acid manufacturing source category. The basic chronic inhalation risk estimates presented here are the maximum
individual lifetime cancer risk, the maximum chronic hazard index, and the cancer incidence. We also present results from our acute inhalation impact screening in the form of maximum hazard quotients, as well as the results of our preliminary screen for potential non

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

- specific risk assessment results is available in Appendix 4 of this document, Draft Detailed Risk Modeling Results

.

Baseline Inhalation Risk Assessment Results Based on Actual Emissions

Table 4 .2

- 1 summarizes the preliminary inhalation risk results for this source ca tegory. The
results indicate that maximum lifetime individual cancer risks are less than 1 in a million. The total estimated cancer incidence from this source category is 0.00 02 excess cancer cases

per year

. The maximum chronic non cancer target organ sp ecific hazard index ( TOS HI) value for the source category could be up to 0.2 associated with emissions of hydrofluoric acid

, indicating no significant potential for chronic noncancer impacts.

Worst

- case acute hazard quotients (HQs) were calculated for e very HAP that has an acute
benchmark , t wo facilities wer e identified with HQ values > 1. For cases where the screening acute HQ was greater than 1, we further refined the estimates by determining the highest HQ value that is outside facility boundaries. The highest refined worst

- case acute HQ value is 2 (based on the acute REL for hydrofluoric acid ) as shown in Table 4 .2

- 1. The HQ values of 2
represent an upper

- bound risk estimate for both facilities ; the off

- site locations for these sites

were either lo cated in a rural location in which public access is limited or in an off

- site area that maybe owned by the facility.

For phosphoric acid manufacturing facilities a multiplier of 10 (x) was developed for point sources based upon the ICR data and engineer ing knowledge of the source category processes and for emissions from area sources (gypsum ponds and cooling ponds) an acute multiplier of

1 was used. The hydrogen fluoride emissions from the phosphoric acid manufacturing gypsum ponds drove the acute risk s. This emission source was considered stable and homogeneous and not subject to major fluctuations in hourly emissions over the year and therefore an acute refined multiplier of 1 was applied. This was applied to all area sources in
the entire source cat egory except for one facility that had site

- specific data for their gypsum ponds, an acute multiplier of 2 was applied for this facility. This data was considered unique to the facility and not applicable for any other site. For further information on th e acute multipliers applied for this source category refer to the memo entitled “ Emissions Data Used in Residual Risk Modeling: Phosphoric Acid and Phosphate Fertilizer Production SourceDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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43 Categories ” available in the docket for this action. Table 4 .2

- 2 pr ovides more information on
the refined acute risk estimates for HAP that had an acute HQ greater than 1 for any
benchmark , refer to Appendix 8 to this document ( A cute Noncancer Ris k Analysis for Phosphate Fertilizer and Phosphoric Acid Manufacturing) Table 2 for further information.

For acute risks, 4 facilities exceeded the HEM

- 3 screen for hydrofluoric acid exceeding the REL by a factor of 2. A refined analysis of these sites identified 2 facilities with off

- site concentrations exceeding the REL. T he worst

- case maximum estimated 1

- hour exposure to hydrofluoric acid outside the facility fence line for the phosphoric acid manufacturing source category is 530 u g/m 3 . This estimated worst

- case exposure exceeds the 1

- hour REL by a
factor of 2 (HQ REL = 2 ) a nd is below the 1

- hour AEGL

- 1 (HQ AEGL

- 1 = 0. 6 ).

Worst

- case a cute hazard quotients (HQs) were calculated for every HAP shown in Table 4

- 1 that has an acute benchmark, and the highest acute HQ (and ass ociated HAP) is shown in
Table 4 .2

- 1.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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44 Table 4 .2

- 1 S ummary of Source Category Level Inhalation Risks for Phosphoric Acid Manufacturing

Result HAP “Drivers” Facilities in Source Category

Number of Facilities Estimated to be i n Source Category 12 n/a

Number of Facilities Modeled in Risk

Assessment 12 n/a

Cancer Risks

Maximum Individual Lifetime Cancer Risk (in 1 million) 0.09 chromium (VI) compounds, arsenic compounds, nickel 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 Greater than or equal to 1 in 1 million 0

Chronic Noncancer Risks

Maximum Skeletal Hazard Index 0.2 hydrofluoric acid Maximum Neurological Hazard Index 0.002 manganese c ompounds Number of Facilities with Maximum Skeletal or Neurological Hazard Index:

Greater than 1 0 n/a

Acute Noncancer Refined Results

Maximum Acute Hazard Quotient 2
0.6
0.3
0.03
0.03 hydrofluoric acid (REL)

hydrofluoric acid (AEGL

- 1) hydrofluoric ac id (ERPG

- 1) hydrofluoric acid (AEGL

- 2) hydrofluoric acid (ERPG

- 2)

Number of Facilities With Potential for Acute
Effects 2 hydrofluoric acid

Population Exposure Number of People Living Within 50 Kilometers
of Facilities Modeled 5, 2 00,000 n/a

Number of People Exposed to Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a Greater than or equal to 10 in 1 million 0 n/a Greater than or equal to 1 in 1 million 0 n/a Number of People Exposed to Noncancer Skeletal or Neurological Hazard Index:

Greater than 1 0 n/a

Estimated Cancer Incidence (excess cancer cases per year) 0.00 02 n/a

Contribution of HAP to Cancer Incidence chromium (VI) compounds 56 % n/a

arsenic compounds 23 % n/a

nickel compounds 1 2 % n/aDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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4 5 Table 4 .2

- 2 Summary of Acut e Refined Results for Phosphoric Acid Manufacturing

MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE

- RESPONSE VALUES

Screening Results

Based on

REL Based on

AEGL

- 1/
ERPG

- 1 Based on

AEGL

- 2/
ERPG

- 2 REL

(mg/m 3 ) AEGL

- 1

(1

- hr) (mg/m 3 ) ERPG

- 1

(mg/m 3 ) AEGL

- 2

(1

- hr) (mg/m 3 ) ERPG

- 2

(mg/m 3 )
HAP Max. 1

-

hr. Air
Conc. (mg/m 3 ) Hydrofluoric acid 0.5 2 0.6 / 0.3 0. 03 / 0. 03 0.24 0.82 1.6 20 16

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

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

- response values which are not in the table do not carry any potential for posing acute health risks, b ased on an analysis of currently
available emissions data.

Notes on Acute Dose

- Response Values:

REL

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

- hour exposures.
AEGL

– Acute exposure guideline leve ls represent emergency exposure (1

- hour) limits for the general public.

AEGL

- 1 is the exposure level above which it is predicted that the general population, including susceptible individuals, could exp erience effects that are
notable di scomfort, but which are transient and reversible upon cessation of exposure.
AEGL

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

- lasting adverse health effects or an impaired ability to escape.

ERPG

– Emergency Removal Program guidelines represent emergency exposure (1

- hour) limits for the general public.
ERPG

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

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

.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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46 Baseline Inhalation Assessment Results Based on Allowable Emissio ns

Analysis of potential differences between actual emissions levels and the maximum emissions allowable under the MACT standards were also calculated for this source category. Based upon the above analysis we multiplied the modeled actual risks for the MIR facility with process site

- specific multipliers to estimate allowable risks under the MACT. This approach was deemed sufficient due to the low actual modeled risks for the source category. The
maximum lifetime individual cancer risks based upon allowa ble are still less than 1 in a
million

. The maximum chronic noncancer TOSHI value for allowable emissions was
estimated at an HI = 0.3.

Baseline Multipathway Assessment Results Based on Actual Emissions

To identify potential multipathway health risks fro m PB

- HAP other than lead, we first performed a screening analysis (Tier 1 ) that compared emissions of PB

- HAP emitted from the phosph oric acid manufacturing s ource category (based on actual emissions) to screening emission rates ( see section 2.5) see Append ix 5 for a more detailed discussion of the screening emission rates

. The PB

- HAP emitted by facilities in this category include mercury compounds (1 2 facilities), le ad compounds (12 facilities), dioxin/furan compounds (1 facilit y ), POM compounds (1 facilit y ) and cadmium compounds (1 2 facilities ) . We compared reported emissions of PB

- HAP to the Tier 1 screening emission thresholds established by the EPA for the purposes of the RTR risk assessments. One facility , PCS in Aurora, NC (NEI 455 71 ) emitted divalent mercury (Hg 2+ ) and cadmium compounds above the
Tier 1 screening threshold level, exceeding the mercury screening threshold by a factor of 7 and cadmium by a factor of 2 , we than proceeded to conduct a Tier 2 screening assessment for
di valent mercury and cadmium

.

For the se PB

- HAP ’s and facility that did not screen out during our initial Tier 1 multipathway screening analysis, we improved our analysis with some additional site

- specific i nformation to develop a Tier 2 screen. (See Append ix 5 of this document, Technical Support Document for TRIM

- Based Multipathway Screening Scenario for RTR: Summary of Approach and
Evaluation , for more information about the Tier 2 screen.) The additional site

- specific
information included the location of fishable l akes and local wind direction and speed. The result of this analysis was the development of site

- specific emission screening levels for each
of the four PB

- HAP for the farmer and fisher scenarios.

Based on this Tier 2 screening analysis, th e cadmium is below the non

- cancer screening
threshold with a value of 0.3 and at a value of 1 for mercury for the subsistence fisher scenario. Both screening values for cadmium and mercury are below a l evel of concern

. Due
to the theoretical construct of the screening model, these factors are not directly translatable into estimates of risk or hazard quotients f or these facilities. Table 4 .2

- 3 summarizes the
results of the Tier 1 and Tier 2 screens. We further note that these results are biased high for purposes of screening and are therefore subject to significant uncertainties.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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47 Table 4 .2

- 3 Summary of the “Tier 1 and 2 ” Multipathway Screening Analysis for the Phosphoric Acid Manufacturing Source Category

The Tier 2 Screen includes some hypothet ical elements, namely the hypothetical farmer and
fisher scenarios. It is important to note that even though the multipathway assessment has been conducted, no data exist to verify the existence of either the farmer or fisher scenario
outlined abov e. The farmer scenario involves an individual living for a 70

- year lifetime on a farm homestead in the vicinity of the source and consuming produce grown on, and meat and animal products raised on, the farm. The individual also incidentally ingests surfa ce soil at
the location of the farm homestead. The fisher scenario involves an individual who regularly consumes fish caught in freshwater lakes within a radius of 50 km of the emission source. In addition, exposure estimates and risks for infants consuming con taminated breast milk were evaluated in the case of dioxins, with the assumption that the nursing mother was exposed to
chemicals via one of the two scen arios described above.

Baseline Environmental Risk Screening Based on Actual Emissions

We conducted a screening

- level evaluation of the potential for adverse environmental risks associated with emissions of the following environmental HAP from the p hosphoric a cid

m anufacturing source category: mercury compounds, cadmium, POM, dioxins, lead, hydrochlori c acid and hydrofluoric acid. The results of the environmental screening analysis
are summarized in Table 4.2

- 4. In our Tier 1 analysis, emissions of mercury, cadmium, POM,
and dioxins did not exceed the threshold emission rates for any of the ecological benchmarks (either the LOAEL or NOAEL) for any facility in the source category . Therefore, we did not
conduct a Tier 2 environmental screening analysis. For lead, there were no exceedances of the secondary lead NAAQS for any individual data point for an y facility

.

For hydrochloric acid and hydrofluoric acid, the average modeled concentration around each facility (i.e., the average concentration of all offsite data points in the modeling domain) did not exceed any ecological benchmark (either the LOAE L or NOAEL). In addition , each
individual modeled concentration of hydrochloric acid (i.e., ea ch off site data point in the modeling domain) was below the ecological benchmarks for all facilities. The results of theDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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48 environmental screen for hydrofluoric a cid are summarized for each facility in Table 3 of Appendix 7

. For hydrofluoric acid , less th an 1 percent of the off site modeling domain for the
entire source category was above the Canadian LOEL ecological benchmark. The largest facility exceedance area based on the Canadian LOEL ecological benchmark represented 6 percent of th at facility’s total offsite model ed area

.

Table 4 .2

- 4 Summary of Environmental Risk Screen ing Results for the Phosphoric Acid Manufacturing Source Category

Environmental
HAP Num ber of Facilities In Category Exceeding Percent of Modeled Area in Category Exceeding

Tier 1 Screen Tier 2 Screen 1 NOAEL LOAEL NOAEL LOAEL NOAEL LOAEL

PB

HAP Hg None None

- - 0% 0%

Cd N one N one

- - 0% 0%

POM N one N one

- - 0% 0%

Dioxins N one N one

- - 0% 0%

Pb N one N one

- - 0% 0%

Acid

Gases 3 HCl NA N one

- - 0% 0%

HF NA N one

- - NA 1%

NA

– Not applicable.

1

- Tier 2 screen is only performed for PB

- HAP when there are exceedances of the Tier 1 screen. The acid gas
screen is a one tier screen. 2

- A value of 0% indicates that none of the modeled data points exceeded the benchmark. For PB

- HAP the percent area is based on the Tier 2 results, if a Tier 2 analysis is performed. Otherwise, the percent area is based
on the Tier 2 results.

3

– For HF, we evaluated two benchmarks, one from Canada and the other from the State of Washington. Although, they are both considered to be LOELs

- the level between a NOAEL and a LOAEL, we have listed the results under the LOAEL column. The results pre sented in the table are the same for both the LOEL from Canada and the LOEL from the State of Washington (i.e., no facility showing exceedance of averaged values; 1% of area in category showing and exceedance). For HCl, we evaluated one benchmark at the L OAEL level.

Facility

- wide Inhalation Assessment Results

The facility

- wide MIR and TOSHI, available in Appendix 4, are based on emissions as identified in the NEI, from all emissions sources at the identified facilities. The results of the facility

- wide indicate that eleven facilities with phosphoric acid manufacturing processes have a facility

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

- wide TOSHI for the source category is 0.2.



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

5.1 Exposure m odeling u ncertainties
Although every effort has been made to identify all the relevant facilities and emission points, as well as to develop accurate estimates of the annual emission rates for all relevant HAP, theDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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49 uncertainties in our emission inventory likely dominate the uncertainties in our exposure modeling estimates. The chronic exposure modeling uncertainties are considered relatively small in comparison, since we are using EPA’s refined local dispersion mode l with site

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

- or long

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

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

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

A sensitivity analysis performed for the 1999 NATA found that the selection of the meteorology dataset location could result in a range of chronic ambient concentrations which
varied from as much as 17 percent below the estimated value to as much as 84 percent higher
than the estimated value. This variability translates directly to the estimated exposures and risks in our assessment, indicating that the actual risks could vary from 17 per cent lower to 84
percent higher than the estimated values.

We have purposely biased the acute screening results high, considering that they depend upon the joint occurrence of independent factors, such as hourly emissions rates, meteorology and
human acti vity patterns . In cases where multiple acute threshold values are considered scientifically acceptable we have chosen the most conservative of these threshold values, erring on the side of overestimating potential health risks from acute exposures. In th e cases where these results indicated the potential for exceeding short

- term health thresholds post

controls, we refined our assessment by developing a better understanding of the geography of the facility relative to potential exposure locations.



### 5.2 Un certainties in the d ose
- r esponse r elationships
In the sections that follow, separate discussions are provided on uncertainty associated with cancer potency factors and noncancer reference values. Cancer potency values are derived for chronic (lifetime) e xposures. Noncancer reference values are generally derived for chronic exposures (up to a lifetime), bu t may also be derived for acute ( <24 hours), short

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

Although every effort is made to identify peer

- review ed dose

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

- reviewed cancer potency values or reference values for chronic non

- cancer or acute effects (inhalation orDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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50 ingestion) . Since exposures to these pollutants cannot be included in a quantitative risk estimate, an understatement of risk for these pollutants at environmental exposure levels is possible.

Additionally, chronic dose

- response values for certain compounds included in the assessment may be under EPA IRIS review

, and revised assessments may determine that these pollutants are more or less potent than currently thought. We will re

- 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

- respo nse uncertainties in the estimation of cancer risk below focuses on the uncertainties associated with the specific approach currently used by the EPA to develop cancer potency factors. In general, these same uncertainties attend the development
of cancer potency factors by CalEPA, the source of peer

- reviewed cancer potency factors
used where EPA

- developed values are not yet available. To place this discussion in context, we provide a quote from the EPA’s Guidelines for Carcinogen Risk Assessment [ 30 ] (here in
referred to as Cancer Guidelines ). “The primary goal of EPA actions is protection of human health; accordingly, as an Agency policy, risk assessment procedures, including default options that are used in the absence of scientific data to the contrary, should be health protective.” The approach adopted in this document is consistent with this approach as

described in the Cancer Guidelines

.

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

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

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

- reviewed methodologies. The EPA Cancer Guidelines describes the Agency’s

recommendations for metho dologies for cancer risk assessment. EPA believes that cancer risk estimates developed following the procedures described in the Cancer Guidelines and outlined below generally provide an upper bound estimate of risk. That is, EPA’s upper

bound estimates represent a “plausible upper limit to the true value of a quantity” (although this is usually not a true statistical confidence limit). 28 In some circumstances, the true risk could be as low as zero; however, in other circumstances the risk could also be g reater. 29

28 IRIS glossary ( http://ofmpub.epa.gov/sor_internet/registry/termreg/searchandretrieve/glossariesandkeywordlists/search.do?deta ils=&glossaryName=IRIS%2 0Glossary ).

29 The exception to this is the URE for benzene, which is considered to cover a range of values, each end of which is considered to be equally plausible, and which is based on maximum likelihood estimates.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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51 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. 30 EPA also uses the upper bound (rather than lower bound or central) estimates in its assessments, although it is noted that this approach can have limitations for some uses (e.g. priority setting, expected benefits analysis).

Such health risk assessments have associated uncertainties, some which may be considered quantitatively, and others which generally are expressed qualitatively. Uncertainties may vary substantially among cancer risk assessments associated with exposures to different pollutants, since the assessments employ different databases with different strengths and limitat ions and the procedures employed may differ in how well they represent actual biological processes for
the assessed substance. EPA’s Risk Characterization Handbook also recommends that risk characterizations present estimates demonstrating the impact on t he assessment of alternative choices, data, models and assumptions [ 31 ]. Some of the major sources of uncertainty and variability in deriving cancer risk values are described more fully below.

(1) The qualitative similarities or differences between tumo r responses observed in experimental animal bioassays and those which would occur in humans are a source of uncertainty in cancer risk assessment. In general, EPA does not assume that tumor sites observed in an experimental animal bioassay are necessarily predictive of the sites at which
tumors would occur in humans. 31 However, unless scientific support is available to show otherwise, EPA assumes that tumors in animals are relevant in humans, regardless of target organ concordance. For a specific polluta nt, qualitative differences in species responses can
lead to either under

- estimation or over

- estimation of human cancer risks.

(2) Uncertainties regarding the most appropriate dose metric for an assessment can also lead
to differences in risk estimates

. For example, the measure of dose is commonly expressed in units of mg/kg/d ingested or the inhaled concentration of the pollutant. However, data may support development of a pharmacokinetic model for the absorption, distribution, metabolism
and excretio n of an agent, which may result 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 uncertain (e.g., as can occur when alternative

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

- assessment process when the correct scientific model is unk nown 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 co ntrary” (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the agency may depart from them in evaluating the risks posed by a specific substance when it believes this to be appropriate. In keeping with EPA’s goal of protecting public health and the environment, default assumptions are used to ensure that risk to chemicals is not underestimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An Examination of EPA Risk Assessment Princ iples and Practices,

EPA/100/B

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

- final.pdf

31 Per the EPA Cancer Guidelines: “The default option is that positive effects in animal cancer studi es 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 Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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52 pharmacokinetic models are available for a compound). Uncertainty in dose estimates may
lead to either over or underestimation of risk.

(3) For the quantitative extr apolation of cancer risk estimates from experimental animals to humans, EPA uses scaling methodologies (relating expected response to differences in physical size of the species), which introduce another source of uncertainty. These methodologies are base d on both biological data on differences in rates of process according to species size and empirical comparisons of toxicity between experimental animals and humans. For a particular pollutant, the quantitative difference in cancer potency between experim ental 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 est imates, whether based on epidemiological or experimental animal data, are generally developed using a benchmark dose (BMD) analysis to estimate a dose at which there is a specified excess risk of cancer, which is used as the point of departure (or POD) fo r the remainder of the calculation. Statistical uncertainty in developing a POD using a benchmark dose (BMD) approach is generally addressed though use of the 95 percent lower confidence limit on the dose at which the specified excess risk occurs (the BMD L), 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 potent ially 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 epidemiologic al studies at higher dose) depending on the available data and understanding of a pollutant’s mode of action (i.e., the manner in which a pollutant causes cancer). EPA’s Cancer Guidelines express a preference for the use of reliable, compound

- specific, 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 consideration in determining how risks should be estimated
for low

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

- dose (straight line from POD) approach is used when available mode of action data suppor t 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 scientific considerations. For example, EPA’s C ancer Guidelines generally
consider a linear dose

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

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

EPA most frequently utilizes a linear low

- dose extrapolation approach as a baseline science

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

- specific determination. This approach is designed to not underestimate risk in the face of uncertaintyDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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53 and variability. EPA believes that linear dose

- response models, when appropriately applied

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

- dose nonlinear, non

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

- probit models) in representing dose response relationships due to the variability in response within human populations. Another National Research Coun cil (NRC) report [ 32 ] 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 individual tolerances to vary extensively in humans depending on genetics, coincident exposures, nutritional status, and various other susceptibility factors...” Thus, if a distribution of thresholds approach is considered for a carcinogen risk as sessment, application would depend on ability of modeling to reflect the degree of variability in response in human populations (as opposed to responses in bioassays with genetically more uniform rodents). Note also that low dose linearity in risk can ari se for reasons separate from population variability: due to the nature of a mode of action and additivity of a chemical’s effect on top of background chemical exposures and biological

processes.

As noted above, EPA’s current approach to cancer risk assess ment typically utilizes a straight line approach from the BMDL. This is equivalent to using an upper confidence limit on the slope of the straight line extrapolation. The impact of the choice of the BMDL on bottom line risk estimates can be quantified by comparing risk estimates using the BMDL value to central estimate BMD values, although these differences are generally not a large contributor to uncertainty in risk assessment (Subramaniam et. al., 2006) [ 33 ]. It is important to note that
earlier EPA ass essments, 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 straight line extrapolation from a POD do not show large differences from those based on the upper confidence limit of the multistage
model.

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

— resulting in another source of uncertainty in assessments. In the diverse human population, some individuals are likely to be more sensitive to the action of a carcinogen than the typica l 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 S upplemental 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 respo nse is to extrapolate human response from results observed in the most sensitive species and sex tested, resulting typically in the highest URE which can be supported by reliable data, thus supporting estimates that are designed not to underestimate risk i n the face of uncertainty and variability.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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54 Chronic noncancer assessment

Chronic noncancer reference values represent chronic exposure levels that are intended to be
health

- protective. That is, EPA and other organizations which develop noncancer reference values (e.g., the Agency for Toxic Substances and Disease Registry

– ATSDR) utilize an approach that is intended not to underestimate risk in the face of uncertainty and variability. When there are gaps in the available information, uncertainty factors ( UFs) are applied to derive reference values that are intended to be protective against appreciable risk of
deleterious effects . Uncertainty factors are commonly default values 32 e.g., factors of 10 or 3, used in the absence of compound

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

- specific information. When data are limited, more assumptions are needed and more default factors are used. Thus there may be a greater tendency to overestimate risk

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

For non

- cancer endpoints r elated to chronic exposures, EPA derives a Reference Dose (RfD) for exposures via ingestion and a Reference Concentration (RfC) for inhalation exposures.
These values provide an estimate (with uncertainty spanning perhaps an order of magnitude)
of a daily oral exposure (RfD) or a continuous inhalation exposure (RfC) to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. 33 To derive values that are intended to be “wi thout appreciable risk,” EPA’s methodology relies upon an uncertainty factor (UF) approach [ 34 ],[ 35 ] which includes consideration of both uncertainty and variability.

EPA begins by evaluating all of the available peer

- reviewed literature to determine non

cancer endpoints of concern, evaluating the quality, strengths and limitations of the available studies. EPA typically chooses the relevant endpoint that occurs at the lowest dose, often using statistical modeling of the available data, and then determin es the appropriate point of departure (POD) for derivation of the reference value. A POD is determined by (in order of preference): (1) a statistical estimation using the benchmark dose (BMD) approach; (2) use of
the dose or concentration at which the to xic response was not significantly elevated (no
observed adverse effect level

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

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

- assessment process when the correct scientific model is unknown or uncerta in.” 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, 1 983a, 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 pu blic health and the environment, default assumptions are used to ensure that risk to chemicals is not underestimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An examination of EPA Risk Assessment Principles and Practi ces, EPA/100/B

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

- final.pdf

33 See IRIS glossaryDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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55 A series of downward adjustments using default UFs is then applied to the POD to estimate
the reference value [ 36 ] . While collectively termed “UFs”, these factors account for a number of different quantitative considerations when utilizing observed animal (usually rodent) or human toxicity data in a risk assessment. The UFs are intended to account for: (1) variation in susceptibility among the members of the human population (i.e., inter

- individual variability); (2) uncertainty in extrapolating from experimental animal data to humans (i.e., interspecies differences); (3) uncertainty in extrapolating from dat a obtained in a study with
less

- than

- lifetime exposure (i.e., extrapolating 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 prob lems with applicability of available studies

. When scientifically sound, peer

- reviewed assessment

- specific data are not available, default adjustment values are selected for the individual UFs. For each type of uncertainty (when
relevant to the assessmen t) , EPA typically applies an UF value of 10 or 3 with the cumulative UF value leading to a downward adjustment of 10

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

- fold factor. If an extrapolation step

or adjustment is not relevant to an assessment (e.g., if applying human toxicity data and an interspecies extrapolation is not required) the associated UF is not used. The major adjustment steps are described more fully below.

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

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

- specific data on human variation, a 10

- fold UF is used to account for uncertainty associated with human variation. Human variation may be larger or smaller; however, data to examine the potential magnitude of human variability are often unavailable. In some situations, a smaller UF of 3 may be applied to reflect a known lack of significant variability among humans.

2) Extrapolation from results of studies in experi mental animals to humans is a necessary step for the majority of chemical risk assessments . When interpreting animal data, the concentration at the POD (e.g. NOAEL, BMDL) in an animal model (e.g. rodents) is extrapolated to estimate the human response. W hile there is long

- standing scientific support
for the use of animal studies as indicators of potential toxicity to humans , there are uncertainties in such extrapolations. In the absence of data to the contrary, the typical approach is to use the most rel evant endpoint from the most sensitive species and the most sensitive sex in assessing risks to the average human. Typically

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

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

.

Pharmacokinetic models are useful to examine species differences in pharmacokinetic processing and associated uncertainties; however, such dosimetric adjust ments are not alwaysDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

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56 possible. Information may not be available to quantitatively assess toxicokinetic or toxicodynamic differences between animals and humans, and in many cases a 10

- fold UF (with separate factors of 3 for toxicokinetic and toxicodynamic components) is used to account for expected species differences and associated uncertainty in extrapolating from laboratory animals to humans in the derivation of a reference value. If information on one or the other of these components is available and a ccounted for in the cross

- species extrapolation, a UF of 3 may be used for the remaining component.

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

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

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

4) Toxicity data are typically limited as to the dose or exposure levels that have been tested in individual studies; in an animal study, for example, treatment groups may differ in exposure by up to an order of magnitude. The preferred approach to arrive at a POD is to use BMD analysis; however, this approach requires adequate quantitative results for a meaningful analysis, which is not always 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 stu dies lack a dose or exposure level at which an adverse effect is not observed (i.e., a NOAEL is not identified). When using data limited to a LOAEL, a UF of 10 or 3

- fold is often applied.

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

- fold is typically applied.

Acute noncancer asses sment

Many of the UFs used to account for variability and uncertainty in the development of acute reference values are quite similar to those developed for chronic durations, but more often using individual UF values that may be less than 10. UFs are app lied based on chemical

specific or health effect

- specific information (e.g., simple irritation effects do not vary appreciably between human individuals, hence a value of 3 is typically used), or based on the purpose for the reference value (see the follow ing paragraph). The UFs applied in acute reference value derivation include: 1) heterogeneity among humans; 2) uncertainty in extrapolating from animals to humans; 3) uncertainty in LOAEL to NOAEL adjustments; and 4) uncertainty in accounting for an inco mplete database on toxic effects of potential concern. Additional adjustments are often applied to account for uncertainty in extrapolation from observations at one exposure duration (e.g., 4 hours) to arrive at a POD for derivation of an
acute reference value at another exposure duration (e.g., 1 hour).

Not all acute reference values are developed for the same purpose and care must be taken when interpreting the results of an acute assessment of human health effects relative to the
reference value or v alues being exceeded. W here relevant to the estimated exposures, theDraft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

57 lack of threshold values at different levels of severity should be factored into the risk characterization as potential uncertainties.Draft Risk Assessment for Phosphate Fertilizer and Phosphoric Acid Sou rce Categories

FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE

58 

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