Draft Risk Assessment for the Pulp & Paper Source Category

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## Deliberative Draft Document for EPA Internal Review

Draft

Residual Risk Assessment for the Pulp & Paper Source Category

by EPA’s Office of Air Quality Planning and Standards

Office of Air and Radiation

November 2011Draft Risk Assessment for the Pulp & Paper Source Category

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### Table of Cont ents

1 Introduction

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

2 Methods

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

2.1 Emissions and source data

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

2.2 Dispersion modeling for inhalation exposure assessment

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

2.3 Estimating human inhalation exposure

................................ ................................ ....... 8

2.4 Acute Risk Screening and Refined Assessments

................................ ........................ 8

2.5 Multipathway and environmental risk screening

................................ ...................... 10

2.6 Dose

- Response Assessment

................................ ................................ ...................... 11

2.6.1 Sources of chronic dose

- response information

................................ .................. 11

2.6.2 Sources of acute dose

- r esponse information

................................ ...................... 22

2.7 Risk Characterization

................................ ................................ ................................ 25

2.7.1 General

................................ ................................ ................................ ............... 25

2.7.2 Mixtures

................................ ................................ ................................ ............. 27

2.7.3 Facility

- wide Risks

................................ ................................ ............................ 28

2.7.4 MACT

- Allowable Risk

................................ ................................ ...................... 28

3 Risk Results for the Pulp & Paper Source Category

................................ ........................ 29

3.1 Source Category Description and Results

................................ ................................ . 29

3.2 Risk Characterization

................................ ................................ ................................ 33

4 General Discussion of Uncertainties and How They Have Been Addressed

................... 38

4.1 Exposure Modeling Uncertaintie s

................................ ................................ ............. 38

4.2 Uncertainties in the Dose

- Response Relationships

................................ ................... 39

5 References

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

Index of Tables

Table 2.2

- 1 AERMOD version 09292 model options for RTR modeling

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

Table 2.6

- 1(a) Dose

- Response Values for Chronic Inhalation Expo sure to Carcinogens

...... 16

Table 2.6

- 1(b) Dose

- Response Values for Chronic Oral Exposure to Carcinogens

............... 18

Table 2.6

- 2(a) Dose

- Res ponse Values for Chronic Inhalation Exposure to Noncarcinogens 18

Table 2.6

- 2(b) Dose

- Response Values for Chronic Oral Exposure to Noncarcinogens

......... 21

Table 2.6

- 3 Dose

- Response Values for Acute Exposure

................................ ........................ 24

Table 3.1

- 1 Summary of Emissions from the Pulp & Paper Source Category Used in the

Residual Risk Assessment and A vailability of Dose

- Response Values

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

Table 3.2

- 1 Summary of Source Category Level Inhalation Risks for Pulp and Paper

.......... 36

Tabl e 3.2

- 2 Summary of Refined Acute Results for Pulp & Paper Facilities

......................... 37

Table 3.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

............................ 38

Appendices

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

- term emission rates relative to long

- term emission

ratesDraft Risk Assessment for the Pulp & Paper Source Category

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Appendix 4 Technical Support Document for TRIM

- Based Multipathway Screening Scenario for RTR: Summary of Approach and Evaluation Appendix 5 Detailed Risk Modeling Results Appendix 6 Acute Impacts Refined Analysis Appendix 7 Dispersion Model Receptor Revisions and Additions for Pulp & Paper Appendix 8 Develop ment of the Chronic Screening Level for Carbonyl Sulfide

Index of Acronyms

AERMOD American Meteorological Society/EPA Regulatory Model

AEGL Acute exposure guideline l evel

ASTDR US Agency for Toxic Substances and Disease Registry

CalEPA California Envir onmental Agency

CTE Central Tendency Estimate

ERPG Emergency Response Planning Guideline

HAP Hazardous Air Pollutant

HEM Human Exposure Model

HI Hazard i ndex HQ Hazard q uotient

IRIS Integrated Risk Information System

MACT Maximum Achievable Control Technology

MIR Maximum Individual Risk

MOA Mode of a ction

NAC National Advisory Committee NAAQS National Ambient Air Quality Standard

NATA National Air Toxics Assessment

NEI National Emissions Inventory

NPRM Notice of Proposed Rulemaking

PB

- HAP Pers istent and Bioaccumulative

- HAP

POM Polycyclic organic matter

REL Reference exposure level

RfC Reference concentration

RfD Reference dose

RME Reasonable Maximum Exposure

RTR Risk and Technology

TOSHI Target

- organ

- specific hazard index

URE Unit ris k estimateDraft Risk Assessment for the Pulp & Paper Source Category

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### 1 Introduction

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

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

- based standards for categories of sources (e.g., petroleum refineries, pulp and paper mills, etc.) [ 1 ]. Under section 112(d)(6), EPA must review each of these technology

- based standards at least every eight years and revise a standard, as necessary, “taking into account developments in practices, processe s and control technologies.” In the second stage, EPA is required under section 112(f)(2) to assess the health and environmental

risks that rema in after implementation of the MACT standards. If additional risk reductions are necessary to protect public health with an ample margin of safety or to prevent an adverse environmental effect, EPA must develop standards to address these remaining risks. This second stage of the regulatory process is known as the residual risk stage. For each source category for which EPA issued MACT standards, the residual risk stage must be completed within eight years of promulgation of the initial technology

- based st andard.

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. Subsequ ent to the consultation, in

June 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 avai lable . Our responses to the key

recommendations of the SAB are ou tlined in a memo entitled, “EPA’s Actions in Response to Key Recommendations from the SAB Review of RTR Risk Assessment Methodologies” [ 4 ].

This document contains the methods and the result s of baseline risk assessments (i.e., after the implementation of the respective MACT standards) performed for the pulp and paper source category . The methods discussion includes descriptions of the methods used to develop

refined estimates of chronic inh alation 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. Since the screening assessme nts indicated low potential for chronic non

- inhalation health effects or environmental impacts, including effects to threatened and endangered species, no further refinement of these assessments was performed.



### 2 Methods

2

. 1 Emissions and source data

Data from a CAA section 114 information collection request (ICR) were us ed for this assessment. In February 2011, we issued an ICR to all U.S. pulp and paper manufacturers toDraft Risk Assessment for the Pulp & Paper Source Category

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gather information needed to conduct the technology review and residual risk requirements o f

the CAA

. The ICR requested available information regarding process equipment, control devices, pulp and paper production, bleaching, inventory data for all pulp and paper point and fugitive emission, practices used to control fugitive emissions, and ot her aspects of facility operations, including s tack parameters and locations. Nex t, EPA engineers who have extensive knowledge of the characteristics of this industry performed an engineering review and thorough QA/QC of the data to identi fy limitations a nd issues. Finally, EPA engineers contacted facility and industry representatives to clarify details and resolve issues with their

ICR data submissions. Details on the development of the emissions and source data for this source category are discussed in a memorandum entitled

, Inputs to the Pulp and Paper Industry October 2011 Residual Risk Modeling

, available in the docket for this rule making

. Section 3 below provides a summary of the emissions.



### 2

. 2 Dispersion modeling for inhalation exposure assessment

Bo th 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) disper sion modeling system ( HEM3 ). The approach used in applying this modeling system is outlined below, and further details are provided in Appendix 1

. The

HEM3 performs three main operations: atmospheric dispersion modeling, estimation of individual human exposures and health risks, and estimation of population risks. This section focuses on the dispersion modeling component. The exposure and risk characterization components are discussed in other subsections of Sections 2 and 3.

The di spersion model in the HEM3 system, AERMOD version 11103 , is a state

- of

- the

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

- by

- hour dispersion from the emission sources into the surrounding atmosphere. Hourly emission rates used for this simulation are generated by evenly dividing the total annual emission rate from the inventory into the 8,760 hours of the year.

The first step in t he application of the HEM3 modeling system is to predict ambient

concentrations at locat ions of interest. The AERMOD model options employed are

summarized in Table 2.2

- 1 and are discussed further below.

Table 2.2

- 1 AERMOD version 09292 mo del options for RTR modeling

Modeling Option Selec ted Parameter for chronic exposure

Type of calculations Hourly Ambient ConcentrationDraft Risk Assessment for the Pulp & Paper Source Category

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Modeling Option Selec ted Parameter for chronic exposure

Source type Point, area represented as pseudo point source

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

- supplied re ceptors

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 represent ative NWS from nearest site (over 200 stations)

In HEM3 , me teorological data are ordina rily selected from a list of over 200 National Weather Service (NWS) surface observation stations across the continental United States, Alaska, Hawaii, and Puerto Rico. In most cases the nearest station is selected as

represent ative 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. Howe ver, because

we had an insufficient number of appropriately formatted model input files derived from available meteorological data, we modeled only a single year, typically 1991. While the selection of a single year may result in under

- prediction of long

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

- prediction at others. For each facility identified by its characteristic latitude and longitude coordinates, the closest meteorological station was used in the dispersion modeling. The average distance between a modeled facility and the applica b le meteorological station was 40 miles (72 km). Appendix 2 ( Meteorological Data Processing Using AERMET for HEM 3 ) provides a complete listing of stations and assumptions along with further detai ls used in processing the data through AERMET. The sensitivity of model results to the selection of the nearest weather station and the use of one year of meteorological data is discussed in “ Risk and Technology Review (RTR) Risk Assessment Methodologies ” [ 2 ].

The HEM3 system estimates ambient concentrations at the geographic centroids of census blocks (using the 2000 Census), and at other receptor locations that can be specified by the user. The model accounts for the effects of multiple facilities when estimating concentration impacts at each block centroid. Typically we combined only the impacts of facilities within the same source category, and assessed chronic exposure and risk only for census blocks with at least one resident (i.e., locations where people may reasonably be assumed to reside rather than receptor points at the fenceline of a facility). Chronic ambient concentrations were calculated as the annual average of all estimated short

- term (one

- hour) concentrations at each

block centroid. Po ssible future residential use of currently uninhabited areas was not considered. Census blocks, the finest resolution available in the census data, are typically comprised of approximately 40 people or about ten households. For each facility in this

sour ce category census block locations were carefully evaluated for proximity to each facilities property line (see Appendix 7 ).Draft Risk Assessment for the Pulp & Paper Source Category

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I n contrast to the development of ambient concentrations for evaluating long

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

- case short

- term (one

- hour) concentrations were estimated both at the census block centroids and at points nearer the facility that represent locations where people may be present for short periods, but generally

no nearer than 100 m eters from the center of the facility (note that for large facilities, this

100

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

- term emission rates were needed to screen for the potential for hazard via ac ute 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 annual hourly emission rate for that source.

The average h ourly emissions rate is defined as the total emissions for a year divided by the total number of operating hours in the year. Th e choice of a factor of ten for 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 Alle n et al

. 2004)[ 7 ]. In that report, the Texas Environmental Research Consortium Project compared hourly and

annual emissions data for volatile organic compound s for all facilities in a heavily

industrialized 4

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

an eleven

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

, Analysis of data on short

- term emission rates

relat ive to long

- term emission rates ). Most peak emission events were less than twice the annual average, the highest was a factor of 74 times the annual average , and the 99 th
percentile ratio of peak hourly emission r ate to the annual hourly emission rate was 9 . Base d on these results, we typically chose a factor of ten for the initial screening . However, for the pulp and paper source category we have maximum hourly emissions estimates for each process group that ind icate that a factor of 2 is more appropriate for this source category. These factors are intended to cover all possible hourly peaks associated with routinely

variable emissions. While there have been some documented emission excursions above this level, our analysis of the data from the Texas Environmental Research Consortium suggests

that this factor should cover more than 99% of the short

- term peak gaseous or volatile HAP

emissions fr om 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 p articulate emissions as well.

Census block elevations for HEM3 modeling were determined nationally from the US

G eological Service 1

- degree digital elevation model (DEM) data files, which have a spatial resolution of about 90 meters. Elevations of polar grid points used in estimating short

- and long

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

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In addition to using receptor elevation to determine plume height, AERMOD adjusts the plume’s flow if nearby elevated hills are expected to influence the wind pat terns. For details on how hill heights were estimated and used in the AERMOD modeling see Appendix 1

.



### 2

. 3 Estimating human inhalation exposure

We used the estimated annual average am bient air concentration of each HAP at each census

block centroid as a s urrogate 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

i nfluence on their exposure.

We did not address short

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

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

- term b ehavior 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

constant over the co urse 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; th e population risk distribution; and the cancer incidence. The assumption of not considering short or long

- term population mobility does not bias the estimate of the theoretical MIR nor does it affect the estimate of cancer incidence since the total popula tion 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 b e at lower risks, thereby increasing the estimated number of people at specific risk levels

.

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

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



### 2

. 4 Acute Risk Screening and Refined Assessments

In establishing a scientifically defensible approach for the assessment of potential health risks due to acute exposures to HAP, w e f ollowed the same general approach that has been used for developing chronic health risk assessments under the residual risk program. That is, we developed a tiered, iterative approach. This approach to risk assessment was endorsed by the

National Acad emy of Sciences in its 1993 publication “Science and Judgment in RiskDraft Risk Assessment for the Pulp & Paper Source Category

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Assessment” and subsequently was adopted in the EPA’s “Residual Risk Report 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 tiered, iterative approach to the asse ssment. This means that we beg i n with a screening assessment, which relies on read ily available data and uses conservative assumptions that in combination approximate a worst

- case exposure . The result of this screening process is that either the facility being 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 meteoro logy. 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 can be used to determine that acute exposures are not a concern, and significant additional data collection is n ot necessary.

Acute health risk screening was performed as the first step. We used conservative assumptions for emission rates, meteorology, and exposure location. We used the following

worst

- case assumptions in our screening approach:

• Peak 1

- hour em issions were assumed to equal 10 times the average 1

- hour emission

rates.

• For facilities with multiple emission points, peak 1

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

• For facilities with multiple emission points, 1

- hou r concentrations at each receptor

were assumed to be the sum of the maximum concentrations due to each emission point, regardless of whether those maximum concentrations occurred during the same

hour.

• Worst

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

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

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

- case 1

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

meters.

• The maximum impact was compared to multiple short

- term he alth benchmarks for the

HAP being assessed to determine if a possible acute health risk might exist. These

ben chmarks are described in section 2.6 of this report.

As mentioned above, when we identify acute impacts which exceed their relevant benchmarks, we pursue refining our acute screening estimates to the extent possible . In some cases, this includes the use of a refined emissions multiplier to estimate the peak hourly emission rates from the average rates (rather than the default factor of 10)

. In other cases, this entails determining the actual physical layout and boundaries of a facility to more accurately gauge where people might reasonable be exposed for an hour. For the pulp and paper s ource

c ategory

, maximum hourly emissions estimates were available by emission process group , so we did not use the default emissions multiplier of 10. T he memorandum ent itled

, Inputs toDraft Risk Assessment for the Pulp & Paper Source Category

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the Pulp and Paper Industry October 2011 Residual Risk Modeling includes a detailed description of how the maximum hourly emissions were developed for this source category and can be found in the docket for this rule making

. We also condu cted a review of the layout of emission points at the facilities with the facility boundaries to determine the maximum off

site acute impact for the facilities that did not screen out during the initial model run. Refer to Append i ces 5 and 6 for the detai led results for these sites.



### 2

. 5 Multipathway and environmental risk screening

The potential for significant human health risks due to exposures via routes other than inhalation (i.e., multipathway exposures) was screened by first determining whether any

sourc es emitted any hazardous air pollutants known to be persistent and bioaccumulative in the environment (PB

- HAP) 1 . The PB

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

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

, toxaphen e, and trifluralin

. Emissions of cadmium, lead, mercury, and POM were ident ified in

the emissions inventories for the pulp and pape r source category

.

These PB

- HAP emissions were evaluated for potential non

- inhalation risks and adverse environmental imp a cts using our recently

- developed screening scenario which was developed

for use with the TRIM.FaTE 2 model. This screening scenario uses environmental media outputs from the peer

- reviewed TRIM.FaTE to estimate the maximum potential ingestion risks for any specified emission scenario by using a generic farming/fishing exposure scenario that simulates a subsistence environment. The screening scenario retains many of the ingestion and scenario inputs developed for EPA’s Human Health Risk Assessment Protocols (HHRAP) for hazardous waste combustion facilities. 3 In the development of the screening scenario a sensitivity analysis was conducted to ensure that its key design parameters were

established such that environmental media concentrations were not underest imated, and to also minimize the occurrence of false positives for human h ealth endpoints. See Appendix 4 for a complete discussion of the development and testing of the screening scenario, as well as for the values of facility

- level emission rates develo ped for screening potentially significant

multi

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

- pathway screening, we derived emission levels for each PB

- HAP (other than lead) at which the

maximum human health risk would be 1 i n a million for lifetime cancer risk or a hazard quotient of 1.0 for noncancer impacts.

In evaluating the potential multi

- pathway risks from emissions of lead compounds, rather than developing a screening emission rate for them , we compared maximum est i mated chronic

1 Although the two

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

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

- letter ch emical symbol for lead is not used in this

document ).

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

3 EPA’s Human Health Risk Assessment Protocol (HHRAP) for Hazardous Waste Combustion Facilities;

htt p://www.epa.gov/epaoswer/hazwaste/combust/riskvol.htm#volume1Draft Risk Assessment for the Pulp & Paper Source Category

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atmospheric concentrations with the current National Ambient Air Quality Standard (NAAQS) for lead. Values below the NAAQS were considered to have a low potential for

multi

- p athway risks

.

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

- HAP

from exceedances of chronic human health inhalation thresholds in the ambient air near these

facilities. Human health dose

- response threshold values are generally derived from studies conducted on laboratory animal s (such as rodents) and developed with the inclusions of uncertainty factors that could be as high as 3000. As a result, these human threshold values are often significantly lower than the level expected to cause an adverse effect in an exposed

rodent. I t should be noted that there is a scarcity of data on the direct atmospheric impact of these HAPs on other receptors, such as plants, birds, and wildlife. Thus, if the maximum inhalation hazard in an ecosystem is below the level of concern for humans, we have generally concluded that mammalian receptors should be at no risk of adverse effects due to inhalation exposures from non PB

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

from the scientific literature.



### 2

. 6 Dose

- Response Assessment

2

. 6

. 1 Sources of chronic dose

- response information

Dose

- response assessment (carcinogenic and non

- carcinogenic) for chronic exposure (either by inhalation or ingestion) for the HAPs reported in the emissions inventory for the pulp and

paper source category were based on the EPA Office of Air Quality Planning and Standards’ existing recommendations for HAPs [ 9 ], also used for NATA [ 10 ]. This information has been obtained from various sources and prioritized according to (1) conceptual consistency with EPA risk assessment guidelines and (2) level of peer review received. The prioritization process was aimed at incorporating into our assessments the best avail able science with respect to dose

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

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

- response assessments for chronic exposure for many of the pollutants in this study. These assessments 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 effe cts 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 spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. ” The RfD is “a n estimate (with uncertainty spanning perhaps an order of magn itude) 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 aDraft Risk Assessment for the Pulp & Paper Source Category

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lifetime. ” The URE is defined as “ the upper

- bound excess cancer risk estimated to res ult

from continuous lifetime exposure to an agent at a concentration of 1 μg/m 3 in air. ” The

SF is “a n upper bound, approximating a 95% confidence limit, on the increased cancer risk from a lifetime exposure to an agent. This estimate, [is] usually expres sed in units of proportion (of a population) affected per mg/kg

- day ...” EPA disseminates dose

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

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

available. Refer to the “IRIS Track” website for detailed inf ormation 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 identify nonlinear MOAs where appropriate,

and we will us e 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 Disea se Registry (ATSDR). ATSDR, which is part of the US Department of Health and Human Services, develops and publishes Minimum Risk Levels (MRLs) [ 12 ] for inhalation and oral exposure to many toxic substances. As

stated on the ATSDR web site: “ Following disc ussions with scientists within the Department of Health and Human Services (HHS) and the EPA, ATSDR chose to adopt a practice similar to that of the EPA's Reference Dose (RfD) and Reference Concentration (RfC) for deriving substance specific health guidanc e levels for non neoplastic endpoints .” The MRL is defined as “an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse effects (other than cancer) over a specified duration of exposure.” ATSDR descri bes 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 assessments for many substances, based both on carcinogeni city and health effects other than cancer. The process for developing these assessments is similar to that used by EPA to develop IRIS values and incorporates significant external scientific peer review. As cited in the CalEPA Technical Support Document for developing their chronic assessments 4 : “The

4 Air Toxics Hot Spots Program, Risk Assessment Guidelines, Part III

- Technical Support Document

for the Determination of Non

- cancer Chronic Reference Exposure Levels. Air Toxicology and Epide miology Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. February 2000 ( http://www.oehha.ca.gov/air/chronic_rels/pdf/relsP32k.pdf )Draft Risk Assessment for the Pulp & Paper Source Category

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guidelines for developing chronic inhalation exposure levels incorporate many recommendations of the U.S. EPA [ 13 ] and NAS [ 14 ].” The non

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

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

In developing chronic risk estimates, we adjusted dose

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

1 ) In the case of HAP categories such as glycol ethers and cyanide compounds, the most

conservative dose

- response value of the chemical category i s used as a surrogate for other compounds in the group f or which dose

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

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

out from further assessment.

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

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

- response value for the category.

3 ) In 2004, the EPA determined that the Chemi ca l Industry Institute of Toxicol ogy ( CIIT )

cancer dose

- response value for formaldehyde (5.5 x 10 - 9 per μg/m 3 ) was based on better

science than the IRIS cancer dose

- response value (1.3 x 10 - 5 per μg/m 3 ), and we switched from using the IRIS value to the CII T value in risk assessments supporting regulatory

actions. S ubsequent research published by EPA suggested that the CIIT model was not appropriate and in 2010 EPA returned to using 1991 IRIS value

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

. 5 EPA will

follow the NAS Report recommendations and will present results obtained by implementing the biologically

- based dose

- response (BBDR) model for formaldehyde. EPA will compare these estimates with those currently presented in the External Review draft of the assessment and will discuss their strengths and weaknesses. As recommended by the NAS committee, appropriated sensitivity and uncertainty analyses will be an integral component of implementing the BBDR model . In the interim, we will present findings using the 1991 IRIS value as a primary estimate, and EPA may also consider

other information as the science evolves.

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

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

risks of cancer due to nickel

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

- emitting sources (including oil combustion, coal combustion,

5 http:/ /www.nap.edu/catalog.php?record_id=13142Draft Risk Assessment for the Pulp & Paper Source Category

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and others) suggested that at least 35 percent of total nickel emissions may be soluble compounds and that the URE for the mixture of inhaled nickel compounds (based on nickel subsulfide, and representative of pure 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 Toxicology Program ( NTP ) in their 12 th Report of the Carcinogens ( ROC ) 6

, Inte rnational Agency for Research on Cancer ( IARC ) 7 , and other international agencies) 8 that consider all nickel compounds to be carcinogenic, we currently consider all nickel compounds to have the potential of being as carcinogenic to humans

. The 12 th Report of the Carcinogens states that the “combined results of epidemiological studies, mechanistic studies, and carcinogenic studies in rodents support the concept that nickel compounds generate nickel ions in target cells at sites 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 is not always clear, studies

indicate that nickel sulfate and the comb inations 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 9 ). The major scientific bodies mentioned above have also recognized that there a re differences in toxicity and/or carcinogenic potential across the different nickel compounds. In this inhalation risk assessment, to take a conservative approach, we have considered all nickel compounds to be as carcinogenic as nickel

subsulfide and hav e applied the IRIS URE for nickel subsulfide without a factor to reflect the assumption that 100 percent of the total mass of nickel may be as carcinogenic as pure

nickel subsulfide. In addition, given that there are two additional URE 10 values derived

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

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

5 ) A substantial propo rtion of POM reported to EPA’s N ati onal E mission I nventory (NEI)

a re not speciated into individua l compounds. As a result, it i s necessary to apply the same simplifying assumptions to assessment s that are used in NATA [ 17 ]. The NATA approach partitions POM into eight different non

- overlapping “groups” that a re modeled

6 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

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

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

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

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

- 7. Available online at http://www.ossup

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

. 10 T wo UREs (other than the current IRIS values) have been derived for nickel compounds as a group: one developed by the California Department of Health Services ( http://www.arb.ca.gov/to xics/id/summary/nickel_tech_b.pdf ) and the other by the Texas Commission on Environmental Quality ( http://www.epa.gov/ttn/atw/nata1999/99pdfs/healtheffectsinfo.pdf ).Draft Risk Assessment for the Pulp & Paper Source Category

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as separate pollutants. Each POM group comprises POM species of similar carcinogenic potency, for which we can apply the same URE.

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

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

7 ) For 1 carcinogenic substance , (propylene dichloride) that lack inhalation assessments from the sources evaluated in this document, oral carcinogenic potency estimates were converted to inhalation UREs. The conversion from oral risk (per mg/kg/d oral i ntake) to inhalation risk (per μ g/m 3 inhaled) was based on EPA’s standard assumptions of a 70

- kg body mass and 20 m 3 /d inhalation rate, as follows:

Where: URE = Unit risk estimate for inhalation (risk per μ g/m 3 )

CPS = Carcinogenic potency slope for ingestion (risk per mg oral intake per kg body mass per day)

EPA understands that conversion of oral dose

- response information to inhalation exposure may add significant uncertainty to the resulting risk estimates. However, the alternative to

this would have been to omit these substances from quantitative inhalation risk estimates altogether, thereby making a de facto assumption of zero carcinogenic potency. For the purposes of the residual risk assessment, EPA prefers to use the approach describe d above to screen these carcinogens for their potential contributions to risk. If a substance is determined to be a potentially important contributor to risk, it will be prioritized for

further dose

- response development through EPA’s IRIS process.

The em issions inventor y for the pulp and paper source category include s emissions of HAP with available chronic quantitative inhalat ion dose

- response values. Of these

, 47 are classified as known, probable, or possible carcinoge ns, with quantitative cancer do se

- response values available. These 47 HAP, their quantitati ve inhalation chronic cancer do se

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

- 1(a). The POM compounds with

chronic oral cancer dose

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

- 1(b). Seventy

- seven HAP have 

## ( )        

×        

× ×        

⋅ =       −

−

g mg

d m kg d kg

mg CPS

m

g URE
μ μ

1000 1 20 70 1 3 1 1

3Draft Risk Assessment for the Pulp & Paper Source Category

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quantitative inhalation chronic noncancer threshold values available

, two of these HAP (mercury and cadmium ), for which a multipathway ass essment was pe rformed, also have quantitative oral chronic noncancer threshold value s available . These 77 HAP, their threshold values, and the source of the value are listed in Table 2.6

- 2(a ) and Table 2.6

- 2 (b)

.

Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhala tion Exposure to Carcinogens

URE (unit risk estimate for cancer) 11 = cancer risk per μg/m 3 of average lifetime exposure. Sources: IRIS = EPA Integrated Risk Information System, EPA ORD = EPA Office of Research & Development, EPA OAQPS = EPA Office of Air Quality Planning & Standards, CAL = California EPA Office of Environmental Health Hazard Assessment.

HEAST = EPA Health Effects Assessment Tables , Conv. Oral = Oral unit risk converted to

inhalation.

Pollutant CAS

Number 12 URE 1 1
(1/μg/m3) Source

1,1,2,2

- Tetrachloroethane 79345 0.000058 IRIS
1,1,2

- Trichloroethane 79005 0.000016 IRIS
1,3

- Butadiene 106990 0.00003 IRIS
1,4

- Dichlorobenzene 106467 0.000011 CAL
2,4,6

- Trichlorophenol 88062 0.0000031 IRIS
2,4

- Toluene diamine 95807 0.0011 CAL

2

- Nitropropane 79469 0.0000056 EPA OAQPS Acetaldehyde 75070 0.0000022 IRIS Acrylamide 79061 0.00016 IRIS Acrylonitrile 107131 0.000068 IRIS

Aniline 62533 0.0000016 CAL
Arsenic compounds 7440382 0.0043 IRIS

Benzene 13 71432 0.0000078 IRIS Beryllium compounds 7440417 0.0024 IRIS Bis(2

- ethylhexyl)phthalate 117817 0.0000024 CAL

Bromoform 75252 0.0000011 IRIS Cadmium compounds 7440439 0.0018 IRIS

Carbon tetrachloride 56235 0.000006 IRIS

Chlorobenzilate 510156 0.000078 HEAST Chromium (VI) compounds 18540299 0.012 IR IS Ethyl benzene 100414 0.0000025 CAL Ethylene dibromide 106934 0.0006 IRIS Ethylene dichloride 107062 0.000026 IRIS

11 The UR E 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.

12 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.

13 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

.Draft Risk Assessment for the Pulp & Paper Source Category

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Table 2.6

- 1 (a) Dose

- Response Values for Chronic Inhala tion Exposure to Carcinogens

URE (unit risk estimate for cancer) 11 = cancer risk per μg/m 3 of average lifetime exposure. Sources: IRIS = EPA Integrated Risk Information System, EPA ORD = EPA Office of Research & Development, EPA OAQPS = EPA Office of Air Quality Planning & Standards, CAL = California EPA Office of Environmental Health Hazard Assessment.

HEAST = EPA Health Effects Assessment Tables , Conv. Oral = Oral unit risk converted to

inhalation.

Pollutant CAS

Number 12 URE 1 1
(1/μg/m3) Source

Ethylene oxide 75218 0.000088 CAL Ethylidene dichloride (1,1

- Dichloroethane) 75343 0.0000016 CAL Formaldehyde 14 50000 0.000013 IRIS

H exachloroethane 67721 0.000004 IRIS Methylene chloride 75092 0.00000047 IRIS Naphthalene 91203 0.000034 CAL Nickel compounds 7440020 0.00048 EPA OAQPS 15

Nitrobenzene 98953 0.00004 IRIS Pentachlorophenol 87865 0.0000051 CAL
Polycyclic Organic Matter 16 ( POM)
7,12

- Dimethylbenz(a)anthracene 57976 0.1136 CAL

3

- Methylcholanthrene 56495 0.01008 CAL Benz(a)anthracene 56553 0.000176 CAL Benzo(a)pyrene 50328 0.00176 CAL Benzo(b)fluoranthene 205992 0.000176 CAL Benzo(k)fluora nthene 207089 0.000176 CAL Chrysene 218019 0.0000176 CAL Dibenzo(a,h)anthracene 53703 0.0019184 CAL Indeno(1,2,3

- c,d)pyrene 193395 0.000176 CAL

POM 71002 187 0.000088 CAL

POM 72002 187 0.000088 CAL Propylene dichloride 17 78875 0.000019 Conv. Oral

Tetrachloroethene 127184 0.0000059 CAL Trichloroethylene 79016 0.000002 CAL Vinyl chloride 75014 0.0000088 IRIS

14 The EPA has used the CIIT URE value, 5.5X10 - 9 per mg/m 3 , to characterize formaldehyde cancer risk in

some instances.

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

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

- 04 per ug/m 3

. 16 POM without a chemical

- specific URE are assigned a URE associated with a m ixture of POM compounds having similar characteristics. Details of this method, also used in the 2002 National Air Toxics Assessment, are

available at http://www.epa.gov/ttn/atw/nata 2002/02pdfs/pom_approach.pdf

. 17 No inhalation unit risk estimates were available for this compound. T herefore we c onverted from a oral potency slope of 0.068 per mg/kg/d. UREs that are converted from the oral route to the inhalation route of

exposure are considered highly uncertain, and are only used in cases where no other URE is available.Draft Risk Assessment for the Pulp & Paper Source Category

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Table 2 .6

- 1(b) Dose

- Response Values for Chronic Oral Exposure to Carcinogens

SF (oral slope facto r 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 Hazard 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 Polycyclic organic matter (POM) Benzo(a)anthracene 56553 1.2 CAL Benzo(a)pyrene 50328 7.3 IRIS
Benzo(b)fluoranthene 205992 1.2 CAL Benzo(k)fluoranthene 207089 1.2 CAL Chrysene 218019 0.12 CAL Dibenz(a,h)anthracene 53703 4.1 CAL

7,12

- Dimethylbenz(a)anthracene 57976 250 CAL
Indeno(1, 2,3

- cd)pyrene 193395 1.2 CAL

3

- Methlycholanthrene 56495 22 CAL

Table 2.6

- 2 (a ) Dose

- Response Values for Chronic Inhalation Exposure to NoncarcinogensDraft Risk Assessment for the Pulp & Paper Source Category

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RfC (reference inhalation concentration) = an estimate (with uncertainty spanning pe rhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRIS = EPA Integrated Risk Informat ion System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables , EPA OAQPS = EPA Office of Air Quality Planning & Standards, EPA ORD = E PA Office of Research and Development

Pollutant CAS Number 12 RfC (mg/m3) Source 18

1,1,1

- Trichloroethane (methyl chloroform) 71556 5 IRIS

- M
1,1,2

- Trichloroethane 79005 0.4 CAL
1,2,4

- Trichlorobenzene 120821 0.2 HEAST
1,3

- Butadiene 106990 0.002 IRIS

- M
1,4

- Dichlorobenzene 106467 0.8 IRIS

- M

2

- Nitropropane 79469 0.02 IRIS

- L Acetaldehyde 75070 0.009 IRIS

- L

Acetonitrile 75058 0.06 IRIS

- M Acrylamide 79061 0.006 IRIS

- M Acrylonitrile 107131 0.002 IRIS

- M

Aniline 62533 0.001 IRIS

- L

Antimon y 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 Bis(2

- ethylhexyl)phthalate 117817 0.01 CAL Cadmium compounds 7440439 0.00001 ATSDR

Carbon disulfide 75 150 0.7 IRIS

- M

Carbon tetrachloride 56235 0.1 IRIS

- M Carbonyl sulfide 463581 0.163 EPA ORD 19

Chlorine 7782505 0.00015 ATSDR

Chlorobenzene 108907 1 CAL

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

- M Cobalt compounds 7440484 0.0001 ATSDR Cresols (mixed) 1319773 0.6 CAL

m

- Cresol 108394 0.6 CAL

o

- Cresol 95487 0.6 CAL

p

- Cresol 106445 0.6 CAL

Cumene 98828 0.4 IRIS

- M
Cyanide & Cyanide Compounds 20

Cyanide compounds 57125 0.0008 IRIS

– L/M Hydrogen cyanide 74908 0.0008 IRIS

– L/M

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

19 A chronic screening level of 0.163 mg/m 3 was developed for carbonyl sulfide by EPA ORD from a No Observed Adverse Effects Level of 200 ppm based on brain lesions and neurophysiological alteration in rodents.

20 The value for hydrogen cyanide was use d as a surrogate for all cyanide compounds without an RfC.Draft Risk Assessment for the Pulp & Paper Source Category

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Table 2.6

- 2 (a ) Dose

- Response Values for Chronic Inhalation Exposure to Noncarcinogens

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning pe rhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRIS = EPA Integrated Risk Informat ion System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables , EPA OAQPS = EPA Office of Air Quality Planning & Standards, EPA ORD = E PA Office of Research and Development

Pollutant CAS Number 12 RfC (mg/m3) Source 18

Diethanolamine 111422 0.003 CAL Ethyl benzene 100414 1 IRIS

- L Ethylene dibromide 106934 0.009 IRIS

- M Ethylene dichloride 107062 2.4 ATSDR Ethylene glycol 107211 0.4 CAL Ethylene oxide 75218 0.03 CAL

Eth ylidene dichloride (1,1

- Dichloroethane) 75343 0.5 HEAST Formaldehyde 50000 0.0098 ATSDR
Glycol Ethers 21

1,2

- Dimethoxyethane 110714 0.02 IRIS

- M Butyl carbitol acetate 124174 0.02 IRIS

- M Ethylene glycol ethyl ether 110805 0.2 IRIS

- M Methyl cellosolve acrylate 3121617 0.02 IRIS

- M Hexachlorocyclopentadiene 77474 0.0002 IRIS

– M/H

Hexachloroethane 67721 0.08 CAL

Hexane 110543 0.7 IRIS

- M Hydrochloric acid (hydrogen chloride) 7647010 0.02 IRIS

- L Lead compounds 7439921 0 .00015 EPA OAQPS Manganese compounds 7439965 0.00005 IRIS

- M
Mercury and Mercury Compounds

Mercuric chloride 7487947 0.0003 IRIS

- M Mercury (elemental) 7439976 0.0003 IRIS

- M

Methanol 67561 4 CAL Methyl bromide 74839 0.005 IRIS

- H

M ethyl chloride 74873 0.09 IRIS

- M Methyl isobutyl ketone 108101 3 IRIS

- L/M Methylene chloride 75092 1 ATSDR Naphthalene 91203 0.003 IRIS

- M Nickel compounds 7440020 0.00009 ATSDR

Nitrobenzene 98953 0.009 IRIS

- M Pentachlorophenol 87865 0.1 CAL

Phenol 108952 0.2 CAL Propionaldehyde 123386 0.008 IRIS

– L/M Propylene dichloride 78875 0.004 IRIS

- M

21 The RfC value for ethylene glycol methyl ether was used as a surrogate for all glycol ethers without an RfC.Draft Risk Assessment for the Pulp & Paper Source Category

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Table 2.6

- 2 (a ) Dose

- Response Values for Chronic Inhalation Exposure to Noncarcinogens

RfC (reference inhalation concentration) = an estimate (with uncertainty spanning pe rhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Sources: IRIS = EPA Integrated Risk Informat ion System, CAL = California EPA Office of Environmental Human Health Assessment, ATSDR = US Agency for Toxic Substances Disease Registry, HEAST = EPA Health Effects Assessment Tables , EPA OAQPS = EPA Office of Air Quality Planning & Standards, EPA ORD = E PA Office of Research and Development

Pollutant CAS Number 12 RfC (mg/m3) Source 18

Selenium compounds 7782492 0.02 CAL Styrene 100425 1 IRIS

- M

Tetrachloroethene 127184 0.27 ATSDR

Toluene 108883 5 IRIS

- H Trichloroethylene 790 16 0.6 CAL Triethylamine 121448 0.007 IRIS

- L Vinyl acetate 108054 0.2 IRIS

- H Vinyl chloride 75014 0.1 IRIS

- M Vinylidene chloride 75354 0.2 IRIS

– H/M Xylenes (mixed) 1330207 0.1 IRIS

- M

m

- Xylene 22 108383 0.1 IRIS

- M

o

- Xylene 22 95476 0.1 IRIS

- M

p

- Xylene 22 106423 0.1 IRIS

- M

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

co ntinuous 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

Pollutant CAS Number RfD (mg /kg/d) Source 23

Mercuric chloride 24 7439976 0.0003 IRIS

- H Cadmium compounds 7440439 0.0005 IRIS

- H

22 The RfC for mixed xylene was used as a surrogate.

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

24 The multipathway exposure assessment for mercury included fate and transport analysis, that included

separat e oral exposure estimates for divalent mercury and methylmercury.Draft Risk Assessment for the Pulp & Paper Source Category

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2

. 6

. 2 Sources of acute dose

- response information

Hazard identification and dose

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

. Depending on availability, the results from screening acute assessments are compared to both “no effects” reference levels for the general public, such as the California

Reference Exposure Levels (RELs), as well as emergency response levels, such as Acute Exposure Guideline Levels (AEGLs) and Emergency Response Planning 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 level and any limitations expressed therein. Comparisons among different available inhalation health effect reference values (both acute and chronic) for selected HA Ps can be found in a newly released EPA document [ 19 ].

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

- response reference values for many

substan ces, expressing the resu lts as a cute 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 adver se 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 individu als in the population by the inclusion of margins of safety. Since margins of safety are incorporated to address data gaps and uncertainties, exceeding the REL does not automatically indicate an adverse health impact. ” Acute RELs are developed for 1

- hour (and 8

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

Acute Exposure Guideli ne 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 “Stan ding 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 rangin g 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 faci lities and from transport carriers.” The

document states that “the primary purpose of the AEGL program and the NAC/AEGL Committee is to develop guideline levels for once

- in

- a

- lifetime , short

- term exposures to airborne concentrations of acutely toxic, high

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

, “ It is anticipated that the AEGL values will be used for regulatory and nonregulatory purposes by U.S. Federal and State agencies, and possibly the inter national 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 andDraft Risk Assessment for the Pulp & Paper Source Category

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preventi on plans, as well as real

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

The NAC/AEGL defines AEGL

- 1 and AEGL

- 2 as:

“ AEGL

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

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 othe r serious, long

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

“ Airborne concentrations below AEGL

- 1 represent exposure levels that can produce mild and progressively increasing but transient and nondisabling odor, taste, and sensory

i rritation 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

th e AEGL values represent threshold levels for the general public, including susceptible subpopulations, such as infants, children, the elderly, persons with asthma, and those with other illnesses, it is recognized that individuals, subject to unique or idio syncratic responses, could experience the effects described at concentration s below the corresponding AEGL.”

Emergency Response Planning Guidelines (ERPGs). The American Industrial Hygiene Association (AIHA) has developed Emergency Response Planning Guid elines (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 ( http://www.aiha.org/1documents/Committees/ERP

- erpglevels.pdf ) are described in their supporting documentation as follows: “ Emergency Response Planning Guidelines (ERPGs) were developed for emergency planning and are intended as health based guideline concentrations for single exposures to chemicals. These guidelin es (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 emergency response plans. The emphasis

is on ERPGs as planning values: When an actual chemical emergency occurs there is seldom

time to measure airborne concentrations and then to take action. ”

ERPG

- 1 and ERPG

- 2 values are defined by AIHA as follows:Draft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 24

“ ERPG

- 1 is the ma ximum 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. ”

“ ERP G

- 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 individual' s ability to take protective action. ”

The emissions inventory for the pulp and paper source category include s emissions of 50

HAP with relevant and available quantitative acute dose

- respon se threshold values. These

HAP , their acute threshold values, and the source of the value are listed below in Table 2.6

- 3

.

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
1,1,1

- Trichloroethane (methyl chloroform) 71556 1300 3300 1900 3800 68

1,3

- Butadiene 106990 1500 12000 22 440 Acetaldehyde 75070 81 490 18 360 0.47

Acetonitrile 75058 22 540
Acrylonitrile 107131 10 130 22 77

Aniline 62533 30 46
Arsenic compounds 7440382 0.0002

Benzene 71432 170 2600 160 480 1.3
Beryllium compounds 7440417 0.025
Biphenyl 92524 61

Carbon disulfide 75150 40 500 3.1 160 6.2

Carbon tetrachloride 56235 280 1200 130 630 1.9
Carbonyl sulfide 463581 140

Chlorine 7782505 1.5 5.8 2.9 8.7 0.21

Chloroaceti c acid 79118 26

Chlorobenzene 108907 46 690

Chloroform 67663 310 240 0.15

Cumene 98828 250 1500
Hydrogen cyanide 74908 2.2 7.8 11 0.34
Ethyl benzene 100414 140 4800
Ethylene dibromide 106934 130 180
Ethylene dichloride 107062 20 0 810
Ethylene oxide 75218 81 90 Formaldehyde 50000 1.1 17 1.2 12 0.055Draft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 25

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
Glycol Ethers 25

1,2

- Dimethoxyethane 110714 0.093
Butyl carbitol acetate 124174 0.093
Ethylene glycol ethyl ether 110805 0.37
Methyl cell osolve acrylate 3121617 0.093

Hexane 110543 12000 Hydrochloric acid 7647010 2.7 33 4.5 30 2.1
Mercury (elemental) 7439976 1.7 2 0.0006

Methanol 67561 690 2700 260 1300 28
Methyl bromide 74839 820 190 3.9
Methyl chloride 74873 1900 830
Methyl iodide 74884 150 290 Methylene chloride 75092 690 1900 1000 2600 14
Nickel compounds 7440020 0.006

Phenol 108952 58 89 38 190 5.8
Propionaldehyde 123386 110 620 Styrene 100425 85 550 210 1100 21

Tetrachloroethene 127184 240 1600 680 1400 20

Toluene 108883 750 4500 190 1100 37
Trichloroethylene 79016 700 2400 540 2700
Triethylamine 121448 2.8
Vinyl acetate 108054 24 630 18 260 Vinyl chloride 75014 640 3100 1300 13000 180
Xylenes (mixed) 1330207 560 4000 22

m

- Xylene 26 108383 22

o

- Xylene 2 6 95476 22

p

- Xylene 2 6 106423 22



### 2

. 7 Risk Characterization

2

. 7

. 1 General

25 The acute REL for ethylene glycol methyl ether was used as a surrogate for glycol ether compounds without

an acute REL.

26 The REL for mixed xylenes was used as a surrogate.Draft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 26

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

Handbook [ 23 ], in 2002 by the Agency’s information quality guidelines [ 24 ], and in the OMB/OSTP September 2007 Memorandum on Updated Principles for Risk Analysis 27 , and are incorporated in these assessments.

Estimates of health risk are presented in the context of uncertainties and limitations in the data and methodology. Through our tiered, iterative analytical approach, we have attempted to reduce both uncertainty and bias to the greatest degree possible in these assessments, within

t he limitations of available time and resources. We provide summaries of risk metrics (including maximum individual cancer risks and noncancer hazards, as well as cancer incidence estimates) along with a discussion of the major uncertainties associated wit h their derivation to provide decision makers with the fullest picture of the assessment and its

limitations.

For each carcinogenic HAP included in the assessment that has a potency estimate available,

individu al and population cancer risks we re calculate d 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 exposur e. Because UREs for most HAPs are upper

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

zero.

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

- of

- action [ 25 ], we applied

EPA’s Supplemental Guidance for Assessing Susceptibility from Early

- Life Exposure to Carcinogens [ 26 ]

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

- 1), 3 (for children aged 2

- 15), or 1.6 (for 70 years of exposure beginning at birth) , as needed in risk assessments . In this case, this has the effect of increasing the estimated life time risks for these pollutants by a factor of 1.6. In addition, although only a

small fraction of the total POM emissions may be reported as individual c ompounds, EPA expresses carcinogenic potency for compounds in this group in terms of benzo[a]pyrene equivalence, based on evidence that carcinogenic POM have the same mutagenic mechanism

of action as does benzo[a]pyrene. For this reason

, EPA implem entatio n policy [ 27 ] recommends applyi ng the Supplemental Guidance to all carcinogenic PAHs for which risk

27 Memorandum f or t he Heads o f Executive Departments a nd Agencies

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

- 24.pdf )Draft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 27

estimates are based on relative potency. Accordingly, we applied the Supplemental Guidance to all unspeciated POM mixtures.

Increased cancer incidence for the entire receptor population within the area of analysis wa s estimated by multiplying the estimated lifetime cancer risk for each census block by the number of people residing in that block, then summing the results for the entire modeled

domain. This l ifetime population incidence estimate wa s divided by 70 years to obtain an estimate of the number of cancer cases per year.

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

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

results.

Unlike linear dose

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

The risk characterization for chronic effects other than cancer is expre ssed 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 n ot necessarily suggest the onset of adverse effects. The HQ cannot be translated to a probability that adverse effects will occur, and is unlikely to be proportional to adverse health effect outcomes in a population

.

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

- term threshold value to develop an array of HQ values relative to the various acute endpoints and thresholds. In general, w hen 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 significant acute risks.

2

. 7

. 2 Mixtures

Since mos t or all receptors in these assessments receive exposures to multiple pollutants rather than a single pollutant, we estimated the aggregate health risks associated with all the exposures from a particular source category combined.Draft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 28

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

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

In assessing noncancer hazard from chronic e xposures, 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 mixtures guidelines support aggregatin g effects of different substances in specific and limited ways. To conform to these guidelines, we aggregated non

- cancer HQs of HAPs that act by similar toxic modes of action, or (where this information is absent) that affect the same target organ.

This process creates, for each target organ, a target

- organ

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

organ . Because impacts on organs or systems that occur above the critical dose have not been included in the TOSHI calculations, some TOSHIs may have been underestimated. As with the HQ, the TOSHI should not be interpreted as a pr obability of adverse effects, or as strict delineation of “safe” and “unsafe” levels. Rather, the TOSHI is another measure of the potential for adverse health outcomes associated with pollutant exposure, and needs to be interpreted carefully by health sci entists 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 Faci lity

- wide Risks

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

- wide” risks using ICR data and modeling as described in Section 2.2. For the facilities in the pulp and paper

source category , we estimated the maximum inhalation ca ncer 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 common control. We analyzed risks due to the inhalation of HAP for the populations residing within 50 kilometers of each facility. The results of the facility

- wide assessment are summarized below in the Risk characterization section of this document. The complete results of the facility

- wid e assessment are provided in Appendix 5.

2

. 7

. 4 MACT

- Allowable Risk

The emissions data in the data set for the pulp and paper source category are estimates of actual emissions on an annual basis. The risk results presented in the following sections are

based on these actual emissions. To estimate emissions at the MACT

- allowable level, a ratio

of MACT

- allowable to actual emissions for each source type was developed. This ratio wasDraft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 29

based on the level of control required by the MACT standard compared to the level of reported actual emissions and available information from the ICR on the level of control achieved by the emissions controls in use. The memorandum entitled, Inputs to the Pulp and Paper Industry October 2011 Residual Risk Modeling includes a detailed discussion on the development of the MACT

- allow able emissions (available in the docket for this rule making).



### 3 Risk Results for the Pulp & Paper Source Ca tegor y

3

. 1 Source Category Description and Results

The pulp and paper source category includes any fac ility engaged in the production of pulp and/or paper. This category includes, but is not limited to, integrated mills (where pulp and paper or paperboard are manufactured on

- site), non

- integrated mills (where paper/paperboard or pulp are manufactured, but not both), and secondary fiber mills (where waste paper is used as the primary raw material. The pul p and paper pro duction process include operations such as pulping, bleaching, chemical recovery, and papermaking. Pulping methods include chemical proces ses such as kraft, s oda, sulfite, and semi

- chemical, and mechanical, secondary fiber, or non

- wood processes. The MACT standards for the pulp and paper production source category were developed in three parts. This source

- category

- level risk assessment ad dress the emissions sources covered by the MACT I and MACT III standards 28 . Emission sources regulated under the pulp and paper MACT I standard in clude all HAP emissions in the kraft, soda, sulfite, and stand

- alone semi

- chemical pulping processes using woo d and all HAP emission points in the bleaching systems. Mills that mechanically pulp wood, pulp secondary

fib er or non

- wood fibers, and any mills that make paper, paper board, or related products from pulp are entit i es cover ed by the MACT III standard. H AP sources covered by the MACT III standard include emission points along the bleaching process. Specifically, bleaching emissions points include storage tanks, tower vents, washer bents, filtrate tank vents, and

s crubber outlets. HAP sources covered by t he MACT III standard also include paper manufacturing machines and their components (e.g., vacuum pump, storage tank, exhaust). A separate MACT standard 29 applicable to chemical recovery processes at kraft, soda, sulfite,

and stand

- alone semi

- chemical pul p mills was promulgated at a later date. The emissions from the sources covered by this later standard are included in t he facility

- wide risk analysis

. A complete description of the pulp and pap er production source category can be found in the

text of th e NPRM.

We curre ntly estimate that there are 17 1 pulp and paper facilities operating in the U.S. The

ICR data set contains all 171 facilities identified with a pulp and paper production MACT code in the 2005 NEI (updated with the 2010 ICR data) . All 171 of these facilities are identified as major sources in the NEI.

28 40 CFR 63, subpart S: National Emission Standards for Hazardous Air Pollutants from the Pulp and Paper

Indust ry.
29 40 CFR Part 63, Subpart MM: National Emission Standards for Hazardous Air Pollutants for Chemical Recovery Combustion Sources at Kraft, Soda, Sulfite, and Stand

- Alone Semichemical Pulp MillsDraft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 30

The emissions for the pulp and paper source category data set (of 171 facilities) are

summarized in Table 3.1

- 1. The total HAP emissions for the source category are approximately 45 ,000 tons per year. Based on these data, the HAP emitted in the largest quantities are methanol and acetaldehyde. Emissions of these two HAP make up 91 percent of the total emissions by mass. Persistent and bioaccumulative HAP ( PB

- HAP ) 30 reported as

em issions from these facilities include lead, cadmium, mercury, and POM

.

Table 3.1

- 1 Summary of Emissions from the Pulp & Paper Source Category Used in the Residual Risk

Assessment and Availability of Dose

- Response Values

HAP a Emissions (tpy) Numb er of

Facilities Reporting

HAP (171

facilities in

data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit

Risk

Estimate

for

Cancer? Reference

Concentration

for

Noncancer? Health

Benchmark

Values for

Acute

Noncancer?

Met hanol 38,650 165 Y Y Acetaldehyde 2,029 160 Y Y Y

Phenol 454 127 Y Y Cresols (mixed) 439 84 Y

Chloroform 356 128 Y Y

o

- Cresol 315 41 Y Formaldehyde 274 151 Y Y Y Hydrochloric acid (hydrogen chloride) 259 55 Y Y Biphenyl 218 92 Y

Hexachloroethane 207 34 Y Y Propionaldehyde 135 106 Y Y
1,2,4

- Trichlorobenzene 129 94 Y Methylene chloride 120 112 Y Y Y Xylenes (mixed) 98 107 Y Y

Carbon disulfide 90 96 Y Y

Cumene 83 95 Y Y

Toluene 82 126 Y Y Styrene 77 112 Y Y

Tetrachloroethene 75 98 Y Y Y Methyl isobutyl ketone 61 104 Y Acetophenone 60 39

Hexane 56 111 Y Y

Carbon tetrachloride 40 92 Y Y Y Trichloroethylene 37 93 Y Y Y

o

- Xylene 36 64 Y Y

Benzene 25 128 Y Y Y Naphthalene 24 105 Y Y

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

EPa

- 453K

- 04

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

.Draft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 31

Table 3.1

- 1 Summary of Emissions from the Pulp & Paper Source Category Used in the Residual Risk

Assessment and Availability of Dose

- Response Values

HAP a Emissions (tpy) Numb er of

Facilities Reporting

HAP (171

facilities in

data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit

Risk

Estimate

for

Cancer? Reference

Concentration

for

Noncancer? Health

Benchmark

Values for

Acute

Noncancer?

Chlorine 24 53 Y Y
1,1,2

- Trichloroethane 23 88 Y Y
1,1,1

- Trichloroethane (methyl chloroform) 22 85 Y Y

Ethyl benzene 18 76 Y Y Y Vinyl acetate 16 6 Y Y

Chlorobenzene 15 82 Y Y Methyl chloride 14 63 Y Y Hexachlorocyclopentadiene 10 6 Y Vinylidene chloride 8 3 Y Glycol Ethers
1,2

- Dimethoxyethane 7 31 Y Y Ethylene glycol ethyl ether 0.01 2 Y Y Methly cellosolve acrylate 0.001 1 Y Y Butyl carbitol acetate 0.0002 1 Y Y

Acetonitrile 5 2 Y Y

Et hylene dichloride 4 75 Y Y Y Vinyl chloride 4 34 Y Y Y Triethylamine 3 2 Y Y

m

- Cresol 3 4 Y Carbonyl sulfide 3 18 Y d Y Acrylonitrile 3 4 Y Y Y

m

- Xylene 2 11 Y Y

Chloroacetic acid 2 2 Y

p

- Xylene 1 7 Y Y Pentachlorophenol 1 2 Y Y Ethylene glycol 0.8 9 Y

Diethanolamine 0.8 4 Y Hydrogen cyanide 0.6 1 Y Y
1,3

- Butadiene 0.5 59 Y Y Y
2,4,5

- Trichlorophenol 0.4 1

p

- Cresol 0.3 3 Y Methyl bromide 0.3 25 Y Y Nickel compounds 0.2 29 Y Y Y Acrylamide 0.2 2 Y Y Ethylene dibromide 0.1 20 Y Y Y Cyanide compounds 0.1 1 Y

Nitrobenzene 0.09 2 Y Y Antimony compounds 0.08 1 YDraft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 32

Table 3.1

- 1 Summary of Emissions from the Pulp & Paper Source Category Used in the Residual Risk

Assessment and Availability of Dose

- Response Values

HAP a Emissions (tpy) Numb er of

Facilities Reporting

HAP (171

facilities in

data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit

Risk

Estimate

for

Cancer? Reference

Concentration

for

Noncancer? Health

Benchmark

Values for

Acute

Noncancer? Lead compounds 0.05 28 Y Y Propylene dichloride 0.05 3 Y Y

2

- Nitropropane 0.05 2 Y Y
2,4

- Toluene diamine 0.02 3 Y

Met hyl iodide 0.02 3 Y Chromium Coumpounds Chromium (III) compounds 0.02 27 Chromium (VI) compounds 0.0007 25 Y Y Ethylidene dichloride (1,1

- Dichloroethane) 0.01 3 Y Y

Bromoform 0.01 2 Y Cadmium compounds 0.01 28 Y Y Y

Be ryllium compounds 0.01 8 Y Y Y
2,4,6

- Trichlorophenol 0.009 2 Y Polycyclic Organic Matter (POM)

POM 72002 0.008 29 Y Y Dibenzo(a,h)anthracene 0.0007 7 Y Y Indeno(1,2,3

- c,d)pyrene 0.000003 7 Y Y
7,12

- Dimethylbenz(a)a nthracene 0.000002 3 Y Y Benzo(b)fluoranthene 0.0000006 7 Y Y Chrysene 0.0000003 5 Y Y Benz(a)anthracene 0.0000002 6 Y Y Benzo(k)fluoranthene 0.0000002 5 Y Y

POM 71002 0.0000002 1 Y Y

3

- Methylcholanthrene 0.0 000002 3 Y Y Benzo(a)pyrene 0.0000002 6 Y Y Manganese compounds 0.006 29 Y

Catechol 0.006 5

n,n

- Dimethylaniline 0.005 1 Arsenic compounds 0.004 28 Y Y Y Selenium compounds 0.004 9 Y Dibutylphthalate 0.003 5
1,4

- Dichlorob enzene 0.003 7 Y Y

Chlorobenzilate 0.002 1 Y Cobalt compounds 0.002 24 Y Mercury Compounds Mercury (elemental) 0.002 27 Y Y Y

Mercuric chloride 0.002 27 Y Y Bis(2

- ethylhexyl)phthalate 0.001 2 Y YDraft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 33

Table 3.1

- 1 Summary of Emissions from the Pulp & Paper Source Category Used in the Residual Risk

Assessment and Availability of Dose

- Response Values

HAP a Emissions (tpy) Numb er of

Facilities Reporting

HAP (171

facilities in

data set) Prioritized Inhalation Dose

- Response Value Identified by OAQPS b

PB

HAP? Unit

Risk

Estimate

for

Cancer? Reference

Concentration

for

Noncancer? Health

Benchmark

Values for

Acute

Noncancer? 1,1,2,2

- Tetrachloroethan e 0.0007 1 Y Ethylene oxide 0.0003 1 Y Y Y

Aniline 0.00001 3 Y Y Y

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” emis sions modeled as “cadmium & compounds”). In the absence of speciation information, we assume the reported mass is 100 percent metal.

• For emissions reported generically as “chromium” or “chromium & compound,” emissions are speciated “chromium (III) compoun ds” and “chromium (VI) compounds” according to the individual emitting process speciation profile 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

. Further information on the development of the chromium speciation profiles used in this assessment can be found in the memorandum entitled, Inputs to the Pulp and Paper Industry October 2011 Residual Risk Modeling , found

in the docket.

• For emissions reported generically as “mercury” or “mercury & compounds,” emissions are speciated for this category as “mercury (elemental)” and “mercuric chloride.” Mercury speciation profile s can be found on the

EPA’s Techn ology Transfer Network website for emissions inventories at http://www.epa.gov/ttn/chief/net/2005inventory.html

.

• For emissions of any chemicals or chemical groups classified as POM, emissions were grouped into POM subgroups as found on EPA’s Technology Transfer Network website for the 200 5 National

- Scale Air Toxics

Assessment at http://www.epa.gov/ttn/atw/nata2005/methods.html#pom ( Approach to Modeling POM)

.

• For emissions reported generically as “Glycol Ethers” or specific glycol ethers not found on EPA’s Technology Transfer Network for air toxics (see footnote b) , emissions were treated as ethylene glycol methyl ether.

b Specific dose

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

toxics at http:/ /www.epa.gov/ttn/atw/toxsource/summary.html

.

c There is no reference concentration for lead. In considering noncancer hazards for lead in this assessment, we compared rolling three

- month average exposure estimates to the National Ambient Air Quality St andard (NAAQS) for lead (0.15

μ g/m 3 ). These NAAQS for lead were recently reviewed with revisions adopted in October 2008 ( http://www.epa.gov/air/lead/actions.html ). The primary (health

- based) standar d 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.

d A chronic screening level of 0.163 mg/m 3 was developed for carb onyl sulfide by EPA ORD from a No Observed Adverse Effects Level of 200 ppm based on brain lesions and neurophysiological alteration in rodents.



### 3

. 2 Risk Characterization

This section presents the results of the risk assessment for the pulp and paper source c ategory. 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 assessment in the form ofDraft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 34

maximum hazard quotients, as well as the results of our preliminary screen for potential non

inhalation risks from PB

- HAP. Also presented are the HAP “drivers,” which are the HAP that collectively contribute 90 percent of the maximum cance r risk or maximum hazard at the highest exposure location, as well as a summary of the results of our facility

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

- specific risk assessment re sults is available in Appendix 5

.

Tables 3.2

- 1 and 3.2

- 2 summarize the chronic and acut e inhalation risk results for the pulp and paper source category . The results indicate that maximum lifetime individual canc er risks could be as high as 10 in a million . The major contributors to this risk are hexachloroethane and naphthalene from kraft processes such as pulp storage, wastewater, and bleaching

. The

total estim ated cancer incidence from this source category is 0.01 excess cancer cases per year, or one excess case in every 100 years. Approximately 40 people are estimated to have

cancer risks at or above 10 in a million, and approximately 76,000 people are estimated to

have cancer risks at or above 1 in a millio n as a result of the emissions from 68 facil ities. The

maximum chronic non cancer target organ specific hazard index ( TOS HI ) value for the source

category could be up to 0.4 associated with emissions of acetaldehyde

, indicating no significant potential for chronic noncancer impacts.

Analysis of potential differences between actual emissions levels and the maximum emissions

allowable under the MACT standards were also calculat ed for stack emissions for this source category . Risk estimates based on the ma ximum emissions allowable under the MACT

standards were calculated from stack emissions obtained from the ICR. Risk results from the

inhalation risk assessment indicate that the maximum lifetime individual cancer risk could be as high as 10 in a million, and that the maximum chronic noncancer TOSHI value could be as high as 0.6 at the MACT

- allowable emissions level.

Worst

- case a cute hazard quotients (HQs) were calculated for every HAP that has an acute

benchmark. For cases where the screening acute HQ w as 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 20 (based on the acute REL for acetaldehyde ) as shown in Table 3.2

- 1. The HQ of 20 represents an upper

- bound risk estimate and is located in a rural location in which public access is limited. An acute noncancer HQ of 3 for this facility would represent an area in which the public has access. The next highest acute noncancer HQ

for t his source category would be 6 for chloroform. Based on maximum hourly emission estimates available by emission process group, a n emissions multiplier of 2 was used to estimate the peak hourly emission rates for source category. See the memorandum entitl ed, Inputs to the Pulp and Paper Industry October 2011 Residual Risk Modeling for detailed description of how the maximum hourly emissions were developed for this source category (found in the docket for this rule making). Table 3

. 2

- 2 provides more inform ation on the

refined acute risk estimates for HAP that had an acute HQ greater than 1 for any benchmark.

To better characterize the potential health risks associated with estimated worst

- case acute exposures to HAP, and in response to a key recommendati on from the Science AdvisoryDraft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 35

Board’s peer review of EPA’s RTR risk assessment methodologies 31 , we examine a wider range of available acute health metrics than we do for our chronic risk assessments. This is in response to the acknowledgement that there are generally more data gaps and inconsistencies

in acute reference values than there are in chronic reference values. By definition, the acute

CA

- REL represents a health

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

- level exposures is unknown. Therefore, when a CA

- REL is exceeded and an AEGL

- 1 or ERPG

- 1 level is available (i.e., levels at which mild effects are anticipated in the general public for a single

exposu re), we have used them as a second comparative measure. Historically, c omparisons of

the estimated maximum off

- site one

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

. This is because o ccupat ional ceiling values are not generally considered protective for the general public since they are designed to protect the worker population (presumed healthy adults) for short duration (<15 minute) increases in exposure 32 . As a result, f or most chemicals, the 15

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

- hour

AEGL

- 1 , making comparisons to them irrelevant unless the AEGL

- 1 or ERPG

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

T he worst

- case maximum estimated 1

- hour exposure to formaldehyde outside the facility

fence line for the pulp and paper source category is 0.25 mg/m 3 . This estimated worst

- case

e xposure exceeds the 1

- hour REL by a factor of 5 (HQ REL = 5) and is below the 1

- hour

AEGL

- 1 (HQ AEGL

- 1 = 0.2). This exposure estimate is below the AEGL

- 1, and exceed the workplace ceiling level guideline for the formaldehyde value developed by National Inst itutes for Occupational Safety and Health (NIOSH) 33 “ for any 15 minute period in a work day ” (NIOSH REL

- ceiling value of 0.12 mg/m 3 ; HQ NIOSH = 2 ). T he estimate is at the value developed by the American Conference of Governmental Industrial Hygienists (ACGI H) 34 as “not to be exceeded at any time” (ACGIH TLV

- ceiling value of 0.37 mg/m 3 ; HQ ACGIH = 1). Additionally, the estimated maximum acute exposure exceeds the Air Quality Guideline value that was developed by the World Health Organization 35 for 30

- minute exp osures (0.1 mg/m 3 ; HQ WHO = 2.5 )

.

31 The SAB peer review of RTR Risk Assessment Methodologies is available at:

http://yosemite.epa.gov/sab/sabproduct.nsf/4AB3966E263D943A8525771F00668381/$File/EPA

- SAB

- 10

- 007

- unsigned.pdf

32 U.S. EPA. (20 09) Chapter 2.9 Chemical Specific Reference Values for Formaldehyde in Graphical Arrays of

Chemical

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

- 09/061, and available on

- line at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=211003

33 National Institutes for Occupational Safety and Health (NIOSH). Occupational Safety and Health Guideline

for Formaldehyde; http://www.cdc.gov/niosh/docs/81

- 123/pdfs/0293 .pdf

34 ACGIH (2001) Formaldehyde. In Documentation of the TLVs® and BEIs® with Other Worldwide

Occupational Exposure Values. ACGIH, 1300 Kemper Meadow Drive, Cincinnati, OH 45240 (ISBN: 978

- 1

- 882417

- 74

- 2) and available on

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

35 WH O (2000). Chapter 5.8 Formaldehyde, in Air Quality Guidelines for Europe, second edition. World Health

Organization Regional Publications, European Series, No. 91. Copenhagen, Denmark. Available on

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

.Draft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 36

To identify potential multipathway health risks from PB

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

- HAP emitted from the pulp and paper source category to screening emission r ates (see section 2.5). The PB

- HA P emitted by facilities in this category include cadmium, mercury, and POM (as benzo(a)pyr ene toxicity equivalents ). Thirty

- eight facilities in the source category reported emissions of one or more of these PB

- HAP

. At al l 38 facilities, the e missions rat e for each PB

- HAP was below the screening thresholds, with the exception of one facility’s emission rate of POM which

exceed ed the screening threshold by 2 times. For POM, exceeding the screening emission rate

relates to a potential for creating a cancer risk in excess of 1 in a million.

In evaluating the potential for multipathway effects from emissions of lead , modeled maximum annual lead concentrations were compared to the NAAQS value for lead (0.15 μg/m 3 ) , which take s into account multipathway exposures, so a separate multipathway screening value was not developed

. Since none of our maximum estimated annual lead concentrations were even close to the NAAQS , we do not expect any significant multipathway exposure and r isk due to lead emissions from these facilities.

Table 3.2

- 1 Summary of Source Category Level Inhalation Risks for Pulp and Paper

Result HAP “Drivers”
Facilities in Source Category

Number of Facilities Estimated to be in Source Category 171 n/a

Nu mber of Facilities Identified in the NEI and

Modeled in Preliminary Risk Assessment 171 n/a

Cancer Risks Maximum Individual Lifetime Cancer Risk (in 1 million) 10 hexachloroethane, naphthalene

Number of Facilities with Maximum Individual Lifetime Cancer Risk: Greater than or equal to 100 in 1 million 0 n/a Greater than or equal to 10 in 1 million 2 hexachloroethane Greater than or equal to 1 in 1 million 6 hexachloroethane , naphthalene

Chronic Noncancer Risks

Maximum Respiratory Hazard Index 0.4 acetaldehyde

Num ber of Facilities with Maximum Respiratory Hazard Index:

Greater than 100 0 n/a

Greater than 10 0 n/a

Greater than 1 0 n/a

Acute Noncancer Refined Results

Maximum Acute Hazard Quotient 20

6

5

2 acetaldehyde (REL ) chloroform (REL) formaldehyde (REL) methanol (REL)

Number of Facilities With Potential for Acute

Effects 9 a cetaldehyde

, chloroform, formaldehyde, methanol Population ExposureDraft Risk Assessment for the Pulp & Paper Source Category

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Table 3.2

- 1 Summary of Source Category Level Inhalation Risks for Pulp and Paper

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

of Facilities Modeled 50, 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 40 n/a Greater than or equal to 1 in 1 million 76,000 n/a

Number of People Exposed to Noncancer Respirator y Hazard Index:

Greater than 100 0 n/a

Greater than 10 0 n/a

Greater than 1 0 n/a Estimated Cancer Incidence (excess cancer cases per year) 0.0 1 36 n/a

Contribution of HAP to Cancer Incidence: acetaldehyde 38 % n/ a formaldehyde 36% n/a

hexachloroethane 9 % n/a naphthalene 4 % n/a

tetrachloroethene 3% n/a
1,1,2

- trichloroethane 2% n/a

Table 3.2

- 2 Summary o f Refined Acute Results f or Pulp & Paper Facilities

Refined Results MAXIMUM ACUTE HAZARD QUOTIENTS ACUTE DOSE

- RESPONSE VALUES

Based on

REL Based on

AEGL

- 1/

ERPG

- 1 Based on

AEGL

- 2/

ERPG

- 2 REL (mg/m 3 ) AEGL

- 1 (1

- hr) (mg/m 3 ) ERPG

- 1 (mg/m 3 ) AEGL

- 2 (1

- hr) (mg/m 3 ) ERPG

- 2 (mg/m 3 )

HAP Max. 1

- hr. Air

Conc. (mg/m 3 )

a cetaldehyde 7.1 20 0.09/0.4 0.01/0.02 0.47 81 18 490 360

chloroform 0.9 6 0.003/0.004 0.15 310 240

f ormaldehyde 0.25 5 0.2/0.2 0.01/0.02 0.055 1.1 1.2 17 12

m ethanol 64 2 0.09/0.2 0.02/0.05 28 690 260 2700 1 300

Notes on Refined Process:

1 ) The screening was performed for all emitted HAP with available acute dose

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

2 ) HAP wi th available acute dose

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

Notes on Acute Dose

- Response Values:

REL

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

- hour exposures.

36 We note that the MIR for this source category would not change if the CIIT URE for formaldehyde had been used in the assessment; however, t he total ca ncer incidence would decrease by about 36%. There is an ongoing IRIS reassessment for formaldehyde, and future RTR risk assessments will use the cancer potency for formaldehyde that results from that reassessment. As a result, the current results many not match those of future

assessments.Draft Risk Assessment for the Pulp & Paper Source Category

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AEGL

– Acute exposure guideline levels represent emergency exposure (1

- hour) limits for the general public.

AEGL

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

AEGL

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

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

EPRG

– Emergency Removal Program guidelines represent emergency exposure (1

- hour) limits for the general public.

ERPG

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

ERPG

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

The facility

- wi de MIR and TOSHI, available in Appendix 5, are based on emissions, as collected in the ICR, from all emissions sources at the identified facilities. The results of the facility

- wide assessment are summarized in Table 3.2

- 3. The results indicate that 100 facilities with pulp and paper production processes have facility

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

- wide MIR is 30 in a million, with pulp and paper source category contributing 27 percent of the risk. The rema ining 63 percent is driven by emissions of arsenic and chromium (VI) from hazardous waste incineration. The maximum facility

- wide TOSHI is 2 , driven by emissions of antimony compounds from smelt dissolving tank kraft process units. The source category co ntributes approximately 11 percent to the facility

- wide TOSHI.

Table 3.2

- 3 Source Category Contribution to Facility

- Wide Cancer Risks

Polystyrene

Production Number of Facilities Binned by Facility

- Wide MIR (in 1 million) Source Category MIR

Contrib ution to Facility

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

> 90% 19 14 1 0 34

50

- 90% 21 42 1 0 64

10

- 50% 27 31 3 0 61

< 10% 4 5 3 0 12

Total 71 92 8 0 171



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

Addressed

4

. 1 Exposure Modeling Uncertainties

Although ever y 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, the uncertainties in our emission inventory likely dominate the uncert ainties in our exposure estimates. The chronic ambient modeling uncertainties are considered relatively small in comparison, since we are using EPA’s refined local dispersion model with site

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

- or long

- term population mobility, andDraft Risk Assessment for the Pulp & Paper Source Category

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by neglecting processes like deposition, plume depletion, and atmospheric degradation. Additionally, estimates of the maximum individua l 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 closure 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 potential downward bias in both the MIR and population risk estimates.

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

We have purposely biased the acute screening results high, considering that they depend upon the joint occurrence of independent factors, such as hourly emissions rates, meteorology and human activity patterns. Furthermore, in cases where multiple acute threshold values are considered scientifically accepta ble we have chosen the most conservative of these threshold

values , erring on the side of overestimating potential health risks from acute exposures. In the cases where these results indicated the potential for exceeding short

- term health thresholds,

we h ave refined our assessment by developing a better understanding of the geography of the facility relative to potential exposure locations and the true variabil ity of short

- term emission

rates

.



### 4

. 2 Uncertainties in the Dose

- Response Relationships

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

- term (>24 hours up to 30 days), and subchronic (>30 days up to 10% of lifetime) exposure durations, all of which are derived based on an assumption of c ontinuous exposure throughout the duration specified. For the purposes of assessing all potential health risks associated wit h

the emissions included in an assessment, we rely on both chronic (cancer and noncancer) and acute (noncancer) benchmarks, which are described in more detail below.

Although every effort is made to identify peer

- review ed dose

- response values for all HAPs

emitted by the source category included in an assessment , some HAP have no peer

- reviewed cancer potency values or reference valu es for chronic non

- cancer or acute effects (inhalation or ingestion) . Since exposures to these pollutants cannot be included in a quantitative riskDraft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 40

estimate, an understatement of risk for these pollutants at environmental exposure levels is possible.

Add itionally, 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

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

- revi ewed 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 ] (herein

referred to as Cancer Guidelines ). “The primar y 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 adopte d in this document is consistent with this approach as

described in the Cancer Guidelines

.

For cancer endpoints EPA usually derives an oral slope factor for ingestion and a unit risk value for inhalation exposures. These values allow estimation of a life time 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, consis tent 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 methodologies for cancer risk assessment. EPA believes that cancer risk estimates developed following the procedures described in the Cancer Guidelines and outlined below generally provide an upper bound estimate of risk. That is, EPA’s upper bound estimates represent a “plausible upper limit to the true val ue of a quantity” (although this is usually not a true statistical confidence limit). 37 In some circumstances, the true risk could be as low as zero; however, in other circumstances the risk could also be greater. 38
When developing an upper bound estimat e of risk and to provide risk values that do not

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

38 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 i s based on maximum likelihood estimates.Draft Risk Assessment for the Pulp & Paper Source Category

-- November 2011 FOR PUBLIC COMMENT, DO NOT CITE OR QUOTE 41

underestimate risk, EPA generally relies on conservative default approaches. 39 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 qualitative ly. Uncertainties may vary substantially among cancer risk assessments associated with exposures to different pollutants, since the assessments employ different databases with different strengths and limitations and the procedures employed may differ in h ow well they represent actual biological processes for

the assessed substance. EPA’s Risk Characterization Handbook also recommends that risk characterizations present estimates demonstrating the impact on the assessment of alternative choices, data, mode ls 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 tumor responses observed in experimental animal bioa ssays and those which would occur in humans is a source of uncertainty in cancer risk assessment. In general, EPA does not assume that tumor sites observed in an experimental animal bioassay are necessarily predictive of the sites at which

tumors would oc cur in humans. 40 However, unless scientific support is available to show otherwise, EPA assumes that tumors in animals are relevant in humans, regardless of target organ concordance. For a specific pollutant, qualitative differences in species responses can lead to either under

- estimation or over

- estimation of human cancer risks.

(2) Uncertainties regarding the most appropriate dose metric for an assessment can also lead to differences in risk predictions. For example, the measure of dose is commonly expressed in units of mg/kg/d ingested or the inhaled concentration of the pollutant. However, data may support development of a pharmacokinetic model for the absorption, distribution, metabolism and excretion of an agent, which may result in improved dos e 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 uncer tain (e.g., as can occur when alternative pharmacokinetic models are available for a compound). Uncertainty in dose estimates may

lead to either over or underestimation of risk.

39 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

ele ments of the risk

- assessment process when the correct scientific model is unknown or uncertain.” The 1983 NRC report Risk Assessment in the Federal Government: Managing the Process defined default option as “the option chosen on the basis of risk assessme nt policy that appears to be the best choice in the absence of data to the contrary” (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the agency may depart from them in evaluating the risks posed by a specific su bstance when it believes this to be appropriate. In keeping with EPA’s goal of protecting public health and the environment, default assumptions are used to ensure that risk to chemicals is not underestimated (although defaults are not intended to overtly overestimate risk). See EPA 2004 An Examination of EPA Risk Assessment Principles and Practices,

EPA/100/B

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

- final.pdf.

40 Per the EPA Cancer Guidelines: “The default option is that positive effects in a nimal cancer studies indicate that the agent under study can have carcinogenic potential in humans.” and “Target organ concordance is not a prerequisite for evaluating the implications of animal study results for humans.”Draft Risk Assessment for the Pulp & Paper Source Category

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

test data and the correctness of scaled estimates.

(4) EPA cancer risk estimates, whether based on epidemiological or exp erimental animal data, are generally developed using a benchmark dose (BMD) analysis to estimate a dose at which there is a specified excess risk of cancer, which is used as the point of departure (or POD) for

the remainder of the calculation. Statistica l uncertainty in developing a POD using a benchmark dose (BMD) approach is generally addressed though use of the 95% lower confidence limit on the dose at which the specified excess risk occurs (the BMDL), decreasing the likelihood of understating risk. E PA 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 potentially large, source of uncertainty in cancer risk asse ssment. EPA uses different approaches to low dose risk assessment (i.e., developing estimates of risk for exposures to environmental doses of an agent from observations in experimental or epidemiological studies at higher dose) depending

on the available data and understanding of a pollutant’s mode of action (i.e., the manner in which a pollutant causes cancer). EPA’s Cancer Guidelines express a preference for the use of reliable, compound

- specific, biologically

- based risk models when feasible; however, s uch 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

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

- dose (straight line from POD) approach is used when available mode of action data support a linear (e.g., nonthreshold response) or as the mos t 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 Cancer Guidelines generally

consider a linear dose

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

- dose linear responses, although the slope o f 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 comp ound

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

- response models, when appropriately applied as part of EPA’s cancer risk assessment process, provid e an upper bound estimate of risk andDraft Risk Assessment for the Pulp & Paper Source Category

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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 Council (NRC) report [ 32 ] suggests that

models based on dis tributions 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

hu mans depending on genetics, coincident exposures, nutritional status, and various other susceptibility factors...” Thus, if a distribution of thresholds approach is considered for a carcinogen risk assessment, application would depend on ability of model ing to reflect the degree of variability in response in human populations (as opposed to responses in bioassays with genetically more uniform rodents). Note also that low dose linearity in risk can arise for reasons separate from population variability: d ue to the nature of a mode of action and additivity of a chemical’s effect on top of background chemical exposures and biological

processes.

As noted above, EPA’s current approach to cancer risk assessment typically utilizes a straight line approach from the BMDL. This is equivalent to using an upper confidence limit on the slope of the straight line extrapolation. The impact of the choice of the BMDL on bottom line risk estimates can be quantified by comparing risk estimates using the BMDL value to cent ral 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 assessments, including the majority of those for which ri sk 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 huma n 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 typical individual, although compound

- specific

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

Chronic no ncancer assessmentDraft Risk Assessment for the Pulp & Paper Source Category

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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 Dis ease 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 i ntended to be protective against appreciable risk of

deleterious effects . Uncertainty factors are commonly default values 41 e.g., factors of 10 or 3, used in the absence of compound

- specific data; where data are available, uncertainty factors may also be d eveloped 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 sense that further study might support development of

ref erence values that are higher (i.e., less potent) because fewer default assumptions are needed. However, for some pollutants it is possible that risks may be underestimated.

For non

- cancer endpoints related to chronic exposures, EPA derives a Reference D ose (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 daily oral exposure (RfD) or of a continuous inhalation expo sure (RfC) to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. 42 To derive values that are intended to be “without appreciable risk,” EPA’s methodology relies up on 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 determines the appropriate point of departure (POD) for deri vation of the reference value. A POD is determined by (in order of preference): (1) a statistical estimation using the benchmark dose (BMD) approach; (2) use of the dose or concentration at which the toxic response was not significantly elevated (no

obser ved adverse effect level

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

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

elements of the risk

- assessment process when the correct scientific model is unknown or uncertain.” The 1983 NRC report

, Risk Assessment in the Federal Government: Managing the Process defined default option as “the option chosen on the basis of risk assessment policy that appears to be the best choice in the absence of data to

th e contrary” (NRC, 1983a, p. 63). Therefore, default options are not rules that bind the agency; rather, the agency may depart from them in evaluating the risks posed by a specific substance when it believes this to be appropriate. In keeping with EPA’s go al 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 Pr inciples and Practices,

EPA/100/B

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

- final.pdf

.

42 See IRIS glossaryDraft Risk Assessment for the Pulp & Paper Source Category

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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 fa ctors 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 data obtained in a study with

less

- than

- lifetime exposur e (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 problems with applicability of available studies

. When s cientifically sound, peer

- reviewed assessment

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

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

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

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

smaller

- sized population, often of one sex or of a narrow range of life stages (typical of occupational epidemiologic studies), to a larger, more diverse popu lation. 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 var iability 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 experimental animals to humans is a necessary step for the majority of chemical risk assessments . When interpreting animal data, the concentration at the POD (e.g. NOAEL, BMDL) in an animal model (e.g. rodents) is extrapolated to estimate the human response. While there is long

- standing scientific support

for th e 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 relevant endpoint from the most sensitive species and th e 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 resp onses may be greater or less than this value

.

Pharmacokinetic models are useful to examine species differences in pharmacokinetic processing and associated uncertainties; however, such dosimetric adjustments are not always possible. Information may not b e available to quantitatively assess toxicokinetic orDraft Risk Assessment for the Pulp & Paper Source Category

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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 d ifferences and associated uncertainty in extrapolating from laboratory animals to humans in the derivation of a reference value. If information on one or the other of these components is available and accounted for in the cross

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

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

- day subchronic studies in rodents) or when such data are judged more appropriate for de velopment 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 ind ividual 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 studies lack a dose or exposure level at which an advers e 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 deriving an underprotective RfD/RfC due to a data gap preventing complete characterization of the chemical’s toxicity. In the absence of studies for a known or suspected endpoint of concern, a

UF of 10 or 3

- fold is typically applied.

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

air

- related lead and the associated risk (73FR at 66979). EPA als o explicitly considered the uncertainties associated with both the human health evidence and the exposure and risk analyses when developing the NAAQS for lead. For example, EPA considered uncertainties in the relationship between ambient air lead and bloo d lead levels (73FR at 66974), as well as uncertainties between blood lead levels and loss of IQ points in children (73FR at 66981). In considering the evidence and risk analyses and their associated uncertainties, the EPA

Administrator noted his view tha t there is no evidence

- or risk

- based bright line that indicates a single appropriate level. Instead, he noted, there is a collection of scientific evidence and judgments and other information, including information about the uncertainties inherent in

many relevant factors, which needs to be considered together in making this public health policy judgment and in selecting a standard level from a range of reasonable values (73FR at 66998). In so doing, the Administrator decided that, a level for the primary lead standard of 0.15 μg/m 3 , in combination with the specified choice of indicator, averaging time, and form,Draft Risk Assessment for the Pulp & Paper Source Category

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is requisite to protect public health, including the health of sensitive groups, with an adequate margin of safety (73FR at 67006). A thorough d iscussion of the health evidence, risk and exposure analyses, and their associated uncertainties can be found in EPA’s final rule revising the lead NAAQS (73 FR 66970

- 66981, November 12, 2008).

We also note the uncertainties associated with the health

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

- response values developed for many of the other HAP, particularly those HAP for which no human health data exist. In 1988, EPA’s IRIS program reviewed the health effec ts data regarding lead and its inorganic compounds and determined that it would be inappropriate to develop an RfD for these compounds, saying, “A great deal of information on the health effects of lead has been obtained through

decades of medical observat ion and scientific research. This information has been assessed in the development of air and water quality criteria by the Agency's Office of Health and Environmental Assessment (OHEA) in support of regulatory decision

- making by the Office of Air Quality Planning and Standards (OAQPS) and by the Office of Drinking Water (ODW). By comparison to most other environmental toxicants, the degree of uncertainty about the health effects of lead is quite low. It appears that some of these effects, particularly

ch anges in the levels of certain blood enzymes and in aspects of children's neurobehavioral development, may occur at blood lead levels so low as to be essentially without a threshold. The Agency's RfD Work Group discussed inorganic lead (and lead compounds) at two meetings (07/08/1985 and 07/22/1985) and considered it inappropriate to develop an RfD for inorganic lead.” EPA’s IRIS assessment for Lead and compounds (inorganic) (CASRN 7439

- 92

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

.

We note further that because of the multi

- pathway, multi

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

related multi

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

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

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

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

evidence

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

Acute noncancer a ssessment

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 applied based on chemical

specific or health effect

- specific information (e.g., simple irritation effects do not vary appreciably between human individuals, hence a value of 3 is typically used), or based on the purpose for the reference value (see the fo llowing 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; andDraft Risk Assessment for the Pulp & Paper Source Category

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4) uncertainty in accounting for an incomplete database on toxic effects of potential concern. Additional adjustments are often applied to account for uncertainty in extrapolation from observations at one exposure duration (e.g., 4 hours) to arrive at a POD for derivation of an

acute refere nce value at another exposure duration (e.g., 1 hour).

Not all acute reference values are developed for the same purpose and care must be taken when interpreting the results of an acute assessment of human health effects relative to the

reference value or values being exceeded. W here relevant to the estimated exposures, the lack of threshold values at different levels of severity should be factored into the risk characterization as potential uncertainties.



### 5 References

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