EPA 600/R-14/217F | September 2014 | www.epa.gov/ncea
United States
Environmental Protection
Agency
Child-Specific Exposure
Scenarios Examples
National Center for Environmental Assessment
Office of Research and Development
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EPA/600/R-14/217F
September 2014
www.epa.gov/ncea
Child-Specific Exposure Scenarios Examples
National Center for Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Washington, DC 20460
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DISCLAIMER
This final document has been reviewed in accordance with U.S. Environmental Protection
Agency policy and approved for publication. Mention of trade names or commercial products does
not constitute endorsement or recommendation for use.
ABSTRACT
The purpose of the Child-Specific Exposure Scenarios Examples is to outline scenarios
for various child-specific exposure pathways and to demonstrate how data from the Exposure
Factors Handbook (hereinafter EFH) (U. S. EPA, 2011 a) may be applied for estimating dose.
Exposure scenarios are tools to help the assessor develop estimates of exposure and dose to
assess potential health risks. An exposure scenario generally includes facts, data, assumptions,
inferences, and sometimes professional judgment about how the exposure takes place. In 2004,
EPA published the Example Exposure Scenarios (U.S. EPA, 2004a) using human physiological
and behavioral data from the Exposure Factors Handbook (U.S. EPA, 1997a), which has been
superseded by the EFH (U.S. EPA, 201 la). This document provides an update of the 2004
Example Exposure Scenarios, focusing specifically on scenarios involving children. The
example scenarios presented here have been selected to best demonstrate the use of the various
key data sets in the EFH (U.S. EPA, 201 la) and to represent commonly encountered exposure
pathways. An exhaustive review of every possible exposure scenario for every possible receptor
population would not be feasible and is not provided. Instead, readers may use the representative
examples provided here to formulate scenarios that are appropriate to the assessment of interest
and to apply the same or similar data sets and approaches as shown in the examples.
Preferred citation:
U.S. Environmental Protection Agency (EPA). (2014) Child-Specific Exposure Scenarios Examples. National
Center for Environmental Assessment, Washington, D.C.; EPA/600/R-14/217F. Available from the National
Technical Information Service, Springfield, VA and online at http://www.epa.gov/ncea.
11
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CONTENTS
LIST OF TABLES VII
LIST OF FIGURES VIII
ABBREVIATONS AND ACRONYMS IX
PREFACE X
AUTHORS, CONTRIBUTORS, AND REVIEWERS XII
1. INTRODUCTION AND PURPOSE 1
.1. PURPOSE 2
.2. RELATIONSHIP TO OTHER RELEVANT EPA REPORTS 2
.3. EXPOSURE ASSESSMENT GENERAL PRINCIPLES 2
.4. EXPOSURE SCENARIOS 7
.5. CUMULATIVE EXPOSURES 13
.6. OTHER SOURCES OF INFORMATION ON EXPOSURE ASSESSMENT 14
.7. COMMON CONVERSION FACTORS 16
2. EXAMPLE INGESTION SCENARIOS 18
2.1. PER CAPITA INGESTION OF CONTAMINATED HOMEGROWN
EXPOSED VEGETABLES: CHILDREN AGED 1 TO <11 YEARS, IN
GARDENING HOUSEHOLDS, CENTRAL TENDENCY, CHRONIC
AVERAGE DAILY DOSE 18
2.1.1. Introduction 18
2.1.2. Dose Algorithm 19
2.1.3. Input for Exposure Factor Variables 19
2.1.4. Calculations 22
2.1.5. Uncertainties 23
2.2. INGESTION OF CONTAMINATED SOIL AND DUST IN AND AROUND
THE HOME: YOUNG CHILDREN AGED 1 TO <6 YEARS, CENTRAL
TENDENCY, LIFETIME AVERAGE DAILY DOSE 24
2.2.1. Introduction 24
2.2.2. Dose Algorithm 25
2.2.3. Input for Exposure Factor Variables 25
2.2.4. Calculations 26
2.2.5. Uncertainties 27
2.3. INGESTION OF CONTAMINATED INDOOR DUST: CHILDREN AT
SCHOOL AGED 6 TO <11 YEARS, CENTRAL TENDENCY,
SUBCHRONIC AVERAGE DAILY DOSE 28
2.3.1. Introduction 28
2.3.2. Dose Algorithm 28
2.3.3. Input for Exposure Factor Variables 29
2.3.4. Calculations 30
2.3.5. Uncertainties 30
2.4. INGESTION OF AN ENVIRONMENTAL CONTAMINANT BY
NONDIETARY HAND-TO-MOUTH BEHAVIORS: INFANTS AND
iii
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TODDLERS 3 MONTHS TO <2 YEARS, BOUNDING, ACUTE DOSE
RATE 31
2.4.1. Introduction 31
2.4.2. Dose Algorithm 32
2.4.3. Input for Exposure Factor Variables 32
2.4.4. Calculations 34
2.4.5. Uncertainties 35
2.5. EXPOSURE TIME OF INCIDENTAL INGESTION OF CONTAMINATED
POOL WATER TO REACH A REFERENCE DOSE LEVEL OF
EXPOSURE: CHILDREN AGED 6 TO <11 YEARS, BOUNDING 36
2.5.1. Introduction 36
2.5.2. Dose Algorithm 36
2.5.3. Input for Exposure Factor Variables 37
2.5.4. Calculations 38
2.5.5. Uncertainties 38
2.6. INGESTION OF CONTAMINATED DRINKING WATER: CHILDREN
AGED <21 YEARS, DISTRIBUTION OF CHRONIC AVERAGE DAILY
DOSE 39
2.6.1. Introduction 39
2.6.2. Dose Algorithm 39
2.6.3. Input for Exposure Factor Variables 40
2.6.4. Calculations 42
2.6.5. Uncertainties 44
2.7. INGESTION OF CONTAMINATED HUMAN MILK: INFANTS AGED
BIRTH TO <12 MONTHS, HIGH-END, SUBCHRONIC AVERAGE
DAILY DOSE 45
2.7.1. Introduction 45
2.7.2. Dose Algorithm 45
2.7.3. Input for Exposure Factor Variables 46
2.7.4. Calculations 47
2.7.5. Uncertainties 48
2.8. INGESTION OF CONTAMINATED RECREATIONAL ATLANTIC
MARINE FINFISH: CHILDREN AGED 3 TO <6 YEARS, CENTRAL
TENDENCY, SUBCHRONIC AVERAGE DAILY DOSE 49
2.8.1. Introduction 49
2.8.2. Dose Algorithm 49
2.8.3. Input for Exposure Factor Variables 50
2.8.4. Calculations 50
2.8.5. Uncertainties 51
3. EXAMPLE INHALATION EXPOSURE SCENARIOS 54
3.1. INHALATION OF CONTAMINATED AIR WHILE PLAYING IN A
SCHOOL YARD: SCHOOL CHILDREN AGED 6 TO <11 YEARS,
CENTRAL TENDENCY, SUBCHRONIC ADJUSTED AIR
CONCENTRATION 55
3.1.1. Introduction 55
iv
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3.1.2. Exposure Algorithm 55
3.1.3. Input for Exposure Factor Variables 56
3.1.4. Calculations 56
3.1.5. Uncertainties 57
3.2. INHALATION OF AEROSOLIZED CONTAMINANTS FROM WATER
DURING AND AFTER SHOWERING: CHILDREN AND TEENS AGED 6
TO <18 YEARS, CENTRAL TENDENCY, LIFETIME ADJUSTED AIR
CONCENTRATION 57
3.2.1. Introduction 57
3.2.2. Exposure Algorithm 58
3.2.3. Input for Exposure Factor Variables 58
3.2.4. Calculations 59
3.2.5. Uncertainties 60
3.3. INHALATION OF CONTAMINATED INDOOR AIR: RESIDENTIAL
CHILDREN AGED 3 TO <11 YEARS, BOUNDING, ACUTE DOSE RATE 60
3.3.1. Introduction 60
3.3.2. Dose Algorithm 61
3.3.3. Input for Exposure Factor Variables 61
3.3.4. Calculations 64
3.3.5. Uncertainties 64
3.4. INHALATION OF CONTAMINATED AIR DURING BUS
TRANSPORTATION: SCHOOL CHILDREN AND TEENS AGED 6 TO
<16 YEARS, HIGH-END, CHRONIC AVERAGE DAILY DOSE 64
3.4.1. Introduction 64
3.4.2. Dose Algorithm 65
3.4.3. Input for Exposure Factor Variables 65
3.4.4. Calculations 66
3.4.5. Uncertainties 67
4. EXAMPLE DERMAL EXPOSURE SCENARIOS 68
4.1. DERMAL CONTACT WITH CONTAMINATED SOIL: TEEN ATHLETES
AGED 11 TO <16 YEARS, CENTRAL TENDENCY, SUBCHRONIC
AVERAGE DAILY DOSE 68
4.1.1. Introduction 68
4.1.2. Dose Algorithm 68
4.1.3. Input for Exposure Factor Variables 69
4.1.4. Calculations 71
4.1.5. Uncertainties 71
4.2. DERMAL CONTACT WITH INORGANIC CONTAMINANTS WHILE
WADING IN A RECREATIONAL POND: CHILDREN AGED 6 TO
<16 YEARS, BOUNDING, ACUTE DOSE RATE 73
4.2.1. Introduction 73
4.2.2. Dose Algorithm 73
4.2.3. Input for Exposure Factor Variables 73
4.2.4. Calculations 76
4.2.5. Uncertainties 76
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4.3. DERMAL CONTACT WITH AN ORGANIC CONTAMINANT IN WATER
WHILE SHOWERING: CHILDREN AND TEENS, AGED 6 TO
<16 YEARS HIGH-END, LIFETIME AVERAGE DAILY DOSE 77
4.3.1. Introduction 77
4.3.2. Dose Algorithm 77
4.3.3. Input for Exposure Factor Variables 78
4.3.4. Calculations 82
4.3.5. Uncertainties 82
GLOSSARY 84
REFERENCES 96
VI
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LIST OF TABLES
Table 1. Exposure durations and dose metrics 9
Table 2. Child-Specific Exposure Scenarios Examples roadmap 11
Table 3. Common conversion factors 17
Table 4. Estimation of age specific per capita mean homegrown exposed vegetable intake
rates for children in gardening households (g/kg-day) for four age ranges among
children aged 1 to
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LIST OF FIGURES
Figure 1. Distribution of average daily doses (ADD) from birth to 21 years of age 43
Vlll
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ABBREVIATONS AND ACRONYMS
ADAF Age-dependent adjustment factors
ADD Average daily dose
ADR Acute dose rate
BW Body weight
EPA U.S. Environmental Protection Agency
HEC Human equivalent concentration
IRIS Integrated Risk Information System
IUR Inhalation Unit Risk
LADD Lifetime average daily dose
NCEA National Center for Environmental Assessment
RfC Reference concentration
RfD Reference dose
IX
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PREFACE
The National Center for Environmental Assessment (NCEA) of EPA's Office of
Research and Development has prepared the Child-Specific Exposure Scenarios Examples to
outline scenarios for various exposure pathways and to demonstrate how data from the EFH
(U.S. EPA, 201 la) may be applied for estimating exposures for children. A similar document
entitled Example Exposure Scenarios was published by EPA in 2004 (U.S. EPA, 2004a). The
Child-Specific Exposure Scenarios Examples updates the children's exposure scenarios included
in U.S. EPA2004a.
An exposure scenario considers the physical setting, potential uses of a contaminated
resource (e.g., future residential land use or consumption offish), the population that may be
exposed (infant, child, or adolescent), fate and transport of contaminants, and how exposure may
occur including ingestion, dermal contact, and inhalation. Consideration of frequency and
duration of exposure as well as seasonal variations are part of the development of an exposure
scenario. The Child-Specific Exposure Scenarios Examples is intended to be a companion
document to the EFH. The example scenarios were compiled from questions and inquiries
received from users of the earlier versions of the EFH on how to select data from the Handbook.
The scenarios presented in this report promote the use of the standard set of age groups
recommended by the EPA in the report entitled Guidance on Selecting Age Groups for
Monitoring and Assessing Childhood Exposures to Environmental Contaminants (U.S. EPA,
2005a).
Each scenario examined in this report refers to a single-chemical exposure route and
pathway. EPA recognizes that individuals may be exposed to mixtures of chemicals through
more than one pathway and one route. In the past few years there has been an increased
emphasis in cumulative risk assessments1, aggregate exposures2, and chemical mixtures
(U.S. EPA, 2008a, 2003). Detailed and comprehensive guidance for evaluating cumulative risk
is not currently available. The Agency has, however, developed a framework that lays out a
broad outline of the assessment process and provides a basic structure for evaluating cumulative
Cumulative risk assessment—An analysis, characterization, and possible quantification of the combined risks to
health or the environment from multiple agents or stressors.
2Aggregate exposures—The combined exposure of an individual (or defined population) to a specific agent or
stressor via relevant routes, pathways, and sources.
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risks. This basic structure is presented in the Framework for Cumulative Risk Assessment
published in May 2003 (U.S. EPA, 2003). Additional guidance is available from EPA's
Concepts, Methods and Data Sources for Cumulative Health Risk Assessment of Multiple
Chemicals, Exposures and Effects: A Resource Document (U.S. EPA, 2007a). EPA encourages
and supports the use of new and innovative approaches and tools to improve the quality of public
health and environmental protection.
In general, the Child-Specific Exposure Scenarios Examples document provides examples
using the point-estimate approach, but also includes an example of a simple probabilistic
assessment for one scenario. In contrast to the point-estimate approach, probabilistic methods
allow for a better characterization of variability and/or uncertainty in risk estimates. The use of
probabilistic methods is contingent on the availability and quality of the data. Additional
information on characterization of variability and uncertainty can be found in Chapter 2 of the
(U.S. EPA, 201 la).
XI
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AUTHORS, CONTRIBUTORS, AND REVIEWERS
The National Center for Environmental Assessment (NCEA), Office of Research and
Development was responsible for the preparation of this document. This document has been
prepared by Battelle under EPA contract No. EP09H001685. Jacqueline Moya served as a Work
Assignment Manager, providing overall direction, technical assistance, and contributing author.
AUTHORS AND CONTRIBUTORS
U.S. EPA
Jacqueline Moya
Linda Phillips
John Schaum, retired
Laurie Schuda
Battelle
Ann Gregg
Marcia Nishioka
Technical Editing
Vicki Soto, U.S. EPA
REVIEWERS
The following EPA individuals reviewed an earlier draft of this document and provided valuable
comments:
Heidi Bethel, OW Eva McLanahan, ORD/NCEA-RTP
Iris Camacho, OW detail Margaret McDonough, retired, Region 1
Becky Cuthbertson, OSWER David Miller, OPP
Lynn Delpire, OPPT Marian Olsen, Region 2
Peter Egeghy, ORD/NERL Haluk Ozkaynak, ORD/NERL
Michael Firestone, OCHP Yvette Selby-Mohamadu, OPPT
Ann Johnson, ORPM Nicolle Tulve, ORD/NERL
Youngmoo Kim, Region 3 Dana Vogel, OPP
Geneice Lehmann, ORD/NCEA-RTP
xn
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AUTHORS, CONTRIBUTORS, AND REVIEWERS (continued)
This document was reviewed by an external panel of experts. The panel was composed of the
following individuals:
Dr. David O. Carpenter, Director, Institute for Health and the Environment University at Albany
Dr. Alesia Ferguson, University of Arkansas for Medical Science
Dr. Annette Guiseppi-Elie, Principal Consultant, Risk Assessment DuPont Engineering
Dr. P. Barry Ryan, Emory University Atlanta, Georgia
Dr. Alan H. Stern, University of Medicine and Dentistry of New Jersey
xin
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1. INTRODUCTION AND PURPOSE
Children's environmental exposures to contaminants can change significantly as they
develop through infancy, childhood, and adolescence. These exposure differences are a result of
both behavioral and rapid physiological changes as they grow. Children, therefore, may be
physiologically susceptible to some environmental contaminants during certain life stages.
Greater susceptibility due to greater exposure can lead to greater risk of adverse health effects for
children relative to adults exposed to the same contaminants.
Since 1995, the U.S. Environmental Protection Agency (EPA) has specified that children
must be explicitly considered when conducting risk assessments as part of a public health
decision-making process. Subsequently, the Supplemental Guidance for Assessing Susceptibility
from Early-Life Exposure to Carcinogens (U.S. EPA, 2005b) stressed the importance of
considering life stage differences in both exposure and dose-response when assessing cancer
risks from early life exposures. The guidance promotes the summing of doses or risks across all
relevant life stages instead of averaging an age-specific dose over the entire lifetime. For
carcinogens acting via a mutagenic mode of action, age-dependent adjustment factors (ADAFs)
are used to account for susceptibility at various life stages (U.S. EPA, 2005b).
In 2002, EPA published the interim final version of the Child-Specific Exposure Factors
Handbook, which was designed specifically to address the exposure factors related to children
(U.S. EPA, 2008a). In 2008, the Child-Specific Exposure Factors Handbook was republished
(U.S. EPA, 2008a), incorporating information from the Guidance on Selecting Age Groups for
Monitoring and Assessing Childhood Exposures to Environmental Contaminants (U.S. EPA,
2005a). The 2008 version of the Child-Specific Exposure Factors Handbook rearranged the data
and recommendations, to the extent possible, to be consistent with the standard set of childhood
age groups provided in the 2005 guidance. The Exposure Factors Handbook published in 2011
retained the same age groupings for children. These childhood age groups are as follows:
• Less than 12-months old: birth to <1 month, 1 to <3 months, 3 to <6 months, and 6 to
<12 months
• Greater than 12-months old: 1 to <2 years, 2 to <3 years, 3 to <6 years, 6 to <11 years,
11 to <16 years, and 16 to <21 years
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1.1. PURPOSE
The purpose of the Child-Specific Exposure Scenarios Examples is to present childhood
exposure scenarios using data from the Child-Specific Exposure Factors Handbook and updated
children's data from the Exposure Factors Handbook (U.S. EPA, 201 la, 2008a; referred to
throughout as EFH). These scenarios are not meant to be inclusive of every possibility, but they
are intended to provide a range of scenarios that show how to apply exposure factors data to
characterize childhood exposures. As such, these scenarios are not meant as templates for
exposure assessors, but can be modified to meet specific needs.
1.2. RELATIONSHIP TO OTHER RELEVANT EPA REPORTS
In 2011, EPA published the EFH, which supersedes the Child-Specific Exposure Factors
Handbook and previous versions of the EFH (U.S. EPA, 201 la, 2008). The Child-Specific
Exposure Scenarios Examples supersedes the children's exposure scenarios included in U.S.
EPA 2004a.
1.3. EXPOSURE ASSESSMENT GENERAL PRINCIPLES
Exposure assessment is a "process of estimating or measuring the magnitude, frequency,
and duration of exposure to an agent, along with the number and characteristics of the population
exposed" (Zartarian et al., 2007a). Exposure assessments are conducted for a variety of purposes
including risk assessments, trend analyses, and epidemiological studies (U.S. EPA, 1992a). In
the risk assessment context, the output of an exposure assessment is typically the estimation of
the potential dose (U.S. EPA, 1992a). The potential dose is dependent on the concentration of
the contaminant in a medium (e.g., soil, water, air) and the intake or contact rate of the
population with the medium. This potential dose can be adjusted to include additional factors
that further characterize the population being assessed and describe the exposure in terms of
exposure duration and frequency.
The terms exposure and dose are closely related. Exposure is defined as the "contact of
an organism with a chemical or physical agent, quantified as the amount of chemical available at
the exchange boundaries of the organism and available for absorption" (TPCS, 2001). The dose
refers to the amount of agent (e.g., chemical) that enters a target in a specified period of time
after crossing a contact boundary. The units of dose are typically mg/kg-day. The example
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scenarios provided in this report focus on the calculation of dose and not exposure. Often times,
dose is calculated and combined with toxicity information to calculate risk. However,
calculations of risk are outside the scope of this document. The principal focus of this document
is on childhood doses from exposure to chemicals, but the concepts may apply to other agents.
Exposure can occur via ingestion, inhalation, or direct contact (i.e., dermal). Chemicals
can be introduced into the gastrointestinal tract through dietary ingestion of foods and beverages
or nondietary ingestion of foreign substances (e.g., soil). The outer contact boundary for
ingestion exposures is the mouth. A chemical can enter the respiratory tract through the
inhalation of particles, gases, vapors, and aerosols. For inhalation exposure, the outer contact
boundary is the oral/nasal boundary. The characteristics of the inhaled agent affect its
deposition, retention, translocation, and distribution within the respiratory system and other
tissues in the body (U.S. EPA, 1994). Dermal absorption is governed by the characteristics of
the skin (contact boundary) on the exposed part of the body, and the characteristics of the agent
(e.g., physical-chemical properties) and the matrix in which it exists (e.g., water, soil);
environmental conditions (e.g., temperature and humidity) can also play a role. The example
scenarios presented in this document are organized according to these three routes of exposure
(i.e., ingestion, inhalation, and dermal contact).
The population of interest in an exposure assessment, also known as the receptor
population, may include children at various life stages to account for their rapidly changing
physiology and behavior. In addition, the exposure assessment can evaluate only the population
that is potentially exposed (i.e., "doers-only," "consumers-only") or it can assess the exposure
over the entire population on a per capita basis. If one could sample everyone in the population,
the "doers-only" or "consumers-only" will be those individuals who engage in the specific
activity of interest. "Per capita" will be everyone in the population. Since not everyone in the
population can be studied, in this report, "doers only" refers to only those individuals who
reported doing the activity during the survey period. "Consumers-only" refers to only those
individuals who reported food or water intake during the survey period. "Doers-only" or
"consumers-only" contact rates are calculated by averaging activity rates or food or water intake
rates across only the individuals in the survey who engaged in those activities or consumed those
foods or beverages. Conversely, "per capita" contact rates are generated by averaging
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consumer-only rates over the entire population, including those individuals that reported no
activity or intake during the survey period. Generally, "per capita" contact rates are appropriate
for use in exposure assessments for which average dose estimates are of interest. They are also
useful for comparisons with other population groups. For example, for foods, they represent
both individuals who ate the foods during the survey period and individuals who may eat the
food items at some time, but did not consume them during the survey period. Per capita intake
may underestimate consumption for the subset of the population that consumed the food in
question (U.S. EPA, 201 la).
The equation used to express dose is based on the intensity, duration, and frequency of
the exposure to the receptor population. The intensity typically is expressed as the concentration
of the contaminant per unit mass or volume (i.e., ug/g, ug/L, mg/m3, ppm, etc.) in the medium
multiplied by the contact rate (e.g., intake rate, inhalation rate). In the following examples, the
concentration of a contaminant "x" is used as a generic term. Except for the concentration, the
terms used in the dose equation are referred to as exposure factors. Exposure factors are factors
related to human behavior and characteristics that help determine an individual's exposure to an
agent. The concentration is based on site- and chemical-specific data that are not provided in the
EFH.
Each of the main exposure routes has a range of exposure descriptors that explains the
distribution of exposures occurring in the exposed population. The central tendency scenario is
developed using means or 50th percentiles for contaminant concentration and exposure factors or
by selecting the mean or median from the dose distribution. A high-end exposure scenario
typically represents an individual in the upper end of the exposure distribution (i.e., over the
90th percentile, but less than the most exposed individual [U.S. EPA, 1992a]). High-end
scenarios are developed using a combination of central and upper estimates for the contaminant
concentration and/or exposure factors or by selecting an upper-percentile from the dose
distribution. The choice of the parameters the assessor sets at a central tendency value versus an
upper-percentile depends on judgement, the sensitivity of the parameters, and regulatory
requirements.
A bounding scenario is defined as an exposure higher than any expected to occur in the
actual population (U.S. EPA, 1992a). A theoretical upper bound is estimated by assuming limits
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for all the variables used to calculate exposure and dose that, when combined, will result in the
mathematically highest exposure or dose (highest concentration, highest intake rate, lowest body
weight [BW]) (U.S. EPA, 1992a). However, it is generally not necessary to use the theoretical
upper bound to assure that the exposure or dose calculated is above the actual distribution
(U.S. EPA, 1992a). Thus, bounding estimates in the examples included in this report are
estimated using upper-percentile estimates for most of the dose equation, but keeping some
variables at the mean value (i.e., BW, surface area). An upper-percentile estimate of an exposure
factor is defined as a value between the 90th and the 99.9th percentile in the exposure factor
distribution (U.S. EPA, 201 la). In the EFH, the 95th percentile, if available, was used to
represent the upper-percentile in the recommendations because it is the middle of the range
between the 90th and 99.9th percentiles. For some factors, a specific upper-percentile could not
be defined because the data were not available.
Another aspect of exposure assessment is the duration and the frequency over which the
exposure occurred. An acute exposure is a one-time exposure to a contaminant by the oral,
dermal, or inhalation route for 24 hours or less. Chronic exposure is defined as a repeated
exposure by the oral, dermal, or inhalation route for more than approximately 10% of the life
span in humans (more than approximately 90 days to 2 years in typically used laboratory animal
species). A subchronic exposure is defined as a repeated exposure by the oral, dermal, or
inhalation route for more than 30 days, up to approximately 10% of the life span in humans
(U.S. EPA, 201 Ib).
The potential dose may be calculated as a potential average daily dose (ADD), lifetime
average daily dose (LADD), or the acute dose rate (ADR). The ADD, calculated for a
noncarcinogenic contaminant exposure, is a dose averaged over a specified timeframe. The
general equation used for ADD is presented below (see eq 1). Equations used to calculate a
dermal dose include some additional terms (e.g., surface area, dermal permeability coefficient)
and are presented in Section 4. Historically, theLADD is calculated for contaminant exposure
that is expressed over an adult lifetime (e.g., 70 years). LADD is generally used when assessing
exposure to carcinogens. However, consistent with the Supplemental Guidance for Assessing
Susceptibility from Early-Life Exposure to Carcinogens, if exposure is less than lifetime, the
dose is calculated by summing time weighted doses that occur during each life stage and
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averaging across the total exposure period (U.S. EPA, 2005b). It is important to note that the
average life expectancy has increased to an average of 78 years for males and females combined,
as stated in the EFH (U.S. EPA, 201 la). The increase in life expectancy in humans is largely
attributed to decreases in nonmalignant disease mortality, with little change in malignant disease
mortality. The use of 70 years has been a policy decision due to the fact that there is no evidence
to suggest that cancer risk per year of exposure has changed simply due to increased life
expectancy. Dividing the LADD over a period of 78 years instead of 70 years will have the
effect of lowering the cancer risk by approximately 10%. Although this is not a significant
difference, for consistency, an average lifetime of 70 years is used as a reference value when
calculating the LADD. For noncarcinogenic acute exposures, the ADR is used. To calculate the
ADR, the exposure frequency, exposure duration, and averaging time are all set equal to 1 to
adjust the calculation for a one-time exposure.
C X CR X EF X ED
ADD = (1)
BW XAT ^ '
where:
ADD = potential average daily dose of the contaminant of interest (mg/kg-d);
C = concentration of the contaminant within the media of interest (mg/g;
mg/L; mg/cm2; mg/m3);
CR = average daily contact rate of the media of interest (g/d; L/d; cm2/d;
m3/d);
EF = exposure frequency (d/yr);
ED = exposure duration (yr);
BW = body weight (kg); and
AT = averaging time (d).
Note that, in some cases, contact rate may be expressed in units of less than a day (e.g.,
L/hr). When this occurs, an additional term (e.g., exposure time) may be included to account for
the portion of a day spent engaging in the activity of interest (e.g., hours/day). Also, for some
exposure pathways, contact rates are expressed as intake rates. In some cases, the contact rate is
provided on a body-weight (BW) basis (e.g., g/kg-day or L/kg-day); therefore, BWis not needed
in the denominator of the dose equation. Also note that other algorithms or approaches may be
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used to calculate dose depending on available data, software capabilities, regulatory goals, and
statutory requirements. EPA program offices may also have guidances specific to their
programs. In addition, the assessor may need to consider the bioavailability of the contaminant in
the specific medium. The bioavailability will vary depending on the physicochemical
characteristics of the contaminant and the characteristics of the medium (e.g., particle size in
soil).
In the risk assessment context, the dose calculations are often combined with toxicity
information to estimate risk. Exposure assessors are encouraged to consult with toxicologists
regarding the appropriate application of toxicity values with the exposure assessment. For
example, it may not be appropriate to use toxicity values derived to reflect chronic exposures
(e.g., Reference Dose, cancer slope factors) when characterizing acute or subchronic exposures.
In addition, when assessing cancer risk from exposures to mutagenic carcinogens, the assessor
needs to consider the ADAFs to account for early life sensitivities. The reader is referred to the
Supplemental Guidance for Assessing Susceptibility from Early-Life Exposure to Carcinogens
for further information about ADAFs and their application (U.S. EPA, 2005b).
The EPA uses inhalation dosimetry methodology for estimating exposure through the
inhalation pathway because the amount of chemical that reaches the target organ is not a simple
function of the inhalation rate and BW(U.S. EPA, 2009). In contrast with the ingestion pathway,
the inhalation dosimetry methodology only requires a derivation of a time weighted average
concentration adjusted for the duration and frequency of exposure (U.S. EPA, 2009). To
estimate risk, the adjusted concentration is then compared with a Reference Concentration (RfC)
or an Inhalation Unit Risk (IUR), which are expressed in units of concentration and the inverse
of concentration, respectively. There may be cases in which an inhalation dose is of interest
(e.g., the estimation of aggregate and cumulative doses; an analysis of relative pathway
contribution).
1.4. EXPOSURE SCENARIOS
This document is intended to present example exposure scenarios that reflect the possible
ways that data reported in the EFH (U.S. EPA, 201 la) may be used in childhood exposure
assessments and risk assessments. The scenarios are representative of generic applications and
should be tailored to specific program needs and the population and life stages of interest. As
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such, they are not intended to supplant specific guidance issued by EPA program offices. In
developing risk assessments under specific EPA programs, the risk assessor should consult
specific programmatic guidance and requirements. The selection of life stages used in each
scenario is not meant to imply that those are the only life stages for which the scenario could
apply.
This report shows multiple examples for each of the main exposure routes (ingestion,
inhalation, and dermal penetration), a range of exposure descriptors (e.g., central tendency,
high-end, or bounding exposure), exposure durations (i.e., acute, subchronic, or chronic), and
receptor populations (e.g., single or multiple age ranges, only participants in an activity called
"doers-only," "consumers-only," and per capita population). For demonstration purposes, only
one exposure descriptor was chosen for each exposure scenario. This is not meant to imply that
only those chosen descriptors will be of interest for that particular scenario. Throughout the
report, high-end scenarios are constructed using a combination of central tendency estimates and
high-end estimates for the various parameters of the dose equation. The intent of the report is
not to provide prescriptive guidance on how to estimate a high-end dose, since subjective
judgement is required.
Specific scenarios were selected based on inquiries received from users of the past
version of the EFH. These are scenarios that exposure and risk assessors may frequently
encounter. For example, food intake scenarios were selected to illustrate the use of per capita
versus consumer-only data. Fish consumption was of particular interest because of the
associations between contaminants that may be found in fish and children's susceptibility to
these chemicals. Human milk intake and nondietary exposures are pathways that are unique to
children. Likewise, the inhalation and dermal scenarios were selected based on locations where
children spend their time and activities in which they are engaged (e.g., schools, indoor
environments, outdoor activities). Exposure durations and the corresponding dose metrics are
presented in Table 1.
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Table 1. Exposure durations and dose metrics
Exposure type
Acute
Sub chronic
Chronic
Lifetime
Exposure duration
<24 hours
>30 days <10% life span in humans
>10% life span in humans
Life span
Dose metric
ADR
AL)L)subchronic
AL)L) chronic
LADD
The example scenarios are presented according to exposure route. Each scenario
assumes that the concentration of the chemical in the specific medium is known, either measured
or modeled. Mean values for the exposure concentration are used throughout the report when
calculating central tendency dose estimates. It should be noted that some exposure assessors use
the upper confidence limit of the mean for a more conservative estimate. Since the concentration
values are assumed to be known, this report does not address fate and transport considerations
for the estimation of the concentration term. In addition, the scenarios do not address exposures
via multiple routes. This is not meant to imply that exposures from other routes are negligible
for a particular scenario. For example, exposure to contaminated homegrown vegetables implies
contaminated soils, which may also result in exposures via the nondietary pathway. In addition,
the scenarios described do not include potential exposures that may be experienced by the
parents, care givers, or other workers present in the same microenvironments. Each example
provides an introduction describing the scenario, the algorithm used for estimating dose, the
suggested input values of exposure factors with the calculation of the estimated dose, and the
uncertainties and limitations of the data and/or approach used in the example. Exposure factors
input values were derived from the recommendations published in the EFH (U.S. EPA, 201 la).
Table 2 provides a summary of the example exposure scenarios presented in this
document. The outcome for most of the scenarios included in this document is a point estimate
for the described scenario. However, one scenario (2.6—Ingestion of Contaminated Drinking
Water: Children <21 Years, Distribution of Chronic Daily Exposure) presents a simple example
of the use of a probabilistic approach for estimating dose. Toxicity values needed to calculate
risk from each exposure scenario described in Table 2 should match the exposure duration of
interest (i.e., acute, subchronic, chronic). The exposure duration should also match the health
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end point of interest (i.e., carcinogens and noncarcinogens). For additional information on
exposure assessment, refer to Chapter 1 of the EFH (U.S. EPA, 201 la).
10
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Table 2. Child-Specific Exposure Scenarios Examples roadmap
#
Scenario Title
Exposure
media
Receptor
population
Exposure
distribution
Calculated
dose or
concentration
Age range
(yr, unless
stated otherwise)
Ingestion scenarios
2.1
2.2
2.3
2.4
2.5
2.6
2.7
2.8
Per Capita Ingestion of Contaminated Homegrown
Exposed Vegetables: Children Aged 1 to <11 Years, in
Gardening Households, Central Tendency, Chronic
Average Daily Dose
Ingestion of Contaminated Soil and Dust in and Around
the Home: Young Children Aged 1 to <6 Years, Central
Tendency, Lifetime Average Daily Dose
Ingestion of Contaminated Indoor Dust: Children at
School Aged 6 to <1 1 Years, Central Tendency,
Subchronic Average Daily Dose
Ingestion of an Environmental Contaminant by
Nondietary Hand-to-mouth Behaviors: Infants and
Toddlers 3 Months to <2 Years, Bounding, Acute Dose
Rate
Exposure Time of Incidental Ingestion of Contaminated
Pool Water to Reach a Reference Dose (RfD) Level of
Exposure: Children Aged 6 to <1 1 Years, Bounding
Ingestion of Contaminated Drinking Water: Children
Aged <21 Years, Distribution of Chronic Average Daily
Dose
Ingestion of Contaminated Human Milk: Infants Aged
Birth to <12 Months, High-end, Subchronic Average
Daily Dose
Ingestion of Contaminated Recreational Atlantic
Marine Finfish: Children Aged 3 to <6 Years, Central
Tendency, Subchronic Average Daily Dose
Homegrown
exposed
vegetables
Soil and dust
Indoor dust
Nondietary
hand-to-mouth
activity
Pool water
Drinking water
Human milk
Recreational
Marine fish
Children,
per capita
Young children
School children
Infants and
toddlers
Children,
doers-only
Children,
consumers -only
Infants,
consumers -only
Children,
consumers -only
Central
Tendency
Central
tendency
Central
tendency
Bounding
Bounding
Distribution
High-end
Central
tendency
ADD,
chronic
LADD",
chronic
ADD,
Subchronic
ADR,
acute
RfD used to
calculate ET
ADD,
chronic
ADD,
Subchronic
ADD,
Subchronic
lto
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Table 2. Child-specific Exposure Scenarios Examples roadmap (continued)
#
Scenario Title
Exposure
media
Receptor
population
Exposure
distribution
Calculated
dose
Age range
(years, unless
stated otherwise)
Inhalation scenarios
3.1
3.2
3.3
3.4
Inhalation of Contaminated Air while Playing in a
School Yard: School Children Aged 6 to <1 1 Years,
Central Tendency, Subchronic Adjusted Air
Concentration
Inhalation of Aerosolized Contaminants from Water
During and After Showering: Children and Teens Aged
6 to <18 Years, Chronic Central Tendency, Lifetime
Adjusted Air Concentration
Inhalation of Contaminated Indoor Air: Residential
Children Aged 3 to <1 1 Years, Bounding, Acute Dose
Rate
Inhalation of Contaminated Air During Bus
Transportation: School Children and Teens Aged 6 to
<16 Years, High-end, Chronic Average Daily Dose
Outdoor air
Aerosolized
water
Indoor air
Air on bus
transportation
School
children,
doers-only
Children and
teens,
doers-only
Residential
children,
doers-only
Children and
teens,
doers-only
Central
tendency
Central
tendency
Bounding
High-end
C air adjusted,
Subchronic
C air adjusted*,
chronic
ADR
ADD,
chronic
6to
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1.5. CUMULATIVE EXPOSURES
This report provides childhood exposure scenario examples, each relating to one route of
exposure and one chemical. EPA recognizes that childhood exposure can occur from multiple
routes and to one or multiple stressors. The Framework for Cumulative Risk Assessment (U.S.
EPA, 2003) provides a simple and flexible structure for conducting and evaluating cumulative
risk assessment. EPA (2003) defines cumulative risk as "the combined risks from aggregate
exposures to multiple agents or stressors." Agents or stressors are defined in a broader sense to
include chemicals, as well as biological or physical agents (e.g., noise, nutritional status), or the
change or loss of a necessity such as habitat.
Considerations regarding the cumulative evaluation of chemical stressors are discussed in
EPA's report entitled^ Framework for Assessing Health Risks of Environmental Exposures to
Children (U.S. EPA, 2006). The first step in quantifying exposure for a cumulative risk
assessment is the characterization of the population and study area so that all existing and future
pathways can be identified (U.S. EPA, 2007a). It is particularly important when assessing
childhood exposures to identify the relevant and unique exposure factors that may be used to
adjust the exposure estimate based on differential exposures (U.S. EPA, 2007a). The next step is
to group the chemicals of concern according to the timing, medium, or exposure pathway
(U.S. EPA, 2007a). This step typically requires the exposure analyst to consult with
toxicologists to determine the types of chemical exposures that could be associated with a
particular end point. Information about the potential chemicals' co-occurrence in each
compartment/medium and their potential interactions affecting transformation, fate, and transport
are also useful (U.S. EPA, 2007a).
Concepts, methods, and data sources for cumulative health risk assessment are described
in more detailed in EPA's report entitled Concepts, Methods, and Data Sources for Cumulative
Health Risk Assessment of Multiple Chemicals, Exposures and Effects: A Resource Document
(U.S. EPA, 2007a). Cumulative exposure assessments can be complex and may require the use
of models. Modeling tools have been developed that facilitate the evaluation of cumulative
exposures (e.g., U.S. EPA Stochastic Human Exposure and Dose Simulation Model for
Multimedia, Multipathway Chemicals (SHEDS-Multimedia);
http://www.epa.gov/heasd/products/sheds_multimedia/sheds_mm.html) (U.S. EPA 2008b;
Zartarian et al., 2007b).
13
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1.6. OTHER SOURCES OF INFORMATION ON EXPOSURE ASSESSMENT
For additional information on exposure assessment resources, the reader is encouraged to
refer to EPA-Expo-Box (a toolbox for exposure assessors) (available at
http://www.epa.gov/risk/expobox/). Links to the following EPA resources included in EPA-
Expo-Box may be useful:
• Methods for Assessing Exposure to Chemical Substances, Volumes 1-13 (U.S. EPA,
1983-1989);
• Pesticide Assessment Guidelines, Subdivisions K and U (U.S. EPA, 1984, 1986a);
• Standard Scenarios for Estimating Exposure to Chemical Substances During Use of
Consumer Products (U.S. EPA, 1986b);
• Selection Criteria for Mathematical Models Used in Exposure Assessments: Surface
Water Models (U.S. EPA, 1987);
• Selection Criteria for Mathematical Models Used in Exposure Assessments: Groundwater
Models (U.S. EPA, 1988a);
• Superfund Exposure Assessment Manual (U.S. EPA, 1988b);
• Risk Assessment Guidance for Superfund, Volume I, Part A, Human Health Evaluation
Manual (U.S. EPA, 1989);
• Methodology for Assessing Health Risks Associated with Indirect Exposure to
Combustor Emissions (U.S. EPA, 1990);
• Risk Assessment Guidance for Superfund, Volume I, Part B, Development of Preliminary
Remediation Goals (U.S. EPA, 1991a);
• Risk Assessment Guidance for Superfund, Volume I, Part C, Risk Evaluation of
Remedial Alternatives (U.S. EPA, 1991b);
• Guidelines for Exposure Assessment (U.S. EPA, 1992a);
• Dermal Exposure Assessment: Principles and Applications (U.S. EPA, 1992b);
• Soil Screening Guidance (U.S. EPA, 1996a);
14
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Occupational and Residential Exposure Test Guidelines: OPPTS 875.1000 Background
for Application Exposure Monitoring Test Guidelines. Group A (U.S. EPA, 1996b);
Occupational and Residential Exposure Test Guidelines: OPPTS 875.2000 Background
for Postapplication Exposure Monitoring Test Guidelines. Group B. (U.S. EPA, 1996c);
Guiding Principles for Monte Carlo Analysis (U.S. EPA, 1997b);
Policy for Use of Probabilistic Analysis in Risk Assessment at the U.S. Environmental
Protection Agency (U.S. EPA, 1997c);
Sociodemographic Data Used for Identifying Potentially Highly Exposed Populations
(U.S. EPA, 1999a);
Report of the Workshop on Selecting Input Distributions for Probabilistic Assessments
U.S. EPA, 1999b);
Options for Development of Parametric Probability Distributions for Exposure Factors
(U.S. EPA, 2000a);
Revised Methodology for Deriving Health-Based Ambient Water Quality Criteria (U.S.
EPA, 2000b);
Risk Assessment Guidance for Superfund, Volume I, Part D, Standardized Planning,
Reporting, and Review of Superfund Risk Assessments (U.S. EPA, 2001a);
Risk Assessment Guidance for Superfund Volume III, Part A, Process for Conducting
Probabilistic Risk Assessments (U.S. EPA, 2001b);
Framework for Cumulative Risk Assessment (U.S. EPA, 2003b);
Risk Assessment Guidance for Superfund, Volume I, Part E, Supplemental Guidance for
Dermal Risk Assessment (U.S. EPA, 2004b);
Guidance on Selecting Age Groups for Monitoring and Assessing Childhood Exposures
to Environmental Contaminants (U.S. EPA, 2005a);
Supplemental Guidance for Assessing Susceptibility from Early-Life Exposure to
Carcinogens (U.S. EPA, 2005b);
Cancer Guidelines for Carcinogen Risk Assessment (U.S. EPA, 2005c);
15
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• Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities
(U.S. EPA, 2005d);
• A Framework for Assessing Health Risk of Environmental Exposures to Children from
Environmental Exposures (U.S. EPA, 2006);
• Concepts, Methods, and Data Sources For Cumulative Health Risk Assessment of
Multiple Chemicals, Exposures and Effects: A Resource Document (U.S. EPA, 2007a);
• Dermal Exposure Assessment: A Summary of EPA Approaches (U.S. EPA, 2007b);
• Child-Specific Exposure Factors Handbook (U.S. EPA, 2008a);
• Stochastic Human Exposure and Dose Simulation Model for Multimedia, Multipathway
Chemicals (SHEDS-Multimedia) Dietary Model. Details of SHEDS-Multimedia Version
3: Technical Manual (U.S. EPA, 2008);
• Risk Assessment Guidance for Superfund Volume I: Human Health Evaluation Manual
Part F, Supplemental Guidance for Inhalation Risk Assessment (U.S. EPA, 2009);
• Exposure Factors Handbook: 2011 Edition (U.S. EPA 201 la);
• Highlights of the Exposure Factors Handbook (U.S. EPA 201 Ic);
• Recommended Use of Body Weight374 (BW3/4) as the Default Method in Derivation of the
Oral Reference Dose (U.S. EPA, 201 Id);
• Standard Operating Procedures for Assessing Residential Pesticide Exposure Assessment
(U.S. EPA, 2012a); and
• The Stochastic Human Exposure and Dose Simulation Model for Multimedia,
Multipathway Chemicals (SHEDS-Multimedia): Dietary Module. SHEDS-Dietary
version 1. Technical Manual. (U.S. EPA, 2012b).
1.7. COMMON CONVERSION FACTORS
Frequently, exposure assessments require the use of volume, mass or area conversion
factors. Conversion factors may be used to convert these units of measure to those needed to
calculate dose. These factors are used, for example, to ensure consistency between the units used
to express exposure concentration and those used to express intake. Table 3 provides a list of
common conversion factors that may be required in the exposure equations.
16
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Table 3. Common conversion factors
To Convert
cubic centimeters (cm3)
cubic centimeters (cm3)
cubic meters (m3)
gallons (gal)
liters (L)
liters (L) (water)
liters (L)
liters (L)
milliliters (mL)
milliliters (mL) (water)
grams (g)
grams (g) (water)
grams (g) (water)
grams (g)
grams (g)
kilograms (kg)
micrograms (jig)
milligrams (mg)
milligrams (mg)
pounds (Ib)
square centimeters (cm2)
square meters (m2)
Multiply
Volume
0.000001
0.001
1,000,000
3.785
0.264
1,000
1,000
1,000
0.001
1
Mass
0.0022
1
0.001
1,000
0.001
1,000
0.001
0.001
1,000
454
Area
0.0001
10,000
To Obtain
cubic meters (m3)
liters (L)
cubic centimeters (cm3)
liters (L)
gallons (gal)
grams (g) (water)
milliliters (mL)
cubic centimeters (cm3)
liters (L)
grams (g) (water)
pound (Ib)
milliliters (mL) (water)
liters (L) (water)
milligrams (mg)
kilograms (kg)
grams (g)
milligrams (mg)
grams (g)
micrograms (jig)
grams (g)
square meters (m2)
square centimeters (cm2)
17
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2. EXAMPLE INGESTION SCENARIOS
2.1. PER CAPITA INGESTION OF CONTAMINATED HOMEGROWN EXPOSED
VEGETABLES: CHILDREN AGED 1 TO <11 YEARS, IN GARDENING
HOUSEHOLDS, CENTRAL TENDENCY, CHRONIC AVERAGE DAILY DOSE
2.1.1. Introduction
At sites with soil or water contamination, or where deposition of atmospheric
contaminants has been observed or is expected based on modeling, the potential exists for locally
grown exposed vegetables to become contaminated. Exposed vegetables are those that are grown
above ground and do not have outer protective coatings that are removed before consumption.
Thus, chronic exposure to these contaminants may exist among children who ingest exposed
vegetables grown in gardens in the contaminated area. The dose via intake of contaminated
exposed vegetables is a function of the concentrations of the contaminants in the vegetables, the
rate at which children consume the food, and the frequency and duration of exposure.
This example assumes exposure via contaminated homegrown exposed vegetables. The
example calculates the central tendency average daily dose from the ingestion of homegrown
exposed vegetables for consumers consisting of children aged 1 to <11 years. This example uses
intake data for four age ranges (1 to <2 years, 2 to <3 years, 3 to <6 years, and 6 to <11 years)
derived from the EFH (U.S. EPA, 201 la). Values obtained from tables within the EFH (U.S.
EPA, 201 la) are cited as EFH Table X-X. The mean consumer-only homegrown exposed
vegetable intake rate, based on the population that gardens, from Table EFH 13-60 is converted
to a mean per capita rate. This value is the per capita mean for the entire survey population that
gardens (i.e., all ages combined). It is used with age-specific per capita intake data for all
exposed vegetables (i.e., not just homegrown exposed vegetables, and not just gardening
households) from EFH Table 9-20 to develop age-specific mean per capita intake rates for
homegrown exposed vegetables in gardening households for the four age groups of children
between the ages of 1 and <11 years. The information on homegrown intake originates from
analyses performed by EPA on data from the 1987-1988 Nationwide Food Consumption
Survey, which currently is the best source of data available to EPA on consumption of
home-produced food. This example assumes that the quantity of homegrown exposed vegetables
produced in the garden is sufficient to support intake at this rate. The intake rates used in this
example represent per capita intake rates for households that participate in home gardening. In
18
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addition, the intake rates are adjusted to account for losses during food preparation, as described
in U.S. EPA (20 11 a).
This scenario assumes that the children live within the contaminated area over the
duration of the exposure (and thus are continually exposed from 1 to <1 1 years of age) and that
they eat homegrown exposed vegetables throughout each year. It is also assumed that all of the
homegrown exposed vegetables are obtained from the contaminated area.
2.1.2. Dose Algorithm
For consumers, the dose of a specified contaminant via ingestion of homegrown exposed
vegetables is expressed as an average daily dose (ADDhgexp-veging) per BWand is calculated as
follows:
_ Chg exp-veg x ^hg exp-veg per capita mean-adj x EF x ED
TZ
where:
ADDhgexp-veging = potential average daily dose per kg BWof the contaminant from
ingestion of homegrown exposed vegetables (mg/kg-d);
Chg exp-veg = concentration of the contaminant in the homegrown exposed vegetables
(mg/g);
IRhg exp-veg per capita mean-adj = age-specific daily intake rate of homegrown exposed
vegetables among children in gardening households; per capita mean,
adjusted for preparation losses (g/kg-d);
EF = exposure frequency (d/yr);
ED = exposure duration (yr); and
AT = averaging time (d).
As detailed in the following subsections, the ADD hg exp-veg ing values are calculated for
each of the four age ranges of 1 to <2 years, 2 to <3 years, 3 to <6 years, and 6 to <1 1 years,
using available data from the EFH). These estimates are then summed to obtain an ADD hg exp-veg
ing estimate for the entire 1- to <1 1 -year-old age range.
2.1.3. Input for Exposure Factor Variables
Chg exp-veg — The concentration of the contaminant in homegrown exposed vegetables is
either the measured or predicted concentration (e.g., based on modeling). Since the scenario is
19
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estimating central tendency dose, the mean or median contaminant concentration would be used.
For the purposes of the example calculations shown below, it is assumed that the mean
concentration of the contaminant in homegrown exposed vegetables is 1 x 1CT3 mg/g for all
consumers within the 1- to <11-year age range.
IRhgexp-vegper capita mean-adj—The age-specific average intake rates of homegrown exposed
vegetables for children in gardening households are estimated by first converting the consumer-
only mean intake rate of homegrown exposed vegetables for the total population of gardening
households (IRhg exP-veg-consumer only mean) from EFH Table 13-60 to the mean per capita rate (IRhgexp-
veg-per capita mean) aS tOllOWS.
exp-veg.per capita mean
where:
Nc = weighted number of gardening individuals who consumed homegrown exposed
vegetables during the survey period (EFH Table 13-60); and
Nt = weighted total number of individuals who garden (EFH Table 13-4).
1.57 x 25,737,000
fig exp-veg.per capita mean — 68 1 52 000
in _ n rq §
ln-hg exp-veg-per capita mean ~ v.oj ^
This mean value (IRhg exp-veg-per capita mean-unadj) represents the quantity of food brought into
the house, and does not account for preparation or postcooking losses (i.e., unadjusted value).
The value can be adjusted to represent the quantity of food as-eaten (IRhg exp-veg-per capita mean-adj) as
follows:
' "kg exp-veg-per capita mean-adj ~
, „ /,. % preparation loss\ /,. % post cooking loss\ -..
' "kg exp-veg-per capita mean-unadj X ^1 j^ J X ^1 j-^ j (4)
20
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where:
Preparation loss
Postcooking loss
12% (see EFH Table 13-69); and
22% (see EFH Table 13-69).
g / 12 \ / 22 \
j n _ n ro ° v I 1 __ I V I 1 __ I
1 n-hg exp-veg-per capita mean.adj ~ fra-d \ IQQJ \ IQQJ
in _ o A-I
lnhg exp-veg-per capita mean-adj ~ u.t.L
This mean per capita value represents the average rate of homegrown exposed vegetable
intake across all age groups of the population that gardens; age-specific intake rates are not
available in the EFH for homegrown exposed vegetable intake among gardening households.
Thus, age-specific intake rates are estimated by assuming that the ratios of age-specific intake to
total population intake for homegrown exposed vegetables for children in gardening households
would be the same as the ratios for intake of all exposed vegetables (i.e., not just homegrown
exposed vegetables, and not just gardening households), based on data from EFH Table 9-20 and
presented here in Table 4.
Table 4. Estimation of age specific per capita mean homegrown exposed
vegetable intake rates for children in gardening households
(g/kg-day) for four age ranges among children aged 1 to <11 years
Age
Total Population
1 to <2 yr
2 to <3 yr
3 to <6 yr
6to
-------
EF — Exposure frequency is 365 days per year for each age range because the intake rate
used in this example represents a long-term average daily intake over the entire year. (It does not
mean that contaminated homegrown exposed vegetables are consumed each day of the year;
instead, any intake that occurs during the year is averaged over the year to yield an average daily
rate.)
ED — Exposure duration is the length of time over which exposure occurs, in years. This
example assumes that a child is exposed continuously from ages 1 to <1 1 years. Thus, exposure
duration is assumed to be 1, 1, 3, and 5 years for the 1 to <2 year, 2 to <3 year, 3 to <6 year, and
6 to <1 1 year age ranges, respectively, for a total of 10 years.
AT — Because the chronic average daily dose is being calculated in this example, the
averaging time is equivalent to the exposure duration expressed in days. To determine this
value, 365 days/year is multiplied by the value of exposure duration for the given age range, and
summed for all age ranges.
2.1.4. Calculations
Using the dose algorithm and exposure factors shown above, the potential ADDhgexp-veging
for a child in a specific age range from consuming homegrown exposed vegetables is estimated
by applying eq 2 to the exposure factor data for that age range. The value of ADDhgexp-veging
depends on values established for IRhg exp-veg per capita mean-adj, Chgexp-veg, EF, ED, and AT. For
children within the four age ranges, Table 5 presents mean point estimates
Table 5. Summary of average daily dose of contaminant associated with
consumption of homegrown exposed vegetables (mg/kg-day) for four
age ranges among children in gardening households, aged 1 to <11
years
Dose Equation
Parameters and Output
Chgexpo-vegfag/g)
-itf-hg exp-veg per capita mean-adj
(g/kg-d)
£F(d/yr)
ED (yr)
AT(d)
ALfLfhg expo-veg ing
(mg/kg-d)
Age Ranges
1 to <2 yr
1.0 X ID"3
0.63
365
1
365
6.3 x 1(T4
2 to <3 yr
1.0 X 1Q-3
0.63
365
1
365
6.3 x 1(T4
3 to <6 yr
1.0 X 1Q-3
0.50
365
3
1,095
5.0 x 1(T4
6 to <11 yr
1.0 X ID"3
0.38
365
5
1,825
3.8 x 1(T4
22
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In the following calculation, the ADDs for each age group are averaged over the 10-year
time period representing ages 1 to <11 years.
[(,3 x
10"4S x lyr) + (6.3 x lO'4,
Kpl xlyr)+ (5.0 x]
LO~4F^ci x 3yr) + I3'8 x ]
LO"4S x 5yr)]
10 yr
_4
ing = 4.7 X 10
2.1.5. Uncertainties
The example here presents results for the mean per capita dose via homegrown exposed
vegetable ingestion for the population of children aged 1 to <11 years, in gardening households.
High-end dose may be estimated by replacing the mean intake rates with upper-percentile values,
or by using a high-end concentration with mean intake rates. The choice of which parameter
should be set to the high-end would be dependent upon the sensitivities of the parameters,
professional judgement, and regulatory requirements. U.S. EPA (201 la) and Phillips and Moya
(2012) provide information about converting upper-percentile consumer only intake rates to per
capita upper-percentile rates. If a bounding estimate is desired, both the concentration in the
homegrown exposed vegetables and the intake rates may be set to high-end or maximum values.
The estimate reflects per capita doses among children in households that garden. The per
capita data for the population that gardens includes both individuals who ate homegrown
exposed vegetables during the survey period as well as those that did not, but may eat
homegrown exposed vegetables at some other time during the year. The uncertainties associated
with this example include the source data for the intake rate and concentration data. The
concentration of the chemical will vary depending on preparation and cooking methods. The
intake data were collected more than 30 years ago and over a short period of 1 week for an
estimated 3,000 children in 4,300 households across the U.S. The extrapolation of a short survey
data over a long period adds to the uncertainty of the intake rate data. Therefore, these data may
not reflect current eating patterns and long-term distributions. These data were considered to be
collected using sound methodology and were considered to have a high degree of quality
assurance. Although the data were adjusted to account for preparation losses, there is added
23
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uncertainty in that adjustment factors based on a mixture of vegetables were used. This may not
always be representative of the mixtures of vegetables eaten by the population of interest. There
may also be uncertainties in the contaminant concentration as a result of sampling or analytical
methods.
2.2. INGESTION OF CONTAMINATED SOIL AND DUST IN AND AROUND THE
HOME: YOUNG CHILDREN AGED 1 TO <6 YEARS, CENTRAL TENDENCY,
LIFETIME AVERAGE DAILY DOSE
2.2.1. Introduction
Exposure via ingestion of soil and dust can occur in areas where soil contamination
exists. Indoor dust can also be contaminated with outdoor soil. Receptors could include all
children, especially those who spend time playing both outdoors, and indoors on the floor. The
dose via this exposure pathway is estimated based on the concentration of contaminants in
outdoor soils or indoor dust at or near the child's residence, the intake rate, exposure frequency,
and exposure duration. Young children are exposed to soil and dust primarily through hand-to-
mouth and object-to-mouth activities. As defined in the EFH (U.S. EPA, 201 la), soil and dust
are:
Soil. Particles of unconsolidated mineral and/or organic matter from the earth's
surface that are located outdoors, or are used indoors to support plant growth. It
includes particles that have settled onto outdoor objects and surfaces (outdoor
settled dust).
Indoor Settled Dust. Particles in building interiors that have settled onto objects,
surfaces, floors, and carpeting. These particles may include soil particles that
have been tracked or blown into the indoor environment from outdoors as well as
organic matter.
Outdoor Settled Dust. Particles that have settled onto outdoor objects and
surfaces due to either wet or dry deposition. Note that it may not be possible to
distinguish between soil and outdoor settled dust, since outdoor settled dust
generally would be present on the uppermost surface layer of soil.
In this example, exposure via ingestion of soil and dust is assumed and the central
tendency LADD from this pathway is evaluated for the population of young children who often
play outdoors, and crawl and play on the floor indoors, and handle toys or other objects that may
contain soil and/or dust (ages 1 to <6 years). The LADD is calculated because the contaminant in
24
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this scenario is assumed to be a carcinogen and the carcinogen toxicity values are expressed as
lifetime values; thus, the childhood exposure period must be spread over a lifetime.
Furthermore, it is assumed that the receptor population is not exposed to this carcinogen after
this exposure period.
2.2.2. Dose Algorithm
TheLADD of a specified contaminant via ingestion of contaminated soil and dust is
calculated as follows:
Csoil + dust XCF XlRsoil XEF XED
LADDsoil + dust ing (5)
where:
il + dusting = potential lifetime average daily dose from ingestion of soil and dust
(mg/kg-d);
dust = concentration of contaminant in soil and dust (mg/g);
CF = conversion factor of 0.001 g/mg;
IRsoii + dust = intake rate of soil and dust (mg/d);
EF = exposure frequency (d/yr);
ED = exposure duration (yr);
BW = average body weight (kg); and
LT = lifetime (d).
2.2.3. Input for Exposure Factor Variables
Csoil+(lust — The concentration of contaminants in soil and dust is either the measured level
of the chemical of interest or predicted concentration, based on modeling. For estimating central
tendency doses, the assessor typically uses an estimate of the mean or median concentration. For
this example, the estimated mean concentration of chemical "x" in soil and dust is
1 x icr3 mg/g.
CF — A conversion factor is required to convert between milligrams (mg) and grams (g),
0.001 g/mg to translate the intake rate to units of g/d.
IRsoii + dust — The recommended central tendency intake rate of soil and dust for young
children (1 to <6 years old) is 100 mg/d, (EFH Table 5-1).
25
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EF—This example uses an exposure frequency of 350 days per year, assuming that
young children are away from home (e.g., on vacation), the source of contamination, for two
weeks per year. The home and surrounding yard are assumed to be the only sources of
contamination.
ED—This example uses an exposure duration of 5 years (from age 1 to <6 years), based
on the assumption that after 5 years of age, children no longer play in outdoor soil or crawl on
the floor, and their soil and dust ingestion is limited compared to that of younger children.
BW—The average BWfor children between the ages of 1 and <6 years can be estimated
by calculating a time weighted average for children 1 to <2 years, 2 to <3 years, and 3 to
<6 years. These BWs are provided in EFH Table 8-1. The average BWfor 1 to <6 year old
children is 16.2 kg using the calculation shown below. This BWwas used in these example
calculations.
_ (ll.4 kg x 1 yr) + (13.8 kg x 1 yr) + (l8.6 kg x 3 yr)
~ 5yr
BW = 16.2 kg
LT—Because the contaminant used in this example is assumed to be a carcinogen, the
dose is averaged over the lifetime (i.e., the LADD is calculated). A lifetime (LT) of 70 years for
a member of the general population is used as a reference value. For use in the calculations, this
value is converted to 25,550 days (i.e., 70 years x 365 days/year).
2.2.4. Calculations
Using the dose algorithm and exposure factors shown above, the LADD son +dusting is
estimated as follows for the population of young children:
IxHT3^ x 0.001^- x 100^ x 350-^ x Syr
LADDsoil + dust ing = 16.2 kg x 25,550 d
dust ing ~ 4'2 X 10 kg.d
26
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2.2.5. Uncertainties
The example presented here is used to represent central tendency dose among a
population of young children, ages 1 to <6 years, via ingestion of soil and indoor dust. The high
end dose can be estimated by replacing the mean intake rate with a higher intake rate, or by using
a high-end concentration with a mean intake rate. The choice of which parameter should be set
to the high-end would be dependent upon the sensitivities of the parameters, professional
judgement, and regulatory requirements. If a bounding dose estimate is desired, the
concentration of contaminants may also be set to the maximum measured or modeled
concentration.
The uncertainties associated with this example scenario are mainly related to assumed
activity patterns of the receptor population and the input parameters used. Soil ingestion rates
are highly uncertain. Implicit in this scenario is that young children ages 1 to <6 years ingest soil
and dust at the same intake rate specified in the EFH (U.S. EPA, 201 la). It should be noted that
intake rate might decrease as activity patterns change with age. Also, the intake rate for children
in specific age ranges may not represent long-term behaviors and day-to-day and seasonal
variability. These input parameters are derived from data collected from a variety of studies
focused on soil ingestion with limited data on dust ingestion. The uncertainties associated with
this example are as follows: (1) the assumption is made that 100% of the soil and dust that the
children ingest comes from their home environment (i.e., it does not consider any portion of soil
intake that may come from time spent away from home such as at daycare or school, nor does it
consider difference in contaminant concentration from sources other than the home
environment); (2) the methodologies of the soil/dust intake studies are considered to have
limitations with numerous sources of measurement error; (3) the studies have limited
representativeness of the U.S. population; and (4) eight of the nine EFH supporting studies were
focused on soil or combined soil and dust ingestion with no, or very limited, focus on dust
ingestion. There may also be uncertainties in the contaminant concentration as a result of
sampling or analytical methods. The assessor should also consider the bioavailability of the
contaminant in soil and dust. The bioavailability will vary depending on the physicochemical
characteristics of the contaminant and the characteristics of the soil and dust (e.g., particle size).
27
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2.3. INGESTION OF CONTAMINATED INDOOR DUST: CHILDREN AT SCHOOL
AGED 6 TO <11 YEARS, CENTRAL TENDENCY, SUBCHRONIC AVERAGE
DAILY DOSE
2.3.1. Introduction
Indoor dust can become contaminated from a variety of sources (e.g., use of pesticides,
building materials, particle-bound contaminants infiltrating indoors from outdoors). The
exposure scenario for this example is ingestion of contaminated indoor dust at a school.
Receptors could include all school children. This example assumes that the outdoor soil is not
contaminated, and exposure occurs only to indoor dust at school. Dose via this pathway is
estimated based on the concentration of contaminants in indoor dust, the intake rate of indoor
dust, exposure frequency, exposure time, and exposure duration. In this example, exposure via
ingestion of indoor dust at school is assumed and the central tendency subchronic (<7 years)
average daily exposure from this pathway is evaluated for children ages 6 to <11 years. Values
obtained from tables within the EFH (U.S. EPA, 201 la) are cited as EFH Table X-X.
2.3.2. Dose Algorithm
The ADD of a specified contaminant via ingestion of contaminated dust by children at
school is calculated as follows:
Cdust X CF X IRdust XEF XET XED
ADDdust ina = (6)
dust mg , V !
where:
ADD dust mg = potential subchronic average daily dose of the contaminant from
ingestion of contaminated dust (mg/kg-d);
Cdust = concentration of the contaminant in the ingested dust (mg/g dust);
CF = conversion factor of 0.001 g/mg;
IRdust = average daily intake rate of dust for children aged 6 to <11 years (mg/d);
EF = exposure frequency (d/yr);
ET = exposure time (unitless fraction representing the portion of the day spent
in school);
ED = exposure duration (yr);
BW = average body weight (kg); and
AT = averaging time (d).
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2.3.3. Input for Exposure Factor Variables
Cdust—The concentration of contaminants in indoor dust is either the measured level of
the chemical of interest in the indoor dust or predicted concentration, based on modeling. For
estimating central tendency doses, the mean or median values would be used. In this example, it
is assumed that the mean concentration of chemical "x" in indoor dust is 1 x 1CT3 mg/g.
CF—A conversion factor is required to convert between milligrams and grams,
0.001 g/mg.
IRdust—The recommended central tendency intake rate of indoor dust for young children
(6 to <11 years old) is 60 mg/day (EFH Table 5-1; U.S. EPA, 201 la).
EF—School is in session for approximately 37 weeks/year or 185 days/year. The school
is assumed to be the only source of contamination.
ET—For "doers-only", the average time spent in school for 6 to <11 year-old children is
approximately 400 minutes/day (i.e., 6.7 hours/day) (EFH Table 16-17). Since dust ingestion
only occurs during waking hours, the fraction of time spent in school should be based on waking
hours and not on 24 hours. Children 6 to <11 years spend 613 minutes/day or 10 hours/day
sleeping or napping (EFH Table 16-25; U.S. EPA, 201 la). Thus, these children are awake
approximately 14 hours/day (24 hours/day - 10 hours/day). Assuming that 6.7 hours/day during
the time they are awake is spent at school, 0.48 of the day (i.e., 6.7/14) is spent in school where
they may be ingesting indoor dust. The school is assumed to be the only source of
contamination.
ED—Exposure duration is the length of time over which the exposure occurs. In this
example, an ED of 5 years (from age 6 to <11 years) is used. It is assumed that the children
attend the contaminated school the entire 5 years.
BW— The average BWfor children from 6- to <11-years old of 31.8 kg EFH Table 8-1
(U.S. EPA, 2011 a).
AT—Because the subchronic ADD is being calculated in this example, the averaging
time is equivalent to the exposure duration. The averaging time of 5 years is converted to
1,825 days for this calculation (i.e., 5 years x 365 days/year).
29
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2.3.4. Calculations
Using the dose algorithm and exposure factors shown above, the ADDdust is estimated
as follows for the population of children:
(1 x 1(T3) x 0.001^- x 60^ x 185 - x 0.48 x Syr
31.8kg x 1,82 5 d
ADDdustin0 = 4.6 x
2.3.5. Uncertainties
The example presented here is used to represent central tendency dose among a
population of school children, ages 6 to <1 1 years, via ingestion of indoor dust. For high-end
estimates, a combination of upper-percentile and central tendency inputs would be used. The
choice of which parameter(s) should be set to the high-end would be dependent upon the
sensitivities of the parameters, professional judgement, and regulatory requirements. If a
bounding dose estimate is desired, both the intake rate and the concentration of contaminant may
be set to the upper-percentile values. It is important to note that the bounding estimate results in
dose estimates that may be unreasonably high for the population of interest.
The uncertainties associated with this example scenario are mainly related to assumed
activity patterns of the receptor population and the input parameters used. This scenario
represents a central tendency dose; higher exposures may occur depending on activity patterns.
Implicit in this scenario is that school children ages 6 to <1 1 years ingest indoor dust at the same
intake rate specified in the EFH (U.S. EPA, 201 la). It should be noted that intake rates might
decrease as activity patterns change with age. The periods studied may not represent long-term
behaviors, and day-to-day and seasonal variability were not well characterized. These input
parameters are derived from data collected from a variety of studies. The uncertainties
associated with this example are as follows: (1) the methodologies of the dust intake studies are
considered to have limitations with numerous sources of measurement error; (2) the dust intake
studies have limited representativeness of the U.S. population; and (3) eight of the nine dust
intake studies were focused on soil ingestion with no, or limited, focus on dust ingestion. These
30
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facts make it difficult to characterize the individual contributions from soil and dust to the total
intake.
The assessor may also consider the bioavailability of the contaminant in soil and dust.
The bioavailability will vary depending on the physicochemical characteristics of the
contaminant and the characteristics of the dust (e.g., particle size). Also, this scenario assumes
that the contaminant is not present in outdoor soils and that children are not exposed to the
contaminant in soil or dust outside the school environment. This may be true for some
contaminants, however, indoor dust will often be a mixture of outdoor soils and indoor sources.
Children who participate in after-school programs may spend more time at school. In those
cases, it would be appropriate to use a higher number of hours spent at school to estimate the ET.
It should be noted that the contaminant may be brought into other microenvironments (e.g.,
home) on the children's body, shoes, or clothing, in which case adjustments to theETbased on
the fraction of time spent in school would not be appropriate. In addition, the approach used
here assumes that dust ingestion occurs at a steady rate throughout the time that one is awake.
The supporting studies are not detailed enough to show if this is true. For a more reliable dose
estimate, a study would need to be conducted to specifically estimate the indoor dust intake rate
for children. This scenario only considers exposure via dust ingestion, dermal exposure may also
be a concern and would need to be evaluated.
2.4. INGESTION OF AN ENVIRONMENTAL CONTAMINANT BY NONDIETARY
HAND-TO-MOUTH BEHAVIORS: INFANTS AND TODDLERS 3 MONTHS TO
<2 YEARS, BOUNDING, ACUTE DOSE RATE
2.4.1. Introduction
Infants and toddlers exhibit a high frequency of hand-to-mouth and object-to-mouth
behaviors. In instances where infants and toddlers are playing in a contaminated room, they may
be exposed to contaminants through mouthing of contaminated surfaces and objects and/or
transferring contaminants from surfaces to their hands and subsequently into their mouths.
Potential exposure to contaminants by nondietary hand-to-mouth and object-to-mouth behaviors
may occur, for example, after use of a sprayed biocide or household cleaning product. This
example estimates bounding acute dose via ingestion of contaminants through hand-to-mouth
behaviors for infants and toddlers ages 3 months to <2 years. Values obtained from tables within
the EFH (U.S. EPA, 201 la) are cited as EFH Table X-X.
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2.4.2. Dose Algorithm
Dose via this pathway would be calculated as follows:
"•LJ "hand-to-mouth ing ~
\Csurface * C*hand-to-mouth * CSAhands]x[TEs/fX TEHMX ET X EF X ED\
BWXAT ^ '
where:
ADRhand-to-mouth ing = acute potential dose rate from contaminated surface (mg/kg-d);
Csurface = contaminant loading on surface (mg/cm2);
CRhand-to-mouth = contact rate (contacts/hr);
CSAhands = contact surface area of hand (cm2/contact);
TEsH = transfer efficiency from surface to hand (%);
TEHM = transfer efficiency from hand-to-mouth (%);
ET = exposure frequency (hr/event);
EF = exposure frequency (events/d);
ED = exposure duration (d);
BW = average body weight (kg); and
AT = averaging time (d).
2.4.3. Input for Exposure Factor Variables
(•-surface—The contaminant loading on indoor surfaces can be measured or predicted based
on modeling the chemical of interest on a floor surface or object. For estimating the acute dose
in this example, the maximum value is used. For the purposes of the example calculations
shown below, it is assumed that the modeled maximum loading of chemical "x" on a surface is
1 xl(T6 mg/cm2.
CRfiand-to-mouih—The upper-percentile contact rate for children is presented in EFH
Table 4-1 (U.S. EPA, 201 la). In this example, the 95th percentile contact rates are used to
calculate the acute bounding dose. For children ages 3 months to <6 months, 6 months to
<12 months, and 1 year to <2 years, the 95th percentile contact rates are 65, 52, and 63 contacts
per hour, respectively. The weighted average of these contact rates is 60 contacts per hour and is
calculated as follows:
32
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CR
hand-to-mouth
y.,r contacts „ \ /r~ contacts .. \
(65—j^— x3moj + (52—^— x6moj
/„ contacts . _ \
(63 —r x 12 mo 1
21 mo
CR
hand-to-mouth
= 60
contacts
~hr
CSAhands—The surface area for body parts is presented in EFH Table 7-2 (U.S. EPA,
201 la). In this example, mean surface areas are used because surface area and BWare strongly
correlated and the mean values are most representative of the surface area of individuals with an
average BW. For children 3 months to <6 months, 6 months to <12 months, and 1 year to
<2 years the mean contact surface areas (CSA) for hands are 0.020, 0.024, and 0.030 m2 per
contact, respectively. A square meter is converted to square centimeters using the conversion of
1 m2 = 10,000 cm2. For this example, the contact surface areas used to calculate the weighted
average CSA are 200 cm2 for 3 months to <6 months, 240 cm2 for 6 months to <12 months, and
300 cm2 for 1 year to <2 years. It is assumed that the contact surface area is 100% of the hands
for children. The weighted CSAhands is 269 cm2 and is calculated as follows:
CSA
hands
lY-oo CIT1
^UU cont
act X *mo) +
(°nn cm
^UU conta
/0 cm2
V 1 7 mn I
ct /
x 6moj +
21 mo
CSA
hands
= 269
cnr
contact
TEsH—The transfer efficiency (TEsn) from surface to hand is 14%, as estimated in EFH
Table 7-27 (U.S. EPA, 201 la). This is the highest transfer efficiency reported by Cohen-Hubal
et al. (2005) from a study in which adult volunteers contacted surfaces treated with nontoxic
fluorescent tracer material to estimate the percentage transferred from a variety of surface types
by the hands under a variety of conditions. This maximum value represents the initial surface
contact with "sticky" hands.
T£HM—The transfer efficiency from hand-to-mouth (also referred to as the saliva transfer
efficiency) is assumed to be 16%. This value is based on results reported by Kissel et al. (1998),
33
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who estimated the geometric mean transfer efficiencies from hand-to-mouth from thumb sucking
and finger mouthing to be 10.1% and 15.9%, respectively.
ET — The exposure time is assumed to be a one-time acute exposure. For the purpose of
this example, a 4-hour visit to a contaminated indoor space is assumed.
EF — The exposure frequency is assumed to be one event for acute exposure. This means
that residues are transferred to the hand during the day of exposure without washing and
reloading.
ED — The exposure duration is the length of time over which exposure occurs. For the
purposes of this example, the acute exposure duration is assumed to be 1 day.
BW—EFH Table 8-1 (U.S. EPA, 201 la) reports recommended values for BWs for
children. Using the age-specific mean BWs, the average BWs of 7.4, 9.2, and 1 1.4 kg are used
for the age ranges of 3 to <6 months, 6 to <12 months, and 1 year to <2 years, respectively. The
weighted average BWfor this example is as follows:
(7.4kg x 3 mo) + (9.2kg x 6 mo) + (ll.4kg x 12 mo)
BW = - — -
21 mo
BW = 10.2 kg
AT — Because the acute dose is being calculated, the averaging time is 1 day.
2.4.4. Calculations
Using the dose algorithm and exposure factors shown above, the potential ADR for
hand-to-mouth ingestion of a contaminant, ADR hand-to-mouthing, is estimated:
X !0- x 60 x 269 x
0.14 x 0.16 x 4--r x
4 no _ d
_
ins ~ 10.2 kg x 1 d
_4
^DRhand.to.mouthing = 1.4 x 10 — — -
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2.4.5. Uncertainties
The example demonstrates a bounding estimate of dose to infants and toddlers resulting
from exposure to contaminated surfaces. Central tendency doses may be estimated by replacing
the contact rates and concentrations with central tendency values (e.g., mean or median). The
high-end dose may be estimated by using a combination of mean and upper-percentile values for
the exposure factors. The choice of which parameter should be set to the high-end would be
dependent upon the sensitivities of the parameters, professional judgement, and regulatory
requirements.
The uncertainties associated with this example scenario are related to assumed activity
patterns and contact rates of the receptor populations. This is an acute scenario and the
maximum concentration was used. However, for other measures of dose (e.g., central tendency),
the variability in the chemical concentration in the different rooms of the house where the child
spends his/her time may need to be considered. The studies that derived the recommended
values for contact rates were conducted with very small sample sizes over short data collection
periods and in a small number of locations in the U.S. The data may not be representative of
long duration exposure or of large populations. In addition, the transfer efficiency studies were
conducted using adults with organic fluorescent tracers, rather than children. Chemical-specific
transfer efficiencies may differ from those assumed here. Transfer efficiency studies did not
evaluate surface-to-hand and hand-to-mouth transfer efficiency for particles such as dust.
Hand-to-mouth transfer efficiency was assumed to be 16%, and this value may vary depending
on the chemical as well as other factors. The scenario also assumes that there is a constant
loading of the contaminant into the hand after each mouthing event with no hand washing. In
reality, there may not be a constant replenishment of the chemical into the hand before each
mouthing event and the amount transferred to the mouth is a fraction of the loading that remains
from the prior insertion. Ozkaynak et al. (2011) developed a model to simulate frequent
mouthing events without contaminant replenishment which estimates soil and dust ingestion that
may be used to further refine this scenario example.
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2.5. EXPOSURE TIME OF INCIDENTAL INGESTION OF CONTAMINATED POOL
WATER TO REACH A REFERENCE DOSE LEVEL OF EXPOSURE: CHILDREN
AGED 6 TO <11 YEARS, BOUNDING
2.5.1. Introduction
Children may incidentally ingest chemicals in the water when swimming. This scenario
estimates how long it would take to exceed a reference dose (RfD) for children playing and/or
swimming in a swimming pool containing the chemical of interest. For the purpose of this
example, it is assumed that the chemical is well mixed in the pool water. Receptors in this
example include swimmers in swimming pools (i.e., owned privately, municipally, or by
schools). Values obtained from tables within the EFH (U.S. EPA, 201 la) are cited as EFH Table
X-X.
This example is designed to derive a daily exposure time that one could have over a
subchronic exposure duration, to a specified concentration, without exceeding the RfD. A
bounding dose for acute incidental ingestion of pool water is evaluated here for children aged 6
to <11 years. As a bounding estimate, it is assumed that the children swim every day (i.e.,
365 days/year) in the same pool, and the pool water is not drained or cleaned over the duration of
the exposure. In other cases, the assessor may want to solve the dose equation for the maximum
concentration to which the swimmer can be exposed without exceeding the RfD. In that case, the
assessor needs to assume an exposure time.
2.5.2. Dose Algorithm
The time-to-exceed a given dose via ingestion of contaminated pool water would be
calculated using the following dose equation (eq 8) rearranged to solve for exposure time and
replacing ADDwater ing with the RfD as shown in eq 9.
Cpool water x IRpool water x ET x EF X ED
ADDwater ing — BW x AT
ET _ - Wter ing x BW X AT
Cpoolwater x IRpoolwater x EF X ED
where:
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ering = potential average daily dose of the contaminant from ingestion of
contaminated pool water (mg/kg-d);
ing = reference dose (mg/kg-d);
i water = concentration of chemical in the pool water (mg/L);
i water = water intake rate (L/hr);
ET = exposure time (hr/d), length of time necessary to exceed the reference
for the chemical;
EF = exposure frequency (d/yr);
ED = exposure duration (yrs);
BW = average body weight (kg); and
AT = averaging time (d).
2.5.3. Input for Exposure Factor Variables
RfDwatering—A reference dose is an estimate (with uncertainty spanning perhaps an order
of magnitude) of a daily oral exposure to the human population (including sensitive subgroups)
that is likely to be without an appreciable risk of deleterious effects during a lifetime (U.S. EPA,
201 Ib). For the purposes of the example calculations shown below, it is assumed that the RJD of
chemical "x"is 1 x 1CT3 mg/kg-day.
BW—EFH Table 8-1 (U.S. EPA, 201 la) reports recommended mean values for BWs for
children. The age-specific mean BW for 6- to
-------
ED—Exposure duration is assumed to be 5 years.
2.5.4. Calculations
Using the dose algorithm and exposure factor inputs shown above, the ET would be
calculated as follows for children (ages 6 to <11 years):
(1 x 10~3)jj x 31.8kg x 1,825 d
ET = - ; - j -
O.l£j£ x 0.12 jp x 365^; x Syr
hr
2.5.5. Uncertainties
The example presented is used to represent bounding doses among a specific population
from the incidental ingestion of pool water. This scenario does not include dermal penetration or
inhalation dose, both of which may contribute to total exposure to pool water. Central tendency
doses may be estimated by replacing the intake rate and concentrations with mean or median
values. Also, exposure frequency may be replaced by mean values obtained from EFH
Table 16-1 (U.S. EPA, 201 la). High-end doses may be estimated by using a combination of
central tendency and upper-percentile values for the intake rates, concentrations, and exposure
frequency. The choice of which parameter should be set to the high-end would be dependent
upon the sensitivities of the parameters, professional judgement, and regulatory requirements.
The uncertainties associated with this example scenario are related to assumed activity
patterns and intake rates of the receptor populations and include uncertainties such as ingestion
differences due to playing or swimming behaviors. Implicit in this scenario is the assumption
that the child swimmer or wader actually consumes the chemicals in the pool water at the rates
specified. It also assumes that the child visits the same pool for all 5 years and that the same
chemicals are used in the pool for those 5 years. These assumptions are appropriate for the
bounding estimate, but may be unrealistic for other estimates (e.g., central tendency). Another
uncertainty is that RfDs are developed to represent chronic doses and may not be applicable to
subchronic doses. The intake rate of pool water has a high uncertainty, because the data
available are limited for this factor. The intake rate used in this assessment is 0. 12 L/hour as
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reported from only one study (U.S. EPA, 201 la). This study does not break out age ranges and
encompasses all children less than 16 years of age. It also is not considered representative of the
U.S. population.
2.6. INGESTION OF CONTAMINATED DRINKING WATER: CHILDREN AGED
<21 YEARS, DISTRIBUTION OF CHRONIC AVERAGE DAILY DOSE
2.6.1. Introduction
In areas where contaminated surface water or ground water is used as a source of
drinking water, there is the potential for contaminant exposure via ingestion of tap water. The
dose via ingestion of contaminated drinking water is estimated based on the concentration of
contaminants in the drinking water, the intake rate of drinking water, exposure frequency, and
exposure duration. In this example, exposure via ingestion of drinking water is assumed and a
distribution of chronic average daily doses from this pathway is evaluated for the population of
children, birth to <21 years. It is assumed that the children's community water is contaminated;
therefore, both the home and school drinking water supplies are contaminated, and the children
ingest contaminated water from birth (e.g., formula prepared with water) through childhood until
21 years of age. Values obtained from tables within the EFH (U.S. EPA, 201 la) are cited as EFH
Table X-X.
Instead of a point estimate, this example scenario uses a probabilistic method to estimate
the distributions of contaminant intakes in the exposed population. This approach is used to
demonstrate how a probabilistic method could be used to estimate a dose. It does not mean that
this is the only, or most appropriate, method for this scenario. Distributions are used to represent
the contaminant concentration and intake rates. All other input parameters are held constant at
their central values. The final output distribution is developed using a Monte Carlo simulation
with the Crystal Ball version 7 software.
2.6.2. Dose Algorithm
The ADDdrinking water ing resulting from consumption of contaminated drinking water, is
calculated for each age group as follows:
_ C drinking water x IRi x EF
ADDdrinkingwater — — — (10)
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where:
ADD drinking watering = potential chronic average daily dose from ingestion of
contaminated drinking water (ug/kg-d);
C drinking water = concentration of contaminant in contaminated drinking water
(Hg/mL);
IRi = intake rate of drinking water for age group /' (mL/kg-d);
EF = exposure frequency (d/yr);
ED, = exposure duration for age group /' (yr); and
AT = averaging time (d).
The ADDdriniang water ing can also be calculated as the average over all of the age ranges as
follows:
_ c drinking water * EF
X IR X
drinking water ,,„,
2.6.3. Input for Exposure Factor Variables
C drinking water — The concentration of contaminant in drinking water is either the measured
or predicted concentration based on modeling. For the purposes of this example, it is assumed
that a measurement survey of the contaminated drinking water produced a mean concentration of
1 |ig/mL with a standard deviation of 0.5 ug/mL. Contaminant concentrations in natural
environments typically are log normally distributed (Cullen and Frey, 1999), and this was
assumed for this example.
IRdrinking water — The distribution of intake rate of drinking water for ages birth to
<21 years are presented in EFH Table 3-19 (U.S. EPA, 201 la). These data are summarized in
Table 6 for 1 1 age ranges of children <21 years of age. These data are for consumers-only of
community water including both direct and indirect sources. Water consumption data are
positively skewed and have been found to be well represented by log-normal distributions
(Roseberry and Burmaster, 1992). The Crystal Ball version 7 software was used to fit the data to
log-normal distributions based on the mean and 90th percentile values.
EF — Exposure frequency is assumed to be 350 days per year for each age range. This is
equivalent to 50 weeks of living where the water is contaminated, and accounts for 2 weeks
away from the contaminated area for vacations. This value was held constant in the simulation.
40
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ED—Exposure duration is the length of time over which exposure occurs in each age
group expressed in years. For example, the 1- to <2-year age group has an exposure duration of
1 year. This value was held constant in the simulation.
AT—Because the chronic ADD is being calculated in this example, the averaging time is
equivalent to the exposure duration. This value was held constant in the simulation.
All input values are summarized in Table 7.
Table 6. Consumer-only estimates of direct and indirect water ingestion:
community water (mL/kg-day)
Age range
Birth to <1 mo
1 to <3 mo
3 to <6 mo
6 to <12 mo
1 to <2 yr
2 to <3 yr
3 to <6 yr
6 to <11 yr
11 to <16 yr
16 to <18 yr
18 to <21 yr
Sample
size
37
108
269
534
880
879
985
1,410
2,113
944
1,086
Mean
137a
119
80
53
27
26
21
17
12
10
11
Percentiles
10
IP
12a
7
5
4
4
3
2
1
1
1
25
65a
71
27
12
9
9
8
6
4
4
o
5
50
138a
107
77
47
20
21
17
13
8
8
7
75
197a
151
118
81
36
36
29
23
15
15
15
90
235a
228a
148
112
56
52
43
35
26
23
26
95
238a
285a
173a
129
75
62
52
47
35
30
36
99
263a
345a
222a
186a
109a
121a
83
78
62
47
58
"Estimates are less statistically reliable based on guidance published in the Joint Policy on Variance Estimation and
Statistical Reporting Standards on NHANES III and CSFII Reports: NHIS/NCHS Analytical Working Group
Recommendations (NCHS, 1993).
Source: U.S. EPA (201 la).
41
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Table 7. Input values by age range for ingestion of contaminated drinking
water
Age range
0 to <1 mo
1 to <3 mo
3 to <6 mo
6 to <12 mo
1 to <2 yr
2 to <3 yr
3 to <6 yr
6to
-------
Table 8. Average daily doses (ADD; ug/kg-day) from birth to 21 years of age
for ingestion of contaminated drinking water
Age range
0 to <1 mo
1 to <3 mo
3 to <6 mo
6 to <12 mo
1 to <2 yr
2 to <3 yr
3 to <6 yr
6to
-------
2.6.5. Uncertainties
Log-normal distributions were used to represent drinking water intake rates for the
purposes of this example because water consumption data have been found to be well
represented by log-normal distributions (Roseberry and Burmaster, 1992). The fitted
distributions were based on means and 90th percentiles; however, more accurate fits may be
possible using more data. Alternatively, the raw data could be used to derive empirical
distributions.
This scenario assumes that all of the ingested water is contaminated community tap
water. However, children may ingest water from other sources that are either not contaminated
or have different levels of contamination. The intake rates of drinking water in the EFH
(U.S. EPA, 201 la) are derived from the data collected over a short period of time (2 days). The
extrapolation to chronic intake in this example might introduce some degree of uncertainty and
would not account for variation in children activity levels due to seasonal changes over a long
timeframe of 21 years.
Information on uncertainty and variability and probabilistic risk analysis can be found in
Chapters 1 and 2 of the EFH (U.S. EPA, 201 la). The Monte Carlo simulation conducted for this
example scenario assumed that all variables were independent. However, drinking water intake
rates for the age groups may be positively correlated. This is because generally a high water
consumer at one age is likely to be a high water consumer at other ages. This positive
correlation may not be too strong at the young ages included in this example because children's
habits may change. This is a potential source of uncertainty in the simulation across all ages
(i.e., birth to <21 years). The correlations between variables can be defined in the Crystal Ball
version 7 program. To assess the possible uncertainty associated with the assumption of
independence, a second simulation was run assuming a correlation coefficient of 0.8 between the
drinking water intake rates for all age groups. The results did not change significantly.
The ADD could also be calculated using a deterministic approach. Assuming average
inputs for all exposure parameters, the central tendency point estimate would be:
X °-08 yr+(119 X 0.17 yr) + (80jj X 0.25 yr) + (53 X 0.5 yr) + (27j X 1 yr)
^ X 3 yr)]
_
^'-''-'drinking water — 7 66Q d
44
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ADDdrinkingwater= 17.9jig/kg-d
This ADD is similar to the central tendency estimate derived using the probabilistic
approach as shown in Table 8.
2.7. INGESTION OF CONTAMINATED HUMAN MILK: INFANTS AGED BIRTH TO
<12 MONTHS, HIGH-END, SUBCHRONIC AVERAGE DAILY DOSE
2.7.1. Introduction
For infants who are breastfed, the potential exists for intake of contaminants through
nursing. The mother may be exposed to contaminants through ingestion, inhalation, and dermal
absorption. In addition, the mother may have stores of contaminants in adipose tissue from past
exposures. These contaminants may reenter the maternal circulation during pregnancy or
nursing. Because of the high lipid content in human milk, contaminants that are lipophilic are
likely to be passed to a nursing child via this exposure pathway. The aqueous portion of human
milk also could allow transfer of hydrophilic contaminants to the infant. The potential receptors
are infants who consume human milk with no other milk substitutes. In this example, exposure
via contaminated human milk is assumed for infants who are breastfed from 0 to <12 months of
age. Covered are four age ranges (0 to <1, 1 to <3, 3 to <6, and 6 to <12 months). Values
obtained from tables within the EFH (U.S. EPA, 201 la) are cited as EFH Table X-X. According
to the EFH (U.S. EPA, 201 la), the potential subchronic daily dose for all four of the age ranges
should be calculated separately for each age range and then the weighted average calculated for
the entire age range for this scenario. In this example, the high-end dose of a lipophilic
contaminant is calculated using central estimates of the concentration of the contaminant in the
lipid portion of human milk, the upper-percentile lipid intake rates of human milk, the exposure
frequency, the exposure duration, and the averaging time.
2.7.2. Dose Algorithm
The ADD of a specified contaminant via ingestion of contaminated human milk is
calculated as follows:
x IRlipidhumanmilk x EF X £D
human milk ing ~7Z,
45
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where:
ADD human milk ing = potential subchronic average daily dose from ingestion of
contaminated human milk (mg/kg-d);
Cupid = concentration of contaminants in the lipid portion of contaminated
human milk (mg/g lipid);
IRhpid human milk = lipid intake rate of human milk for infants who are fed human milk
(g lipid/kg-d);
EF = exposure frequency (d/mo);
ED = exposure duration (mo); and
AT = averaging time (d).
2.7.3. Input for Exposure Factor Variables
Cupid—The concentration of a contaminant in the lipid portion of human milk is either the
measured or predicted concentration based on modeling, of the contaminant in this medium.
When estimating central tendency, the mean or median values would be used. For the purposes
of the example calculations shown below, it is assumed that the central tendency concentration
of chemical "x" in human milk is 1 x 1CT3 mg/g lipid.
IRiipidhuman mm—The upper-percentile intake rate of lipids from human milk for infants
from birth to <12 months of age can be estimated based on intake rate of lipids from human milk
for infants provided in EFH Table 15-1 (U.S. EPA, 201 la). The intake rates presented in this
table are normalized to BWand are calculated as the mean for each age range. It is assumed that
in the general population, each age group is equally represented. The recommended intake rates
are then converted from mL/kg-day to g/kg-day assuming the density of human milk is
1.03 g/mL (NAS, 1991). The lipid intake rates for human milk are summarized here in Table 9.
For the purpose of this example, intake rates for exclusively breastfed infants are used.
Exclusively breastfed infants are those whose sole source of milk comes from human milk, with
no other milk substitutes (U.S. EPA, 201 la). Also, it is assumed that the contaminant is only
present in the lipid portion of human milk.
46
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Table 9. Upper-percentile lipid intake rates from human milk
Age range
0 to <1 mo
1 to <3 mo
3 to <6 mo
6 to <12 mo
Lipid intake rate
(mL/kg-d)
8.7
8.0
6.1
5.2
Density-converted
lipid intake rate
(g/kg-d)
9.0
8.2
6.3
5.4
EF—Exposure frequency is 30 days/month.
ED—Exposure duration is the length of time over which the exposure occurs. For the
purpose of this example, it is assumed that infants are breastfed for the first year of life. After
that time, the infant's diet is changed. Thus, the exposure duration is equal to the number of
months within each age range.
AT—Because the subchronic ADD is being calculated in this example, the averaging
time is equivalent to the exposure duration. This value is converted to days using 30 days/month
for the purposes of this calculation and is different for each age range (Table 10).
2.7.4. Calculations
Using the dose algorithm (eq 12) and the input for the exposure factors shown above, the
potential ADDhuman milking from human milk ingestion is estimated for the individual age ranges.
Table 10. Summary of ADD of contaminant associated with human milk for
four age ranges among infants aged birth to <12 months
Equation 12
input and output
C(mg/g)
IR (g/kg-d)
EF (d/mo)
ED (mo)
AT(d)
ADD (mg/kg-d)
Age ranges
Oto
-------
'Human milk ing —
((9.0 x 10-3)j|| x 30 d) + ((8.2 x lO'3)^ x 60 dV
360 d
-3
ADDHumanmiiking = 6.4 x 10 — — -
2.7.5. Uncertainties
The example presented here represents a high-end exposure scenario for the receptor
population of infants 0 to <12 months of age who are breastfed. Central tendency and bounding
dose estimates also can be derived from the data in Tables 9 and 10 using all central tendency or
all upper-percentile input values, respectively.
This scenario specifies that a population of infants is breastfed the first year of life, using
weight-averaged intake rates for human milk specified in the EFH (U.S. EPA, 201 la). It also is
assumed here that the contaminant concentration is constant in human milk composition;
however, studies have shown that contaminant concentrations may be affected by maternal
nutrition (U.S. EPA, 201 la). In addition, the concentration of the chemical may decline as
lactation continues and the mother's body burden declines.
This scenario also assumes a measured concentration. Models used to estimate human
milk concentrations introduce additional uncertainties. Description of these models can be found
in EPA'sHuman Health Risk Assessment Protocol (HHRAP)for Hazardous Waste Combustion
Facilities (U.S. EPA, 2005d). Another assumption in this scenario is that the exposure is to the
contaminant dissolved in the lipid portion of the human milk. However, some of the
contaminant may also be present in the nonlipid portion of the human milk which is not
considered here. The intake rate estimates are a source of uncertainty because they are based on
studies from 1980-2000, where participants were white in the mid-to-upper socioeconomic
classes. The intake rates are based on studies that have small sample sizes and cover short time
periods. These may not be a good representation of intake rates over longer periods of time.
Finally, there is uncertainty in the lipid content correction. It has been reported that the lipid
48
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content of human milk varies with the length of time of nursing and increases from the beginning
(foremilk) to the end (hindmilk) of the nursing session (NAS, 1991).
2.8. INGESTION OF CONTAMINATED RECREATIONAL ATLANTIC MARINE
FINFISH: CHILDREN AGED 3 TO <6 YEARS, CENTRAL TENDENCY,
SUBCHRONIC AVERAGE DAILY DOSE
2.8.1. Introduction
There is the potential for contamination of finfish and shellfish as a result of
bioaccumulation of certain types of chemicals (e.g., methylmercury and lipophilic compounds
such as dioxins and PCBs) in fish tissues. This may result in exposure among the general
population via consumption of marine or freshwater fish. Receptors could include children of
any age who consume contaminated fish. In this example, the dose via consumption of
contaminated recreationally caught Atlantic marine finfish is estimated based on the
concentration of chemicals in Atlantic marine finfish, intake rates of recreationally caught
Atlantic marine finfish, exposure frequency, and exposure duration. In this example, central
tendency subchronic average daily doses via ingestion of recreationally caught Atlantic marine
finfish are evaluated for children (3 to <6 years of age) residing in a contaminated area. Values
obtained from tables within the EFH (U.S. EPA, 201 la) are cited as EFH Table X-X.
2.8.2. Dose Algorithm
The ADD of a specified contaminant via ingestion of contaminated marine finfish can be
estimated as follows:
Cfish x IRfish XEF XED
ADDfishina= — - - - (13)
fisnmg \ }
where:
ADD fmh mg = potential average daily dose from ingestion offish caught at a
contaminated site (mg/kg-d);
Cfish = concentration of a contaminant in uncooked fish (mg/g fish);
IRfish = intake rate of uncooked recreational Atlantic marine finfish for the
population of interest (g/d);
EF = exposure frequency (d/yr);
ED = exposure duration (yr);
49
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BW = average body weight (kg); and
AT = averaging time (d).
2.8.3. Input for Exposure Factor Variables
C — The concentration of a contaminant in Atlantic marine finfish is either the
measured or predicted concentration, based on modeling. For estimating central tendency doses,
the mean or median values would be used. For the purpose of the example calculations, it is
assumed that the mean concentration of chemical "x" in uncooked fish is 1 x 1CT3 mg/g.
IRfish — Survey data for Atlantic marine finfish intake rates for children are relatively
limited. However, a recommended mean consumption of recreationally caught Atlantic marine
finfish for children 3 to < 6 years of age is 2.5 g/day, as measured uncooked, is provided in EFH
Table 10-3. The value represents both survey anglers who ate recreational fish during the survey
period and those that did not, but may eat recreationally caught fish during other periods. EFH
Table 10-3 (U.S. EPA, 201 la) provides intake rates in terms of the wet weight mass of uncooked
fish. The assessor should ensure that measurements of the contaminant concentration in fish also
are on an uncooked, wet weight basis.
EF — Exposure frequency is 350 days/year because the data used in estimating IRflsh are
assumed to represent average daily intake over a long term (i.e., over a year). However, it is
assumed that the children are away from the contaminated source (i.e., on vacation) for 2 weeks
during the year.
ED — Exposure duration is the length of time over which exposure occurs. This example
assumes that children consume recreationally caught marine finfish for only the 3 years of life
indicated.
BW—EFH Table 8-1 (U.S. EPA, 201 la), reports recommended values for BWs for
children aged 3- to <6-years old. The mean BWfor children in this age group is 18.6 kg.
AT — Because the subchronic ADD is calculated in this example, the averaging time is
equivalent to the exposure duration. Thus, ATis 1,095 days (i.e., 3 years).
2.8.4. Calculations
(1 x 1(T3)^ x 2.5f x 350-^ x Syr
ADD, ish inq = - - - - -
7 3 18.6 kg x 1,095 d
50
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ADDfishing = l.3 X 10
-4
kg-d
2.8.5. Uncertainties
The example presented here is used to represent central tendency doses among children,
aged 3 to <6 years, via consumption of contaminated recreationally caught Atlantic marine
finfish. High-end doses may be estimated by replacing the mean intake rate with an
upper-percentile value or by using a high-end concentration and mean intake rate. The choice of
which parameter should be set to the high-end would be dependent upon the sensitivities of the
parameters, professional judgement, and regulatory requirements. In addition, if a bounding
dose estimate is desired, the concentration in fish also may be set to the maximum measured or
modeled concentration. It is important to note that the bounding estimate may result in a dose
estimate that is unreasonably high for the population of interest.
Uncertainties associated with this example scenario are related to assumed activity
patterns of the receptor population and the input parameters used. Implicit in this scenario are
the assumptions that children, aged 3 to <6 years, remain living near the site of contamination
over that timeframe and consume only Atlantic marine recreationally caught finfish that were
obtained from the contaminated site. As an alternative, a term denoting the fraction offish
assumed to be obtained from the source area could be included in the dose algorithm. Ideally,
both concentration and intake rate data on a species-specific basis would be preferred. However,
reliable estimates of species-specific intake rates are rarely available.
In this example, a single value for the average contaminant concentration in fish is used
to estimate central tendency subchronic dose. This assumes that the average concentration of the
fish consumed is equal to the sample/modeled average concentration. The variability in average
contaminant concentration in fish might introduce some degree of uncertainty. In reality, the
contaminant concentration may vary with the species offish. Variability may result from
differences in bioaccumulation of contaminants in different fish species, and in fish differing in
size and placement in the food chain. Finally, the intake rate value associated with this scenario
is derived from short-term consumption survey data used to estimate the distribution of the fish
intake rate over a long period. There are no adjustments made for losses that may occur during
preparation and cooking. The choice of using uncooked or as-consumed intake rate also depends
51
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on how the contaminant concentration is reported. It is more conservative to use the uncooked
intake rate values in this scenario; however, if the as-consumed information is desired, data are
presented in EFH Table 13-69 (U.S. EPA, 201 la) to adjust the intake rate for moisture and fat
loss during preparation.
In some instances, it also may be necessary to convert wet weight (either as-consumed or
uncooked) intakes to dry weight intakes, or to convert wet weight into lipid weight intake rates
(i.e., whichever state of preparation was used in the study reporting contaminant concentrations
should also be used for the intake rates). The equations used in these conversions are presented
in EFH Section 10.9 (U.S. EPA, 201 la). Below are the equations and sample calculations for
converting the 2.5 g/day wet weight of uncooked fish used in this scenario to dry weight and to
lipid weight. For these sample calculations, the average moisture and lipid contents for all
marine fish and shellfish species from EFH Table 10-125 were calculated (U.S. EPA, 201 la).
The average moisture and lipid content for all marine fish and shellfish species were 75.54% and
4.05%, respectively. The dry weight intake rate (g/day) is calculated by
/100-MA
IRdw = IRWW —- (14)
where:
IRdw = dry weight intake rate (g/d);
IRww = wet weight intake rate (g/d); and
W = percentage water content (%).
g/100-75.54
"^ = 2-5!( 100
IRdw = 0.61 |
The lipid weight intake rate (g/day) is similarly calculated by:
IRlw = IRWW (^) (15)
where:
= lipid weight intake rate (g/d);
IRWW = wet weight intake rate (g/d); and
52
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L = percentage lipid (fat) content (%).
IRlw = 1.0 x 10-1 f
d
53
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3. EXAMPLE INHALATION EXPOSURE SCENARIOS
Inhalation of a contaminant is not necessarily a simple function of inhalation rate and
BW. The amount of chemical that reaches the target organ is highly dependent on the human
respiratory anatomy and physiology and the physicochemical properties of the contaminant
(U.S. EPA, 2009). Current EPA methodology uses the principles of inhalation dosimetry to
determine the human equivalent concentration (HEC) for calculating anRfC or IUR (U.S. EPA,
2009, 1994). To apply the RfC methodology, it is unnecessary to calculate an inhaled dose when
using toxicity values from the Integrated Risk Information System (IRIS) in a risk assessment.
To estimate risk via inhalation, EPA recommends the use of the concentration of the chemical in
air as the exposure metric (e.g., mg/m3), rather than inhalation intake of a contaminant in air
based on intake rate and BW(e.g., mg/kg-d). Inhalation risk assessments require an air
concentration adjusted to represent a continuous exposure. The risk calculations are different for
noncarcinogens and carcinogens:
• For noncarcinogens, RfCs are used. These are expressed in concentration units. The RfC
methodology uses the measured or modeled concentration of the chemical in the inspired
air, adjusted to represent a continuous exposure.
• For carcinogens, IRIS uses unit risk values. These are expressed in inverse concentration
units. In this approach, the unit risk is multiplied by the measured or modeled
concentration of the chemical in the inspired air adjusted to represent a continuous
exposure (U.S. EPA, 1994).
Advances in inhalation gas dosimetry show some evidence of higher inhaled doses in
young children (i.e., 3 months) than in adults (U.S. EPA, 2012c). This life stage may warrant
alternative modeling approaches or adjustments based on chemical-specific information. More
information about advances in inhalation gas dosimetry and life stages can be found in EPA's
Advances in Inhalation Gas Dosimetry for Derivation of a Reference Concentration (RfC) and
Use in Risk Assessment (U.S. EPA, 2012c).
Example Exposure Scenarios 3.1 and 3.2 demonstrate how the adjusted air concentrations
may be calculated. Although EPA recommends the use of the chemical concentration in air as
the exposure metric, there may be cases where an inhalation dose is of interest. Estimations of
cumulative doses or analyses of relative pathway contributions are examples where an inhaled
54
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dose may be necessary. Example Exposure Scenarios 3.3 and 3.4 demonstrate the use of
inhalation rates to fully calculate the ADR and ADD, respectively.
3.1. INHALATION OF CONTAMINATED AIR WHILE PLAYING IN A SCHOOL
YARD: SCHOOL CHILDREN AGED 6 TO <11 YEARS, CENTRAL TENDENCY,
SUBCHRONIC ADJUSTED AIR CONCENTRATION
3.1.1. Introduction
Contaminants may be released into the outdoor air from industrial sources or
transportation. This may result in exposure via inhalation by residents, commercial/industrial
workers, students, and recreational populations. The following is an example of an inhalation
exposure estimate for elementary school-age children 6- to <11-years old exposed to
contaminated outdoor air while playing in a school yard. Central tendency subchronic daily
exposure from inhalation is evaluated for this population. This approach would be used in
conjunction with subchronic toxicity values to characterize risk of adverse noncancer health
effects. In this example, the outdoor air concentration is adjusted for the time children spent in
school to reflect a continuous exposure. Values obtained from tables within the EFH (U.S. EPA,
201 la) are cited as EFH Table X-X.
3.1.2. Exposure Algorithm
Adjusted outdoor air concentration via inhalation of contaminated air while playing in a
school yard would be calculated as follows:
_ ^outdoor air x ET X CF X EF X ED
^^outdoor air adjusted ,,„,
where:
ECoutdoor air adjusted = adjusted exposure concentration of contaminant in the outdoor air
(mg/m3);
Coutdoor air = concentration of contaminant in the outdoor air (mg/m3);
ET = exposure time (min/d);
CF = conversion factor (d/min);
EF = exposure frequency (d/yr);
ED = exposure duration (yr); and
AT = averaging time (d).
55
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3.1.3. Input for Exposure Factor Variables
C outdoor air — The concentration of contaminant in air at the site is either the measured or
predicted concentration based on modeling, of the chemical of interest in the air at the site of
interest. For estimating central tendency exposures, the mean or median values are used. For the
purposes of this example, it is assumed that the mean measured concentration of chemical "x" in
air is 1 x 1CT3 mg/m3.
ET—EFH Table 16-19 (U.S. EPA, 201 la) reports the age-specific time spent on the
playground at school for "doers-only." The mean exposure time (ET) is 80 minutes/ day for
children aged 6 to <1 1 years.
CF — The conversion factor needed to convert the exposure time of minutes to days is
1 day/1,440 minutes.
EF — For this example, exposure frequency is assumed to be 185 days/year. This is
equivalent to 37 weeks of full-time school, and accounts for 15 weeks off for summer and winter
vacation, or other school closings.
ED — Exposure duration is the length of time over which exposure occurs. For the
purposes of this example, the ED for 6- to <1 1-year-old school children is assumed to be 5 years
(i.e., first grade through fifth grade). This assumes that the exposure occurs in the same school
yard where outdoor air contamination exists.
AT — The averaging time is equivalent to the exposure duration because this example
assumes the assessor is evaluating risk of noncancer health effects. For the purposes of this
example, the^Tis converted to 1,825 days (i.e., 5 years x 365 days/year).
3.1.4. Calculations
Using the exposure algorithm and the input for the exposure factor variables, the
'outdoor air adjusted f°r elementary school-age children would be as follows:
„ .^.-^ o^ Id . _r d r
1 x 10 x 80— x 1)44Qmin x 185- x Syr
£ ^outdoor air adjusted *
c
- _ 9 R V 1 n~5 _ —
^ outdoor air adjusted ~ ^•° •*• -LU 3
56
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3.1.5. Uncertainties
The example presented here represents a central tendency adjusted air concentration of
contaminant reflecting the inhalation exposures of the general population of elementary school
children playing in a school yard. A high-end adjusted exposure concentration may be estimated
by using a high-end concentration and also increasing exposure time or exposure frequency.
Caution should be used, however, in setting all exposure factor inputs to upper-percentile values,
as the resulting dose estimates may exceed reasonable maximum exposures for the population of
interest. The choice of which parameter should be set to the high-end would be dependent upon
the sensitivities of the parameters, professional judgement, and regulatory requirements.
The uncertainties associated with this example scenario are related to the concentrations
and assumed exposure time and exposure frequency. Uncertainty related to seasonal and
weather variations (e.g., temperature, wind direction and strength) may lead to overestimates or
underestimates of exposure. An underestimate of exposure concentration may also occur if the
contaminant migrates from outdoors to indoors, resulting in additional exposures. This
calculation does not account for these additional potential exposures, season or weather
variations.
3.2. INHALATION OF AEROSOLIZED CONTAMINANTS FROM WATER DURING
AND AFTER SHOWERING: CHILDREN AND TEENS AGED 6 TO <18 YEARS,
CENTRAL TENDENCY, LIFETIME ADJUSTED AIR CONCENTRATION
3.2.1. Introduction
Because volatile contaminants can be released into the air from contaminated water, there
is the potential for exposure among residents via inhalation during and after showering. In this
example, the lifetime average adjusted exposure concentration from this pathway is evaluated for
children and teens aged 6 to <18 years. It should be noted that exposures can also result from
inhalation during other water uses around the household as well as dermal exposures. This
scenario, however, focuses on the exposures via inhalation during and after showering. The
approach below would be used for carcinogen exposure when using chronic toxicity values (e.g.,
from IRIS) in a risk assessment. It is assumed that children move away from the contaminated
source after age 18 (e.g., moving away to attend college). Values obtained from tables within the
EFH (U.S. EPA, 201 la) are cited as EFH Table X-X. If this is a mutagenic carcinogen,
57
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appropriate ADAFs would need to be applied in accordance with Supplemental Guidance for
Assessing Susceptibility from Early-Life Exposure to Carcinogens (U.S. EPA, 2005b).
3.2.2. Exposure Algorithm
The adjusted exposure air concentration (ECair adjusted) via inhalation would be calculated
as follows:
_ Cair X ET X CF X EF X ED
air adjusted , „, \*- ')
Li I
where:
ECair adjusted = adjusted exposure concentration of contaminant in the air during and
after showering (mg/m3);
Cair = concentration of contaminant in the air during and after showering
(mg/m3);
ET = exposure time (min/d);
CF = conversion factor (d/min);
EF = exposure frequency (d/yr);
ED = exposure duration (yr); and
LT = lifetime (d).
3.2.3. Input for Exposure Factor Variables
Cair—The concentration of contaminants in air is either the measured or predicted
concentration based on modeling, of the chemical of interest in the air of the shower room. For
estimating central tendency exposures, mean or median values are used. For the purposes of this
example, it is assumed that mean measured concentration of chemical "x" in air is
1 x icr3 mg/m3.
ET—Exposure time is the estimated time spent showering and in the bathroom after
showering occurs. EFH Table 16-29 (U.S. EPA, 201 la) presents the estimated time spent
showering and time spent in the shower room immediately following showering. For the
purpose of this example, the mean ETfor children ages 6 to <11 years is 24 minutes/day and for
teens ages 11 to <16 years is 26 minutes/day. Although the Guidance on Selecting Age Groups
for Monitoring and Assessing Childhood Exposures to Environmental Contaminants (U.S. EPA,
2005a) recommends 16 to < 21 years as the next age group for children, for this scenario it was
58
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assumed that children moved away from the contaminated source at age 18. Time spent in the
shower and immediately following showering is not available for children 16 to < 18 years.
Therefore, the value for 16 to < 21 years (i.e., 28 minutes/day) is used in this example. The
average of the two 5-year and the 2-year age ranges is calculated as:
(24^p x 5 yr) + (26^p x 5 yr) + (28^p x 2 yr)
** *~\
mm
ET = 25.5 —-
CF—The conversion factor needed to convert the exposure time of minutes to days is
1 day/1,440 minutes.
EF—Exposure frequency is the number of times an exposure is expected to occur in a
year and is expressed in days/year. For the purposes of this example, it is assumed that children
shower 350 days of the year (i.e., once per day) assuming that they are away from the
contaminated sources for approximately 2 weeks out of the year.
ED—Exposure duration is the length of time over which exposure occurs. For the
purpose of this example, the ED is 5 years for the first two life stages and 2 years for the third
life stage, i.e., 12 total years.
LT—The averaging time is equivalent to the lifetime of an individual in the receptor
population because this example calculates the average exposure air concentration over a
lifetime. For the purpose of this example, the average lifetime of 70 years for men and women is
used because the exposure is assumed to reflect the general population. The value is converted
to 25,550 days (i.e., 70 years x 365 days/year).
3.2.4. Calculations
Using the exposure algorithm and exposure factor inputs shown above, the EC air adjustedfor
children and teens during and after showering would be as follows:
v 10-3 x 255^ X ld x S50— X 12
_ x 1U jm3 x Zb.b d x 1)44Qmin x JbUyr x l^
ECair adjusted- 25,550 d
59
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_6m§
ECaif adjusted = 2.9 X 10 —j
3.2.5. Uncertainties
The example presented here is used to represent a central tendency adjusted air
concentration for children and teens from exposure via inhalation to contaminated air during and
after showering. An adjusted air concentration, based on high-end exposures may be estimated
by using a combination of mean and upper-percentile values for the exposure factors. The
choice of which parameter should be set to the high-end would be dependent upon the
sensitivities of the parameters, professional judgement, and regulatory requirements. If a
bounding dose estimate is desired, the concentration of contaminants may be set to the maximum
measured or modeled concentrations.
Uncertainties in this scenario relate to assumptions regarding the concentration variable
used in the calculation. It was assumed that the concentration will be steady. It is unclear how
well the average concentration of contaminant in indoor air represents the true time weighted
average. This example assumes that the concentration was measured. Assessors typically
estimate a different concentration in the shower stall than in the bathroom immediately after
showering using models; however there are uncertainties with the models used to estimate these
concentrations. The concentration will vary depending on various factors including for example:
water temperature, volatility of the chemical, bathroom size, use of exhaust fan, water flow
rate—just to name a few. This scenario also assumes that children are not exposed to the
contaminant at other locations where they may spend their time. Another uncertainty relates to
the amount of time spent showering and in the shower room immediately after. This example
assumes that children take showers instead of baths. The time spent taking baths will be slightly
higher than the time spent taking showers. It also assumes that children take one shower per day.
3.3. INHALATION OF CONTAMINATED INDOOR AIR: RESIDENTIAL CHILDREN
AGED 3 TO <11 YEARS, BOUNDING, ACUTE DOSE RATE
3.3.1. Introduction
At sites where localized volatile contaminants intrude into residences either from the use
of contaminated water in the household or from the use of commercial products or other
materials results in indoor air contamination, there exists the potential for exposure among
60
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residents via inhalation. In this example, a one-time exposure via inhalation of contaminated
indoor air is assumed and the bounding acute dose from this pathway is evaluated for children
aged 3 to <11 years playing at a residence. Values obtained from tables within the EFH (U.S.
EPA, 201 la) are cited as EFH Table X-X. An ADR is calculated in this example to be used as an
input in a cumulative dose estimate or a relative pathway contribution analysis. This inhalation
dose rate is not used to estimate risks. Risks from the inhalation pathway would be estimated by
calculating a time weighted average exposure concentration or a peak exposure concentration to
be used with an acute inhalation toxicity value. For chronic exposure scenarios, RfCs or lURs
would be used, as appropriate.
3.3.2. Dose Algorithm
The ADR via inhalation of contaminated indoor air is calculated as follows:
^indoorair x ET X 7J? X ED
indoor air inh .„,
where:
mdoor air ink = acute dose rate of contaminated indoor air (mg/kg-d);
ir = concentration of contaminants in the indoor air (mg/m3);
ET = exposure time (min/d);
IR = inhalation rate (m3/min-kg);
ED = exposure duration (d); and
AT = averaging time (d).
3.3.3. Input for Exposure Factor Variables
Cindoor air—The concentration of a contaminant in air is either the measured or predicted
concentration, based on modeling, of the chemical of interest in the air at the site of interest. For
estimating bounding doses, the maximum values would be used. For the purpose of the example
calculations, it is assumed that the modeled bounding concentration of chemical "x" in air from
the breathing zone is 1 x 10~3mg/m3.
ET—EFH Table 16-1 (U.S. EPA, 201 la) reports the age-specific time spent indoors at a
residence over a 24-hour period. This scenario represents a one-time exposure for children at
any age within the age range of 3 to <11 years. Therefore, a time weighted average exposure
61
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time was estimated to represent a child within that age range. The upper-percentile times are
1,355 minutes/day (22.6 hours/day) for ages 3 to <6 years and 1,275 minutes/day
(21.3 hours/day) for children ages 6 to <1 1 years. The weighted average of these is calculated as
follows:
(1,355= x 3yr) + (i,275^ x 5yr)
min
ET = 1,305—-
d
IR — The recommended inhalation rates on aBWbasis for children during short-term
exposures are given in EFH Table 6-18 (U.S. EPA, 201 la). For the purpose of this example, it is
assumed that the children spend some time sleeping and napping, some time playing at light
intensity, and some time sedentary. A weighted average inhalation rate is calculated using
inhalation rate data for each age range (i.e., 3 to <6 years and 6 to <1 1 years). Children age 3 to
<6 years spend an average of 681 minutes/day (11.4 hours/day) sleeping or napping (EFH
Table 16-25). Whereas children age 6 to <1 1 years spend 613 minutes/day (10.2 hours/day)
sleeping or napping. In this example, the rest of the time is apportioned equally between
sedentary and light activities for each age range (i.e., [(1,355 minutes/day
- 681 minutes/day) + 2 = 337 minutes/day] for children 3 to <6 years; and [(1,275 minutes/day -
613 minutes/day) -^2 = 331 minutes/day] for children 6 to <1 1 years). The 95th percentile
inhalation rate values for sleeping or napping are 3.5 x 10~4 mVminute-kg for children from age
3 to <6 years and 2.1 x icr4 mVminute-kg for children from age 6 to <1 1 years (EFH
Table 6-18). The 95th percentile sedentary inhalation rate values are 3.5 x 10~4 mVminute-kg for
children from age 3 to <6 years and 2.2 x 10~4 m3/minute-kg for children from age 6 to
<1 1 years. The 95th percentile inhalation rate values for a light intensity activity are 8.7 x 10~4
m3/minute-kg for children from age 3 to <6 years and 5.3 x 10~4 m3/minute-kg for children from
age 6 to <1 1 years. Using these values, the adjusted inhalation rate for activity intensity is
calculated below for each age range.
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to<6 —
>< «l ^ 3-5 x 10- x 337
" >< 10-4 x 337
1,355
= 4.8 x 1(
min-kg
^6 to< l"- ><
= 3.0 x 1(
min-kg
The weighted average IR is calculated as follows:
((4'8 x l°-4)=?kg- x 3yr) + ((3.0 x 10-)^ x Syr)
= 3.7 x 10~4
min-kg
ED — Exposure duration is the length of time over which exposure occurs. For the
purpose of this example, the exposure duration is assumed to be 1 day.
AT — Because the ADR is calculated in this example, the averaging time is equivalent to
the exposure duration — 1 day.
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3.3.4. Calculations
Using the dose algorithm and exposure factors shown above, the ADRmdoor air mh is
estimated using the input for children ages 3- to <1 1 -years old.
JxlO-ffix 1305^X3.7X10-^X1.1
"•LJ ^indoor air inh ,. i
. mg
~
ADRindoorairinh = 4.8 x
3.3.5. Uncertainties
The example presented here is used to represent bounding dose among residential
children from inhalation of contaminated indoor air. Central tendency doses may be estimated
by using mean values for contaminant concentration, exposure time, and inhalation rate. If a
high-end dose estimate is desired, some high-end and some central tendency input values may be
used. The choice of which parameter should be set to the high-end would be dependent upon the
sensitivities of the parameters, professional judgement, and regulatory requirements.
The uncertainties associated with this example scenario are related to the variation in
activity level of the children during the day. Another uncertainty relates to the contaminant
concentration. A contaminant will disperse and have varying concentrations throughout the
residence. These variations may be modeled, but for the purpose of this example it is assumed
that the concentration is constant throughout the home. In reality, the concentration will be
affected by seasonality, temperature, and house characteristics. In addition, this scenario
assumes that children are not exposed to the contaminant outside the residence.
3.4. INHALATION OF CONTAMINATED AIR DURING BUS TRANSPORTATION:
SCHOOL CHILDREN AND TEENS AGED 6 TO <16 YEARS, HIGH-END,
CHRONIC AVERAGE DAILY DOSE
3.4.1. Introduction
Air contamination on a bus may occur via (1) intrusion of volatile contaminants from
outdoor ambient air, (2) volatilization from personal consumer products, and (3) volatilization
from commercial materials in seats and flooring on the bus. This may result in exposure via
inhalation. For the purposes of this example, exposure among school children and teens 6 to
64
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<16 years old via inhalation of contaminated air occurs during bus transportation to and from
school, which may include infiltration of the bus exhaust. Values obtained from tables within
the EFH (U.S. EPA, 201 la) are cited as EFH Table X-X. High-end chronic daily dose from
inhalation is evaluated for doers-only of this population. An ADD is calculated in this example
to be used as input in a cumulative dose estimate or a relative pathway contribution analysis.
This inhalation dose estimate is not used to estimate risks. Risks from the inhalation pathway
would be estimated by calculating a time weighted average concentration or a peak concentration
to be used with a chronic toxicity value (e.g., RfC or IUK).
3.4.2. Dose Algorithm
Dose via this pathway would be calculated as follows:
X IR X ET X EF X ED
ADDairinh= — — (19)
where:
ADDair ink = average daily dose of contaminated air on bus transportation (mg/kg-d);
Coir = concentration of contaminant in the air on bus transportation (mg/m3);
IR = inhalation rate (m3/min-kg);
ET = exposure time (min/event);
EF = exposure frequency (events/yr);
ED = exposure duration (yr); and
AT = averaging time (d).
3.4.3. Input for Exposure Factor Variables
Coir—The concentration of contaminant in air at the site is either the measured or
predicted concentration, based on modeling, of the chemical of interest in the air on bus
transportation. For the purposes of this example, for a high-end dose, the 95th percentile
concentration of chemical "x" in air is 1 x 10~3 mg/m3.
IR—The recommended inhalation rates for children during short-term exposures are
given in EFH Table 6-2 (U.S. EPA, 201 la). For the purpose of this example, it is assumed that
the children's activity level is sedentary/passive. The mean inhalation rate values used for this
example are 1.60 x 10~4 m3/minute-kg for children aged 6 to <11 years and
1.05 x 1Q~4 m3/minute-kg for children aged 11 to <16 years.
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ET— The exposure time is estimated from EFH Table 16-23 (U.S. EPA, 201 la) for
doers-only on bus transportation. The 95th percentiles for school children aged 6 to <11 years
and teens aged 11 to <16 years are 107 minutes and 131 minutes per day, respectively.
EF—Exposure frequency is assumed to be 185 days/year for this example. This is
equivalent to 37 weeks of full-time school, accounting for 15 weeks off for summer and winter
vacation, or other school closings.
ED—Exposure duration is the length of time over which exposure occurs. For the
purpose of this example, the ED is 5 years for each age range (10 years total). This assumes that
all 10 years of the school commuting time are spent traveling through the same contaminated
area and that the same contaminants are present in the bus exhaust.
AT—Because the chronic ADD is being calculated in this example, the averaging time is
equivalent to the exposure duration. For the purposes of this example, the averaging time for
each age group is converted to 1,825 days (i.e., 5 years x 365 days/year).
3.4.4. Calculations
Using the dose algorithm and input for the exposure factors, the ADD for each of the age
ranges is calculated in Table 11.
Table 11. Summary of ADD for children and teens aged 6 to 16 years for
inhalation of contaminated air on bus transportation
Equation 19
input and output
C (mg/m3)
IR (m3/min-kg)
ET (min/d)
£F(d/yr)
ED (yr)
AT(d)
ADD (mg/kg-d)
Age ranges
6 to <11 yr
1 X ID-3
1.60 x 1(T4
107
185
5
1,825
8.7 x 1(T6
11 to <16 yr
1 X 1Q-3
1.05 x IQ-4
131
185
5
1,825
7.0 x 1(T6
The ADD for school children and teens averaged over the 10 years would be calculated as
follows:
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(Q.I x KT6T^%
V kg-d
inn
4 nn _,..,..,.
x 5yrJ + (y.O x ]
, mg
- 7Q x 10~6
L0~6r^% x 5yr)
kg-d J )
3.4.5. Uncertainties
The example presented here represents high-end doses among the general population of
school children and teens from the inhalation of contaminated air during bus transportation and
uses a high-end concentration with a mean inhalation rate. Alternatively, the high-end can be
estimated by using a mean concentration with a high-end inhalation rate. The choice of which
parameter should be set to the high-end would be dependent upon the sensitivities of the
parameters, professional judgement, and regulatory requirements. Central tendency doses may
be estimated by decreasing exposure time and using a mean concentration instead of a
95th percentile concentration.
The uncertainties associated with this example scenario are related to the contaminant
concentration and assumed exposure time and exposure frequency. The concentration may be
uncertain because it is typically obtained from outdoor measurements and using some
penetration modeling factors or tools. The study used to derive the assumption for exposure time
was conducted with small sample sizes and over short data collection period (24 hours) (U.S.
EPA, 201 la). Therefore, the data may not be representative of long term behaviors. The
exposure frequency may be higher if children attend summer school. This scenario also assumes
that children are not exposed to the contaminant at other locations where they may spend time.
There are also uncertainties associated with the inhalation rate data and assumptions regarding
activity levels. These inhalation rates were derived from a wide range of groups within the
U.S. population using indirect methods (U.S. EPA, 201 la).
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4. EXAMPLE DERMAL EXPOSURE SCENARIOS
4.1. DERMAL CONTACT WITH CONTAMINATED SOIL: TEEN ATHLETES AGED
11 TO <16 YEARS, CENTRAL TENDENCY, SUBCHRONIC AVERAGE DAILY
DOSE
4.1.1. Introduction
At sites where localized soil contamination exists, there is the potential for exposure via
dermal contact with soil during outdoor activities. Exposure also may occur from soil that is
tracked into the home or other buildings (i.e., schools, businesses, etc.). Therefore, receptors
could include nearby residents, students, and recreational populations. Estimating the dose via
dermal contact with the soil considers not only the concentrations of contaminants in the soil, but
also the surface area of the skin that contacts the soil, the amount of soil that adheres to the skin
per unit surface area, the fraction of contaminant in the soil that penetrates the skin, and the
frequency and duration of exposure. For the purposes of this example, the dose to teen athletes
via dermal contact with contaminated soil is calculated. Values obtained from tables within the
EFH (U.S. EPA, 201 la) are cited as EFH Table X-X. A subchronic dermal ADD from soil
contact is evaluated for the teen athlete. For this example, a teen athlete (aged 11 to <16 years)
playing soccer for one-half of the year is evaluated. It is assumed that the athlete is exposed to
the same source of contaminated soil during the entire duration of exposure. An average soil
concentration is used to account for the variability of soil concentration at the site.
4.1.2. Dose Algorithm
The ADD of a contaminant by dermal contact in a soil would be calculated as follows:
SA
_ Csoil X CF XEF XED X ABS X — X AFsoil
ADDABS sou contact dermal ~7Z, (20)
where:
ADDABS sou contact dermal = absorbed average daily dose from dermal contact with
contaminated soil (mg/kg-d);
don = concentration of contaminant in the soil at the site (mg/kg);
CF = conversion factor (kg/mg);
EF = exposure frequency (events/yr);
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ED = exposure duration (yr);
ABS = absorption fraction; this value is chemical specific (unitless);
SA/BW = surface area of the skin that contacts the soil (cm2/event-kg);
AFsoii = adherence factor for soil (mg/cm2); and
AT = averaging time (d).
4.1.3. Input for Exposure Factor Variables
Csoil—The concentration of contaminant in soil at the site is either the measured or
predicted concentration based on modeling, of the chemical of interest in the soil at the site of
interest. For the purposes of the example calculations, it is assumed that the mean measured
concentration of chemical "x" in soil to which the athlete is exposed is 1 x 1CT3 mg/kg. Also
assumed is that the concentration of contaminant in the soil that contacts the skin surface and is
available to be absorbed.
CF—A conversion factor of 1 x 1CT6 kg/mg is required to convert between mg/kg and
kg/mg.
EF—Exposure frequency is the number of times that exposure is expected to occur in a
year. Exposure frequency is assumed to be 130 events/year (i.e., 130 days/year). This assumes
that individuals contact soil from athletic fields once per day for 5 days/week, 6 months/year
(i.e., assumes no exposure associated with this athletic activity during the winter and summer
months). It should be noted that this frequency assumption is used for illustrative purposes only.
There may be cases where the exposure frequency is higher or lower. An implicit assumption of
this scenario is that exposure (and absorption of the contaminants through the skin) occurs for
each event in which soil contacts (and adheres to) a given surface area of the skin. This occurs
without regard to the duration of the exposure event because a certain fraction of the contaminant
in the soil on the skin is assumed to be absorbed for each event. Also assumed is that one 'event'
occurs on each of the 130 days/year; on these occasions, soil adheres to the skin and remains
there for the duration of the exposure event (i.e., until the fraction of contaminant specified in the
absorption fraction (ABS) assumption below has been absorbed). However, in some cases
alternate loading and removal mechanisms may affect the frequency of events (i.e., if hand
washing and reloading of soil on the skin occurs).
69
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ED — Exposure duration is the length of time over which exposure occurs. For the
purposes of this example, the ED for 11- to <16-year-old teen is assumed to be 5 years. This
assumes that 5 years are spent playing soccer on contaminated athletic fields.
ABS — This value is chemical specific. Information on absorption fractions can be
obtained from EPA's Dermal Exposure Assessment: Principles and Applications (U.S. EPA,
1992b). EPA also has developed the draft Part E Supplemental Guidance for Dermal Risk
Assessment of the Risk Assessment Guidance for Superfund, Volume I: Human Health
Evaluation Manual (U.S. EPA, 2004b). This document is a source of data on dermal absorption.
For the purposes of the calculations provided below for this example, it is assumed that the
absorption fraction for the chemical of interest (i.e., chemical "x") is 0. 1 (i.e., 10%). Thus, it is
assumed that 10% of the chemical in the soil contacting the skin is absorbed.
SA/BW — SA/BWis the ratio of skin surface area to BWand is expressed as cm2 of skin
surface area per kg ofBW. Assumptions have been made regarding the surface area of specific
body parts that are expected to be exposed to soil per event. For this example scenario (i.e., teen
athlete), it is assumed that an individual will wear short pants and a short-sleeved shirt, and that
the hands, arms, and legs will come into contact with the soil. EFH Table 7-2 provides the mean
recommended surface area contribution of hands, arms, and legs in m2 needed to obtain a
summed surface area value. Next, the summed surface area value is converted into cm2 using the
conversion factor of 1 m2 = 10,000 cm2. The total estimated surface area of the hands, arms, and
legs is divided by the BWio yield the SA/BW ratio (cm2/kg). The mean BWfor children in this
age range, 56.8 kg, was obtained from EFH Table 8-1.
0.072m2 x 10,000^- cm2
c A — rn — -t
0.227m2 x 10,000^- cm2
SAarms = ^^ l-^ = 40.0
56.8kg kg
„ rm
0.483m2 x 10,000^- cm2
56.8kg
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ii—The assessor should use adherence factor data that most closely resemble the
exposure scenario of concern. In this case, the mean AFsou for outdoor activities were used. The
soil adherence factors for this scenario were obtained from EFH Table 7-4 (U.S. EPA, 201 la)
and are tabulated in Table 12.
Table 12. Soil adherence factors (AFsou) for teen athletes playing soccer
Body parts
Hands
Arms
Legs
Mean adherence factors (mg/cm2)
0.11
0.011
0.031
AT — Because the ADD is being calculated for a specific age range (e.g., 1 1- to
<16-year-old teens), the averaging time is equivalent to the exposure duration, except that the
duration is expressed in days. For use in the calculations, this value is converted to 1,825 days
(i.e., 5 years x 365 days/year).
4.1.4. Calculations
Using the dose algorithm and exposure factor inputs shown above, the
ADDABSsoilcontactdermal would be calculated for each body part exposed and summed across body
parts as follows:
(I
x (1
X5yr x
AUU
x 0.031
ABS son contact dermal
1 R2S d
ADD
ABS sou contact dermal =
10
mg
"
4.1.5. Uncertainties
The example presented here is used to represent central tendency doses among teen
athletes, aged 11 to <16 years, from dermal contact with contaminated soil. High-end doses may
be estimated by assuming a different clothing scenario and replacing the assumptions regarding
areas of the body exposed (e.g., including the face and torso). Alternatively, exposure frequency
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may be increased to estimate high-end doses. If a bounding dose estimate is desired, the
concentration in soil may be set to the maximum measured or modeled concentration, the
assumed frequency of exposure may be increased (e.g., 250 times/year; 5 days/week;
12 months/year), and the clothing scenario may be revised to increase the areas of the body
exposed. It is important to note that the bounding estimate results in dose estimates that may be
unreasonably high for the population of interest.
The uncertainties associated with this example scenario are related to the assumed
activity patterns of the receptor population and the input parameters used. Implicit in this
scenario is the assumption that the population of interest contacts the contaminated soil from the
site, and that adherence occurs over the assumed surface area of the skin at the rates shown in the
EFH (U.S. EPA, 201 la; see Table 12). Another implicit assumption is that the soil is on the skin
for the entire exposure event, which is assumed to be a day. This means that each event (whether
it consists of a few minutes or several hours) is assumed to be 1 day. Multiple soil contact events
in a single day are still treated as one event. Use of a 1-day exposure event is consistent with
absorption values, which typically are based on 24-hour exposure periods. The assumption that
absorption from contaminants in soil adhering to the skin occurs over 24 hours contributes to the
uncertainty of the resulting estimates because it is reasonable that individuals may shower or
bathe after a sporting event.
Selection of the clothing scenario or percentage of the body exposed should be based on
the assessor's knowledge of the populations/activities and should be designed to reflect, as
closely as possible, the skin surface area exposed for the activity of interest. However, the
assumptions used regarding the clothing worn and the surface area exposed result in uncertainty
in the assessment. In addition, clothing is not 100% effective in blocking exposure as dust can
penetrate through cloth or deposit under loose clothing. In the EFH (U.S. EPA, 201 la), EPA
recognizes the uncertainty associated with the surface area and adherence data and concludes
that although there may be some selection bias associated with the recommended surface areas,
they are the best available data for use in exposure assessment. The uncertainties associated with
the adherence data result from the limited size of the data set, and the fact that adherence may be
influenced by the clothing worn by the study participants, and soil properties (e.g., moisture
content, particle size) that are not entirely accounted for in the available data.
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4.2. DERMAL CONTACT WITH INORGANIC CONTAMINANTS WHILE WADING
IN A RECREATIONAL POND: CHILDREN AGED 6 TO <16 YEARS,
BOUNDING, ACUTE DOSE RATE
4.2.1. Introduction
The potential for exposure to chemical substances exists at sites where local surface
water bodies (i.e., streams, ponds, lakes, bays, or rivers) have become contaminated. Children
may be exposed to chemicals in the water via dermal absorption as a result of swimming and/or
wading. Acute dose via dermal contact considers not only chemical concentrations in contact
with the skin, but also the surface area of the skin that contacts the water, the absorption of the
chemical in contact with the skin, exposure frequency, and exposure time. For the purposes of
this example, surface water exposure among wading children (aged 6 to <16 years) is evaluated.
Dermal exposure is assessed based on bounding acute exposure to an inorganic chemical while
wading in contaminated surface water. Values obtained from tables within the EFH (U.S. EPA,
201 la) are cited as EFH Table X-X.
4.2.2. Dose Algorithm
The ADR of an inorganic contaminant via dermal contact while wading is calculated as
follows:
_ DAevent X SA X EF X ED
AL)Kwading water dermal RW X AT
where:
ADRWading water dermal = acute potential dose from dermal contact in recreational surface
water while wading (mg/kg-d);
DAevent = absorbed dose per hour (mg/cm2-event);
SA = surface area of the skin (cm2);
EF = exposure frequency (events/d);
ED = exposure duration (d);
BW = body weight of child (kg); and
AT = averaging time (d).
4.2.3. Input for Exposure Factor Variables
DAevent—The absorbed dose per event (£^4event) is estimated considering the following
factors:
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• The permeability coefficient from water;
• The chemical concentration in water; and
• The event duration.
The approach to estimate DAeveai differs with respect to inorganic and organic chemicals.
This is consistent with current EPA policy directives (U.S. EPA, 2004b, 1997a, 1992b). For a
dermal exposure in water using organic chemicals, see the approach presented in Scenario
4.3 — Dermal Contact with an Organic Contaminant in Water while Showering. For inorganic
chemicals, EPA recommends using the steady-state approach to estimate dermally absorbed
doses. In this approach,
DAevent = Kp X ET X Cw (22)
where:
ent = absorbed dose per event (mg/cm2-event);
Kp = dermal permeability coefficient of compound in water (cm/hr);
ET = event time (hr/event); and
Cw = chemical concentration in water (mg/cm3).
For the purpose of this example, the inorganic chemical "x" is used. It is assumed that
chemical "x, " a permeability coefficient of 1 x 1CT3 cm/hour, and a maximum chemical
concentration of 1 x 1CT6 mg/cm3.
ET—EFH Table 16-19 (U.S. EPA, 201 la) reports time spent in selected outdoor
locations for children from 6 to <16 years of age. The 95th percentile exposure time spent in
pool, river, or lake (doers-only) for children aged 6 to <1 1 years is 359 minutes/day
(6.0 hours/day) and 228 minutes/day (3.8 hours/day) for children aged 11- to <16-years old.
Assuming that these exposure times represent an event occurring over the course of 1 day, the
exposure time would be 6 hours/event for children aged 6 to <1 1 years and 3.8 hours/event for
children aged 1 1 to <16 years (i.e., a child's skin is immersed in water for a total of either 6 or
3.8 hours over the course of the daily event, depending on the age of the child).
This results in a DAevent calculation for children aged 6 to <1 1 years of:
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, ,, cm hr , mg
DAevent = (l x 1(T3) — x6 - x (1 x 1(T6) — %
event v ; hr event v J cm3
fluent = 6 X 1(T9 - ^ -
event cm2-event
This results in a DAevent calculation for children aged 11 to <16 years of:
, ,, cm hr , mg
DAevent = l x (1 x 1(T3) — X3.8 - x (1 x 1(T6)
event v y v J
.
hr event v J cm3
= 3.8 X 1(T9 - ^ -
cm2-event
SA — The surface area of the skin of a child (aged 6 to <16 years) for various body parts
can be found in EFH Table 7-2 (U.S. EPA, 201 la). In this scenario, wading is assumed;
therefore, only the SA of the legs and feet will be used. In this example, mean surface areas of
the legs and feet are used because surface area and BWare strongly correlated and the mean
values are most representative of the surface area of individuals with an average BW. Because
surface area is divided by the body weight in the dose equation, using an upper-percentile surface
area with an upper-percentile BW would be similar to using a mean surface area with a mean
BW. The estimates are given in m2 and must be converted to cm2 (1 m2 = 10,000 cm2). For this
example, the surface area is 0.311 m2 for legs and 0.073 m2 for feet (3,110 + 730 = 3,840 cm2),
respectively, for ages 6 to <11 years, and 0.483 m2and 0.105 m2 (4,830 + 1,050 = 5,880 cm2) for
legs and feet, respectively, for ages 1 1 to <16 years.
EF — Exposure frequency is assumed to be one event per day.
ED — Exposure duration is the number of days over which exposure occurs. For the
purposes of this example, the acute ED is assumed to be 1 day.
BW—EFH Table 8-1 (U.S. EPA, 201 la) reports recommended BWs for children from 6
to <16 years of age. The BWfor boys and girls are averaged for ages 6 to <16 years. This
calculation, using the mean of this distribution, also is weight averaged according to the number
of years in each age range. For children aged 6 to <1 1 years of age, the mean recommended BW
is 31.8 kg. For children aged 11 to <16 years of age, the mean recommended B W is 56.8 kg.
AT — Because the potential acute bounding dose is being calculated, the averaging time is
equivalent to the ED of 1 day.
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4.2.4. Calculations
Using the dose algorithm and the input for the exposure factors, the ADRwading water dermal
for children aged 6 to <11 and 11 to <16 is calculated in Table 13.
Table 13. Summary of ADR for children aged 6 to <16 years for acute
potential dose from dermal contact in recreational surface water while
wading
Equation 21
input and output
DA event (mg/cm2-event)
SA (cm2)
EF (events/d)
ED(d)
AT(d)
BW(kg)
ADR (mg/kg-d)
Age ranges
6 to <11 yr
6 x 1(T9
3,840
1
1
1
31.8
7.2 x 1Q-7
11 to <16 yr
3.8 x 1(T9
5,880
1
1
1
56.8
3.9 x 1Q-7
The ADRwading water dermal averaged over the 10 years of exposure for children aged 6 to <11
and 11 to <16 is calculated as follows:
"•V ^
(5 yrx 7.2X10-^)
wading water dermal
10 yr
• wading water dermal
-I n
-LU
~7 "
i _,
4.2.5. Uncertainties
The example presented here is used to represent bounding doses among children aged 6
to <16 years while wading in surface water. Note that central tendency doses may be calculated
by using mean concentrations and exposure time, and a lower FA.
There are uncertainties related to calculation of the absorbed dose per surface water
exposure event (e.g., DAevent). As noted in Dermal Exposure Assessment: Principles and
Applications, "the dermal permeability estimates are probably the most uncertain of the
parameters in the dermal dose equation. Accordingly, the final dose and risk estimates must be
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considered highly uncertain" (U.S. EPA, 1992b). A lack of measured data for a variety of
chemicals makes the validation of the model difficult. There are also uncertainties associated
with the surface areas and exposure times used in this example scenario.
4.3. DERMAL CONTACT WITH AN ORGANIC CONTAMINANT IN WATER WHILE
SHOWERING: CHILDREN AND TEENS, AGED 6 TO <16 YEARS HIGH-END,
LIFETIME AVERAGE DAILY DOSE
4.3.1. Introduction
The potential for exposure to chemical substances exists if children and teens shower in
water from a contaminated source or in water that has been treated with substances that convert
into toxicants over time. Receptors could include any children and teens who shower using such
water. The dose via dermal contact considers not only the chemical concentration in the water,
but also the surface area of the skin in contact with the water, the behavior of the chemical when
it comes in contact with the skin, exposure duration, exposure time, and exposure frequency.
This example examines the high-end dermal dose via showering in contaminated water for
children and teens aged 6 to <16 years (age ranges: 6 to <11 and 11 to <16 years) and calculates
the ADD for both age ranges, then weights the average daily doses according to the length of
time these exposures occur to calculate the LADD. Values obtained from tables within the EFH
(U.S. EPA, 201 la) are cited as EFH Table X-X. In this example, it is assumed that the receptors
are not exposed to the contaminant again for the remainder of their lives. The LADD is
calculated because the contaminant in this scenario is assumed to be a carcinogen and the
carcinogen toxicity values are expressed as a lifetime value.
4.3.2. Dose Algorithm
Dose via this pathway would be calculated as follows:
_ DAevent X SA X EV X EF X ED ( .
'-'"•^-'^-'shower water dermal g^ x AT \ )
where:
LADD shower water dermal = absorbed lifetime average daily dose from dermal contact with
water during showering (mg/kg-d);
DAevent = absorbed dose per event (mg/cm2-event);
SA = surface area of the skin (cm2);
EV = event frequency (events/d);
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EF = exposure frequency (d/yr);
ED = exposure duration (yr);
BW = body weight of child (kg); and
AT = averaging time (d).
4.3.3. Input for Exposure Factor Variables
DAevent—The absorbed dose per event (mg/cm2-event) is estimated considering the
following factors:
• The permeability coefficient from water,
• The chemical concentration in water, and
• The event duration.
Current EPA policy directs differing approaches to estimate DAeVent with respect to
inorganic and organic chemicals (U.S. EPA, 2004b, 1992b). For inorganic chemicals, the EPA
recommends using a steady-state approach to estimate dermal absorption doses. This approach
is illustrated in Scenario 4.2—Dermal Contact with Inorganic Contaminants while Wading in a
Recreational Pond.
For organic chemicals, EPA provides two equations. The choice of appropriate equation
is based on the event duration versus the lag time per event. If the duration of the event (tevent) is
less than the time to reach steady-state (2.4x), then the following equation is used to estimate
vent (U.S. EPA, 2004b, 1992b):
If tevent
-------
If the duration of the event (tevent) is greater than the time to reach steady-state (2.4-r), then
the equation incorporates a new coefficient B, which is a dimensionless ratio of the permeability
coefficient of a compound through the stratum corneum relative to its permeability across the
epidermis. U.S. EPA (2004) indicates that the lag time is the time during which absorption
continues after the exposure has ended; for chemicals that exhibit a long lag time, "some of the
chemical dissolved into skin may be lost due to desquamation during that absorption period." It
should be noted that the fraction available for absorption (FA) is different than the absorption
fraction used in Scenario 4.1 — Dermal Contact with Soil (ABS). The variable FA is used to
account for the loss of chemical due to the desquamation of the outer skin layer and a
corresponding reduction in the absorbed dermal dose.
The following equation is used to estimate this DAevent (U.S. EPA, 2004b, 1992b):
Kteve*>t*,±en:DAevent = FA x Kp x Cw + 2T X *3** f * (25)
where:
DAevent = absorbed dose per event (mg/cm2-event);
FA = fraction absorbed (dimensionless);
Kp = dermal permeability coefficient of compound in water (cm/hr);
Cw = chemical concentration in water (mg/cm3);
T = lag time per event (hr/event);
tevent = event duration (hr/event);
B = dimensionless ratio of the permeability coefficient of a compound
through stratum corneum relative to its permeability coefficient across
the viable epidermis; and
t* = time to reach steady-state.
Guidance for using these equations is detailed in Dermal Exposure Assessment:
Principles and Applications (U.S. EPA, 1992b) and Risk Assessment Guidance for Superfimd,
Part E (U.S. EPA, 2004b). The organic chemical benzene is used for the purposes of this
example. Benzene, estimates for which are given in Appendix B of Risk Assessment Guidance
for Superfund, Part E (U. S . EPA, 2004b), has a molecular weight (MW) of 78 . 1 and a log Kow of
2.13. The Kp for benzene is 1.5 x 10~2 cm/hour and the FA is 1.0. To determine which equation
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must be used to calculate DAevent, the lag time per event (T) must be calculated. The following
equation can be used:
T = -&- (26)
6DSC ^ }
In this equation, 7SC (the thickness of the stratum corneum) is 10~3 cm. This is a default
recommended for use by EPA's Risk Assessment Guidance for Superfund, Part E (U.S. EPA,
2004b). DSC is the stratum corneum diffusion coefficient (cm2/hour), which can be calculated as
follows:
Dsc= io(-2-8°-°-°°56MM0 xlsc (27)
Using eq 26, the lag time per event (T) is 0.29 hour/event, as shown in Table B-3 of Risk
Assessment Guidance for Superfund, Part E (U.S. EPA, 2004b). Because the time to reach
steady-state (t*) is defined as 2.4 T, the t* actually would be 0.70 hour or 42 minutes (U.S. EPA,
2004b). Based on EFH Table 16-1 (U.S. EPA, 201 la), the 95th percentile recommended value
for shower duration is 41 minutes for a child aged 6 to <1 1 years, and 40 minutes for a child
aged 1 1 to <16 years. Using these values as the event duration (tevent), tevent < t*; thus, eq 24
would be used for the calculation of DAevent. If tevent had been greater than t*, eq 25 would be
used, and variable B would need to be calculated, as shown in eq 28:
(28)
^ '
2.6
~3 3
Assuming the mean concentration in water (Cw) is 1 x 10~3 mg/cm3, an example dose
calculation for DAevent is as follows, and is the same for both age ranges using eq 25:
16 x 0.29^r x 0.7" hr
rm ma o /s u.z.:? r /s u./u r
2 x 1.0 x (1.5 x 10-2)^ x (1 x 10-3)^| ^^ 2£nt
hr crn-^ "\J TT
-5 m§
lpvpnf — *-^ ^ ^ T
event cm2-event
DA = l.9 x 10
SA—The total surface area of the skin of a child can be found in EFH Table 7-1
(U.S. EPA, 201 la) for all children according to the age increments in the Guidance on Selecting
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Age Groups for Monitoring and Assessing Childhood Exposures to Environmental Contaminants
(U.S. EPA, 2005a) document. In this example, mean total surface areas are used because surface
area and BW are strongly correlated and the mean values are most representative of the surface
area of individuals with an average BW. Because surface area is divided by the BW'm the dose
equation, using an upper-percentile surface area with an upper-percentile BW would be similar to
using a mean surface area with a mean BW. The estimates are given in m2 and must be
converted to cm2 (1 m2 = 10,000 cm2). For this example, the averages of 1.08 m2 for 6 to
<11 years of age and 1.59 m2 for 11 to <16 years of age are converted and used as 10,800 cm2
and 15,900 cm2, respectively.
ET—Since the LADD accounts for daily exposure, the event frequency is the number of
events per day. For this scenario, it is assumed that one shower is taken daily (i.e., 1 event/day).
EF—Exposure frequency is the number of times an exposure is expected to occur in a
year and is expressed in days per year. For the purposes of this scenario, it is assumed that
children shower at home 350 days/year. This assumes that young children are away from home
(e.g., on vacation) for 2 weeks/year.
ED—Exposure duration is the length of time over which the exposure occurs. This
scenario covers a total duration of 10 years: 5 years from age 6 to <11 years and 5 years from
age 11 to <16 years.
BW—EFH Table 8-1 (U.S. EPA, 201 la) reports recommended BWs for children aged 6
to <16 years. The BWs for boys and girls are averaged from age 6 to <11 years old and 11 to
<16 years old. These calculations, using the mean of this distribution, are 31.8 kg and 56.8 kg,
respectively.
AT—The averaging time (AT) of 5 years is used in the individual calculations of DAevent
for each age range. Note that this assumes that no further exposures to the water contaminant of
interest occur via showering after or before the 10 years examined here (i.e., aged 6 to
<16 years). This ^Tvalue is converted to 1,825 days (that is, 5 years x 365 days/year). Because
the LADD dose is calculated, the overall averaging time is equivalent to the lifetime (LT) of an
individual in the receptor population. For the purposes of this example, the average lifetime of
70 years (25,550 days) for men and women is used because the receptors exposures are assumed
to reflect the general population (U.S. EPA, 201 la).
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4.3.4. Calculations
Using the dose algorithm and input for the exposure factors variables, the dermal ADD
for children and teens while showering, is estimated for each age range in Table 14.
Table 14. Summary of ADD for children aged 6 to <16 years for high-end
potential dose from dermal contact while showering
Equation 23
inputs and output
DA event (mg/cm2-event)
SA (cm2)
£F(events/d)
£F(d/yr)
ED (yr)
AT(d)
BW(kg)
ADD (mg/kg-d)
Age ranges
6 to <11 yr
1.9 x 1(T5
10,800
1
350
5
1,825
31.8
6.2 x 1(T3
11 to <16 yr
1.9 x IQ-5
15,900
1
350
5
1,825
56.8
5.1 x 1(T3
The ADDs shown in Table 14 are then used to estimate the LADDshowering water dermal.
Assuming exposure for 5 years as a 6- to <1 1-year old, 5 years of exposure as an 11- to <16-year
old, and no exposure for the rest of the life time (i.e., 60 years), the weighted average over a
lifetime for the LADD is calculated as:
showering water dermal
+5yr x 5.1X10-'
70 yr
sflowering water dermal
_4
o.l X 1U
4.3.5. Uncertainties
The example presented here is used to represent high-end doses among children aged 6 to
<16 years for showering in contaminated water. Note that central tendency doses may be
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estimated by replacing the 95th percentile shower duration with a mean value. The bounding
estimate can be estimated by setting all the input parameters to upper-percentile values.
There are uncertainties related to calculation of the DAeVent. According to Dermal
Exposure Assessment: Principles and Applications., "The dermal permeability estimates are
probably the most uncertain of the parameters in the dermal dose equation. Accordingly, the
final dose and risk estimates must be considered highly uncertain" (U.S. EPA, 1992b).
Frequently, for organic chemicals, Kp values are predicted using Kow. Dermal Exposure
Assessment: Principles and Applications states that "the uncertainty in the predicted Kps is
judged to be within plus or minus one order of magnitude from the best fit value" (U.S. EPA,
1992b). A lack of measured data for a variety of chemicals makes the validation of the model
difficult.
Because of these uncertainties, U.S. EPA (1992b) recommends that an assessor conduct a
"reality check" by comparing the total amount of contaminant in the water to which an
individual is exposed, to the total estimated dose. U.S. EPA, 1992b states that "As a preliminary
guide, if the dermal dose exceeds 50% of the contaminant in the water, the assessor should
question the validity of the dose estimate." Assessors are cautioned to consider the various
uncertainties associated with this scenario to ensure that dose estimates are adequately
represented.
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GLOSSARY1
Absorbed dose— The amount of a substance penetrating across an absorption barrier (the
exchange boundaries) of an organism, via either physical or biological processes. Sometimes
called internal dose. See also Absorption barrier and Dose.
Absorption barrier—Any exposure surface that may retard the rate of penetration of an agent
into a target. Examples include the skin, respiratory tract lining, and gastrointestinal tract wall.
See also Target and Agent.
Activity pattern data—Information on human activities used in exposure assessments. These
may include a description of the activity, frequency of activity, duration spent performing the
activity, and the microenvironment in which the activity occurs.
Acute dose rate (ADR)—Dose per unit time received over a short period of time. Units may
include mg/day.
Acute exposure—A single exposure to a toxic substance that may result in severe biological
harm or death. Acute exposures are usually characterized as lasting no longer than a day, as
compared to longer, continuing exposure over a period of time. The ADR is used for an acute,
noncarcinogenic exposure.
Adherence factor—The amount of a material (e.g., soil) that adheres to the skin per unit of
surface area.
Age-dependent adjustment factors (ADAFs)—In cases where age-related differences in
toxicity occur, differences in both toxicity and exposure need to be integrated across all relevant
age intervals, by the use of ADAFs. This is a departure from the way cancer risks have
historically been calculated based upon the premise that risk is proportional to the daily average
of the long-term adult dose. For example, for chemicals or compounds with a mutagenic mode
of action for carcinogenesis, in the absence of chemical-specific data, the risk from exposures
that occur at early life stages should be calculated by applying the following ADAFs to the non-
1 Glossary entries are adapted from IPCS (2004) and EPA (U.S. EPA, 1992a, 2004a, 2005a, 201 la, 20lib)
publications.
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age-specific slope factor: a factor of 10 for ages 0 to < 2 years; a factor of 3 for ages 2 to < 16
years; and a factor of 1 for ages >16 years.
Agent—A chemical, biological, or physical entity that contacts a target. See also Target.
Aggregate exposure—The combined exposure of an individual (or defined population) to a
specific agent or stressor via relevant routes, pathways, and sources. Aggregate exposure can
include exposure through multiple routes (e.g., dermal, inhalation, and ingestion).
Assessment—A determination or appraisal of possible consequences resulting from an analysis
of data.
Average daily dose (ADD)—The mean daily amount of an agent to which a person is exposed,
often averaged over a long period of time. EPA is transit!oning from average daily dose
methodologies to more refined aggregate and cumulative approaches for estimating exposure
across each life stage. See also Lifetime average daily dose (LADD) and Time-averaged
exposure.
Bias—A systematic error inherent in a method or caused by some feature of the measurement
system.
Bounding estimate—An estimate of exposure, dose, or risk that is higher or lower than that
incurred by the person with the highest or lowest exposure, dose, or risk in the population being
assessed. Bounding estimates are useful in developing statements that exposures, doses, or risks
are "not greater than" or "less than" the estimated value, because assumptions are used which
define the likely bounding conditions.
Carcinogen—A substance or agent capable of causing cancer.
Central tendency exposure/dose—A measure of the middle or the center of an exposure/dose
distribution. The mean is the most commonly used measure of central tendency.
Childhood exposure—Contact between an agent and a child. See also Agent.
Children—Individuals under the age of 21 years are classified as youth or children. For
children less than 12 months old, the following age groups are recommended: birth to <1 month,
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1 to <3 months, 3 to <6 months, and 6 to <12 months. For children older than 12 months, the
following age groups are recommended: 1 to <2 years, 2 to <3 years, 3 to <6 years, 6 to
<11 years, 11 to <16 years, and 16 to <21 years.
Chronic exposure—Repeated exposure by the oral, dermal, or/and inhalation route for more
than approximately 10% of the life span in humans (more than approximately 90 days to 2 years
in typically used laboratory animal species).
Chronic intake—The long term period over which a substance crosses the outer boundary of an
organism without passing an absorption barrier.
Community water—Includes tap water ingested from community or municipal water supply.
Consumer only—Refers to only those individuals who reported food or water during the survey
period.
Contaminant concentration—Contaminant concentration is the concentration of the
contaminant in the medium (air, food, soil, etc.) contacting the body and has units of
mass/volume or mass/mass.
Cumulative exposure—Exposure via mixtures of contaminants through more than one pathway.
Risk assessments in EPA are placing more emphasis on total exposures via multiple pathways.
Cumulative risk assessment—An analysis, characterization, and possible quantification of the
combined risks to health or the environment from multiple agents or stressors. See also Risk
assessment.
Deposition—The removal of airborne substances to available surfaces that occurs as a result of
gravitational settling and diffusion, as well as electrophoresis and thermophoresis.
Dermal absorption—A route of exposure by which substances can enter the body through the
skin (i.e., uptake across the skin barrier following dermal exposure).
Dermal permeability—Measure of the ability of the substance to penetrate and move through
the skin.
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Direct water ingestion—Consumption of tap water as a beverage. It does not include water
used for preparing beverages such as coffee or tea.
Distribution—A set of values derived from a specific population or set of measurements that
represents the range and array of data for the factor being studied.
Doers—Survey respondents who report participating in a specified activity.
Dose—The amount of an agent that enters a target after crossing an exposure surface. If the
exposure surface is an absorption barrier, the dose is an absorbed dose. If the exposure surface
is not an absorption barrier, the dose is an intake dose.
Dose rate—Dose per unit time, for example in mg/day, sometimes also called dosage. Dose
rates are often expressed on a per-unit-body-weight basis, yielding units such as mg/kg-day.
They are also often expressed as averages over some time period, for example a lifetime.
Drinking water—All water consumed by individuals to satisfy body needs for internal water.
Dry weight intake rates—Intake rates that are based on the weight of the food consumed after
the moisture content has been removed.
Dust ingestion—Consumption of dust that results from various behaviors including, but not
limited to, mouthing objects or hands, eating dropped food, consuming dust directly, or inhaling
dust that passes from the respiratory system into the gastrointestinal tract.
Effect—Change in the state or dynamics of an organism, system, or population caused by
exposure to an agent. See also Agent.
Exclusively breastfed—Infants whose sole source of milk comes from human milk with no
other milk substitutes. See also Infant.
Exposure—Contact between an agent and a target. See also Agent and Target.
Exposure assessment—The process of estimating or measuring the magnitude, frequency, and
duration of exposure to an agent, along with the number and characteristics of the population
exposed. See also Agent, Exposure duration, and Exposure frequency.
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Exposure concentration—The concentration of a chemical in its transport or carrier medium at
the point of contact.
Exposure duration—Length of time over which contact with the contaminant lasts.
Exposure event—The occurrence of continuous contact between an agent and a target.
Exposure factor—Factors related to human behavior and characteristics that help determine an
individual's exposure to an agent.
Exposure frequency—The number of exposure events in an exposure duration. See also
Exposure duration.
Exposure time—The length of time an individual engages in an activity which results in
exposure.
Exposure pathway—The physical course a chemical takes from the source to the organism
exposed.
Exposure route—The way a chemical pollutant enters an organism after contact, e.g., by
ingestion, inhalation, or dermal absorption.
Exposure scenario—A set of facts, assumptions, and inferences about how exposure takes place
that aids the exposure assessor in evaluating, estimating, or quantifying exposures.
General population—All individuals inhabiting an area or making up a whole group.
High-end exposure/dose—An estimate of individual exposure or dose for those persons at the
upper end of an exposure or dose distribution, conceptually above the 90th percentile, but not
higher than the individual in the population who has the highest exposure or dose. See also
Bounding estimate.
Human equivalent concentration or dose (HEC or HED)—The concentration (for inhalation
exposure) or dose (for other routes of exposure) of an agent that is believed to induce the same
magnitude of toxic effect in humans experienced by an experimental animal species. This
adjustment may incorporate toxicokinetic information on the particular agent and/or target, if
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available, or use a default procedure, such as assuming that daily oral doses experienced for a
lifetime are proportional to BWraised to the 0.75 power.
Indirect water ingestion—Includes water added during food preparation, but not water intrinsic
to purchased foods. Indirect water includes for example, water used to prepare baby formulas,
cake mix, or concentrated orange juice.
Infant—A life stage that covers four age ranges, from birth to <1, 1 to <3, 3 to <6, and 6 to
<12 months. See also Children.
Inhalation dosimetry—Process of measuring or estimating inhaled dose.
Inhalation unit risk (IUR)—The upper-bound excess lifetime cancer risk estimated to result
from continuous exposure to an agent at a concentration of 1 ug/m3 in air for a lifetime.
Inhaled dose—The amount of an inhaled substance that is available for interaction with
metabolic processes or biologically significant receptors after crossing the outer boundary of an
organism.
Intake—The process by which a substance crosses the outer boundary of an organism without
passing an absorption barrier (e.g., through ingestion or inhalation).
Intake rate—Rate of inhalation, ingestion, and dermal contact depending on the route of
exposure. For ingestion, the intake rate is simply the amount of food or drink containing the
contaminant of interest that an individual ingests during some specific time period (units of
mass/time). For inhalation, the intake rate is the rate at which contaminated air is inhaled.
Factors that affect dermal exposure are the amount of material that comes into contact with the
skin, and the rate at which the contaminant is absorbed.
IRIS—EPA's Integrated Risk Information System (IRIS) is a human health assessment program
that evaluates information on health effects that may result from exposure to environmental
contaminants. The IRIS database is an online database and contains information on more than
550 chemical substances.
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Key study/data—A study that is useful for deriving exposure factors. Alternatively, studies
may be classified as "relevant" and not "key" for one or more of the following: (1) they provide
supporting data (e.g., older studies on food intake that may be useful for trend analysis); (2) they
provide information related to the factor of interest (e.g., data on prevalence of breastfeeding); or
(3) the study design or approach makes the data less applicable for exposure assessment purposes
(e.g., data on mouthing behavior that was intended to be used in reducing the risk of choking
hazards).
Life stage—A distinguishable time frame in an individual's life characterized by unique and
relatively stable behavioral and/or physiological characteristics that are associated with
development and growth. See also Infant and Children.
Lifetime—The average lifetime of 70 years for men and women is assumed to reflect the general
population for consistency by EPA when calculating cancer risks.
Lifetime average daily dose (LADD)—Dose rate averaged over a lifetime. The LADD is used
for compounds with carcinogenic or chronic effects. The LADD is usually expressed in terms of
mg/kg-day or other mass/mass-time units. Often used in carcinogen risk assessments that
employ linear low-dose extrapolation methods. See also Average daily dose and Time-averaged
exposure.
Mean value—Simple or arithmetic average of a range of values, computed by dividing the total
of all values by the number of values.
Measurement error—A systematic error arising from inaccurate measurement (or
classification) of subjects on the study variables.
Median value—The value in a data set such that half the measured values are greater and half
are less.
Moisture content—The portion of food that is made up by water. The percentage of water is
needed for converting food intake rates and residue concentrations between whole weight and
dry weight values.
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Monte Carlo technique—A repeated random sampling from the distribution of values for each
of the parameters in a generic (exposure or dose) equation to derive an estimate of the
distribution of (exposures or doses in) the population. A form of probabilistic exposure
estimation. See also Distribution.
Mouthing behavior—Activities in which objects, including fingers, are touched by the mouth or
put into the mouth except for eating and drinking, and includes licking, sucking, chewing, and
biting (usually infants and children).
Octanol/water partition coefficient (Kow)—The ratio of the solubility of a compound in
octanol to its solubility in water. The higher the Kow, the more nonpolar the compound is. The
Log Kow of a compound may be used as an indication of how well the compound will adsorb to
soil.
Per capita intake rate—The average quantity of food consumed per person in a population
composed of both individuals who ate the food during a specified time period and those that did
not.
Pica—Pica behavior is the repeated eating of nonnutritive substances, whereas soil-pica is a
form of soil ingestion that is characterized by the recurrent ingestion of unusually high amounts
of soil (i.e., on the order of 1,000-5,000 mg/day or more).
Plain tap water—Water obtained directly from the faucet or tap. It excludes water intrinsic in
foods, juices, and other beverages.
Potential average daily dose (ADD)—is the amount of substance ingested, inhaled, or applied
to skin per day, not all of which will be absorbed.
Potential dose—The amount of a chemical contained in material ingested, air breathed, or bulk
material applied to the skin.
Preparation losses—Net cooking losses, which include dripping and volatile losses,
postcooking losses, which involve losses from cutting, bones, excess fat, scraps and juices, and
other preparation losses, which include losses from paring or coring.
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Random samples—Samples selected from a statistical population such that each sample has an
equal probability of being selected.
Range—The difference between the largest and smallest values in a measurement data set.
Reasonable maximum exposure—A semi quantitative term referring to the lower portion of the
high end of the exposure, dose, or risk distribution. As a semiquantitative term, it should refer to
a range that can conceptually be described as above the 90th percentile in the distribution, but
below the 98th percentile.
Receptor/receptor population—The population of interest, also known as the receptor
population, is described by specific age ranges. For children, these age ranges take into account
their rapidly changing physiology. See also Infant and Children.
Reference Concentration (RfC)—An estimate (with uncertainty spanning perhaps an order of
magnitude) of a continuous inhalation exposure to the human population (including sensitive
target groups) that is likely to be without an appreciable risk of deleterious effects during a
lifetime. It can be derived from a NOAEL, LOAEL, or benchmark concentration, with
uncertainty factors generally applied to reflect limitations of the data used. Generally used in
EPA's noncancer health assessments. Durations include acute, short-term, subchronic, and
chronic.
Reference Dose (RfD)—An estimate (with uncertainty spanning perhaps an order of magnitude)
of a daily oral exposure to the human population (including sensitive target groups) that is likely
to be without an appreciable risk of deleterious noncancer effects during a lifetime. It can be
derived from a NOAEL, LOAEL, or benchmark dose, with uncertainty factors generally applied
to reflect limitations of the data used. Generally used in EPA's noncancer health assessments.
Durations include acute, short-term, subchronic, and chronic.
Representativeness—The degree to which a sample is, or samples are, characteristic of the
whole medium, exposure, or dose for which the samples are being used to make inferences.
Risk—The probability of an adverse effect in an organism, system, or population caused under
specified circumstances by exposure to an agent.
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Risk assessment—A process intended to calculate or estimate the risk to a given target
organism, system, or population, including the identification of attendant uncertainties, following
exposure to a particular agent, taking into account the inherent characteristics of the agent of
concern as well as the characteristics of the specific target system. The risk assessment process
includes four steps: hazard identification, dose-response assessment, exposure assessment, and
risk characterization.
Sample—A small part of something designed to show the nature or quality of the whole.
Exposure-related measurements are usually samples of environmental or ambient medium,
exposures of a small portion of a population for a short time, or biological samples, all for the
purpose of inferring the nature and quality of parameters important to evaluating exposure.
Soil—Particles of unconsolidated mineral and/or organic matter from the earth's surface that are
located outdoors, or are used indoors to support plant growth.
Soil adherence—The quantity of soil that adheres to the skin and from which chemical
contaminants are available for uptake at the skin surface.
Soil ingestion—The intentional or unintentional consumption of soil, resulting from various
behaviors including, but not limited to, mouthing, contacting dirty hands, eating dropped food, or
consuming soil directly. Soil-pica is a form of soil ingestion that is characterized by the
recurrent ingestion of unusually high amounts of soil (i.e., on the order of 1,000-5,000 mg/ day
or more). Geophagy is also a form of soil ingestion defined as the intentional ingestion of earths
and is usually associated with cultural practices.
Subchronic exposure—Repeated exposure by the oral, dermal, or inhalation route for more than
30 days, up to approximately 10% of the life span in humans (more than 30 days up to
approximately 90 days in typically used studies with laboratory animal species).
Surface area—Coating, triangulation, and surface integration are direct measurement techniques
that have been used to measure total body surface area and the surface area of specific body
parts. Consideration has been given for differences due to age, gender, and race.
Target—Any physical, biological, or ecological object exposed to an agent. See also Agent.
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Time-averaged exposure—The time-integrated exposure divided by the exposure duration. An
example is the daily average exposure of an individual to carbon monoxide (also called time
weighted average exposure).
Time use data—Information on activities in which various individuals engage, length of time
spent performing various activities, locations in which individuals spend time, and length of time
spent by individuals within those various environments.
Toddler—A child over the age of 12 months and generally younger than 36 months. See also
Infant and Children.
Transfer efficiency—The percentage of a material that ends up as a coating on the desired
surface.
Uncertainty—Uncertainty represents a lack of knowledge about factors affecting exposure/dose
or risk and can lead to inaccurate or biased. The types of uncertainty include scenario,
parameter, and model.
Unit risk—The quantitative estimate in terms of either risk per (J,g/L drinking water (water unit
risk) or risk per ug/m3 air breathed (air unit risk).
Upper percentile—Values in the upper tail (i.e., between 90th and 99.9th percentile) of the
distribution of values for a particular exposure factor. Values at the upper end of the distribution
for a particular set of data.
Uptake—The process by which a substance crosses an absorption barrier and is absorbed into
the body.
Variability—Variability arises from true heterogeneity across people, places, or time and can
affect the precision of exposure/dose estimates and the degree to which they can be generalized.
The types of variability include spatial, temporal, and inter-individual.
Wet-weight intake rates—Intake rates that are based on the wet (or whole) weight of the food
consumed. This is in contrast to dry-weight intake rates.
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