fir EPA
United States
Environmental Protection
Agency
Office Of Air Quality
Planning And Standards
Research Triangle Park, NC 27711
EPA-453/R-99-007
July 2000
Air
NATIONAL AIR TOXICS
PROGRAM: THE INTEGRATED
URBAN STRATEGY
Report to Congress
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EPA-453/R-99-007
t>
NATIONAL AIR TOXICS PROGRAM:
THE INTEGRATED URBAN STRATEGY
Report to Congress
U S. Environmental Potion Agenc,
Re«.on 5, Library (PL-12J)
77 West Jackson Boulevard, 12UI
Chicago, IL 60604-3590
U.S. ENVIRONMENTAL PROTECTION AGENCY
Office of Air and Radiation
Office of Air Quality Planning and Standards
Research Triangle Park, North Carolina 27711
July 2000
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ACKNOWLEDGEMENTS
This Report was prepared by the U.S. Environmental Protection Agency's (EPA's) Office
of Air Quality Planning and Standards (OAQPS) with input and review by other EPA Offices
and Regions. The Project Leads were Mr. Jaime Pagan and Ms. Laura Me Kelvey.
We would like to acknowledge the contributions of the Agency work group members and
others involved in the development of the report, including staff (too numerous to name) in
OAQPS, the Offices of Transportation and Air Quality; Research and Development; Solid Waste
and Emergency Response; Prevention, Pesticides, and Toxic Substances; and General Counsel,
as well as EPA Regions I, n, IV, and V.
Also, special thanks to the group of external scientific experts that conducted the peer
review of Chapter 6 of this Report. These experts are:
Dr. Viney Aneja Department of Marine, Earth and Atmospheric
Sciences, North Carolina State University
Dr. Gail Charnley Health Risk Strategies
Dr. Merrill Jackson Consultant
Dr. Daland Juberg International Center for Toxicology and Medicine
Dr. Petros Koutrakis Harvard School of Public Health
Dr. Ron Wyzga Electric Power Research Institute
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National Air Toxics Program: The Integrated Urban Strategy
Report to Congress
Table of Contents
Executive Summary ES-1
1. Introduction 1-1
1.1 Characterization of Urban Air Pollution (Chapter 2) 1-2
1.2 Emissions Inventory and Selection of the Urban Pollutants (Chapter 3) 1-2
1.3 Regulatory Programs and Activities to Reduce Air Toxics Emissions
(Chapter 4) 1-3
1.4 Assessment of Progress Toward the Goals (Chapter 5) 1-4
1.5 Research Needed to Address Knowledge Gaps (Chapter 6) 1-5
2. Characterization of Urban Air Pollution 2-1
2.1 Introduction 2-1
2.2 What Do We Know About HAP? 2-1
2.3 What Do We Know About HAP Emissions? 2-2
2.4 What Do Monitoring Data Tell Us? 2-4
2.5 What Do We Know About Urban Populations? 2-5
2.6 Characterization of Air Toxics in Urban Areas 2-6
2.7 Why Is the Urban Strategy Needed? 2-17
2.8 References 2-18
3. Emissions Inventory and Selection of the Urban Pollutants 3-1
3.1 Introduction 3-1
3.2 Baseline Emissions Inventory for the Integrated Urban Air Toxics Strategy .. 3-2
3.2.1 Development of the Baseline Inventory 3-3
3.2.2 Baseline Inventory Results 3-5
3.2.3 Allocating Emissions Between Locations and Source Types 3-7
3.2.4 Limitations of the Emissions Inventory 3-9
3.3 Ranking the Urban Hazardous Air Pollutants 3-11
3.3.1 Exposure/Toxicity Indicators Ranking Analysis 3-13
3.3.2 Risk Assessment/Hazard Ranking Studies in Urban Areas 3-18
3.3.3 CEP Ranking Analysis 3-19
3.4 Selection of the Urban Hazardous Air Pollutants 3-21
3.5 References 3-26
4. Regulatory Programs and Activities to Reduce Air Toxics Emissions 4-1
4.1 Introduction 4-1
4.2 List of Area Source Categories 4-1
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National Air Toxics Program: The Integrated Urban Strategy
Report to Congress
Table of Contents (Continued)
Page
4.3 Regulatory Activities for Area Sources 4-3
"- 4.3.1 Tier 1 - MACT Standards 4-4
4.3.2 Tier 2 - Source Category-Specific GACT Standards 4-4
4.3.3 Tier 3 - Flexible GACT Process 4-4
4.3.4 Issues on the National Versus Local Scope of Area Source Standards . 4-5
4.3.5 Schedule for Area Source Standards 4-6
4.4 Regulatory Activities for Mobile Sources 4-6
4.4.1 Urban HAP Emitted from Mobile Sources 4-6
4.4.2 Diesel Exhaust 4-7
4.4.3 Mobile Source Emission Control Programs 4-9
4.4.4 Mobile Source Air Toxics Assessments and Controls 4-10
4.5 Other Hazardous Air Pollutant Emission Sources 4-12
4.6 Other Programs and Authorities 4-13
4.6.1 Federal Regulatory Activities - CAA Section 112 Authorities 4-16
4.6.2 Other CAA Authorities 4-17
4.6.3 Other Authorities, Laws, Rules, and Programs to Help Reduce
HAP Emissions 4-18
4.7 State, Local, and Tribal Activities 4-21
4.7.1 Why are State, Local, and Tribal Programs Integral to the
Strategy? 4-22
4.7.2 What are the Objectives of State, Local, and Tribal Activities? 4-23
4.7.3 How Can State, Local or Tribal Agencies Participate in the
Strategy? 4-24
4.7.4 What Elements Should a State, Local or Tribal Program Contain? ... 4-25
4.8 References 4-25
5. Assessment of Progress Toward Goals 5-1
5.1 Overview of Health Risks 5-1
5.2 The EPA Risk Assessment Paradigm 5-2
5.2.1 Exposure Assessment 5-3
5.2.2 Dose-Response Assessment 5-6
5.2.3 Risk Characterization 5-13
5.3 Methods, Tools, and Data to Estimate Risk 5-18
5.3.1 Assessing Exposures and Characterizing Risks 5-18
5.3.2 Summary 5-21
5.4 The Overall Risk Assessment Approach for the Strategy 5-22
5.4.1 Designing the Assessments 5-22
5.4.2 Addressing Disproportionate Risks 5-23
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National Air Toxics Program: The Integrated Urban Strategy
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Table of Contents (Continued)
Page
5.5 Designing Future Assessments 5-23
- 5.5.1 Initial Assessments - National 5-24
5.5.2 Initial Assessments - Urban 5-25
5.5.3 Periodic Assessments 5-25
5.6 References 5-26
6. Research Needed to Address Knowledge Gaps 6-1
6.1 Exposure Assessment 6-2
6.2 Health Effects and Dose-Response Assessment 6-13
6.3 Risk Assessment/Characterization 6-22
6.4 Risk Management 6-24
6.5 References 6-26
Appendix
Overview A-l
Acetaldehyde A-3
Acrolein A-9
Acrylonitrile A-15
Arsenic Compounds A-21
Benzene A-29
Beryllium Compounds A-35
1,3-Butadiene A-43
Cadmium Compounds A-49
Carbon Tetrachloride A-55
Chloroform A-63
Chromium Compounds A-71
Coke Oven Emissions A-81
1,2-Dichloroethane (Ethylene Dichloride) A-85
1,2-Dichloropropane (Propylene Dichloride) A-93
1,3-Dichloropropene A-99
Ethylene Dibromide (1,2-Dibromoethane) A-107
Ethylene Oxide A-l 13
Formaldehyde A-l 19
Hexachlorobenzene A-127
Hydrazine A-133
Lead Compounds A-139
Manganese Compounds A-147
Mercury Compounds A-153
Methylene Chloride A-163
Nickel Compounds A-169
-in-
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Table of Contents (Continued)
Page
Polychlorinated Biphenyls (PCBs) A-177
Polycyclic Organic Matter (POM) A-185
Quinoline A-193
2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) A-197
1,1,2,2-Tetrachloroethane A-201
Tetrachloroethylene (Perchloroethylene) A-207
Trichloroethylene A-215
Vinyl Chloride A-223
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National Air Toxics Program: The Integrated Urban Strategy
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List of Exhibits
Pas
Exhibit ES-l
Exhibit ES-2
Exhibit ES-3
Exhibit 2-1
Exhibit 2-2
Exhibit 2-3
Exhibit 2-4
Exhibit 3-1
Exhibit 3-2
Exhibit 3-3
Exhibit 3-4
Exhibit 3-5
Exhibit 3-6
Exhibit 3-7
Exhibit 3-8
Exhibit 3-9
Exhibit 4-1
Exhibit 4-2
Exhibit 4-3
Exhibit 4-4
Exhibit 5-1
Exhibit 5-2
Exhibit 5-3
Exhibit 5-4
Exhibit 6-1
List of Urban HAP for the Integrated Urban Air Toxics Strategy
("Urban HAP List") ES-4
Area Source Categories Already Subject to Standards or
Which Will Be Subject to Standards ES-5
New Area Source Categories Being Listed ES-5
HAP Baseline NTI Emissions by Source 2-3
HAP Emissions by State Based on 1993 NTI 2-3
Risk-Based Assessments Covering Urban Areas 2-10
Overview of Assessments 2-11
Baseline Emissions Inventory Estimates for Each of
the 40 Candidate Urban HAP (1990-1993) 3-6
Sources of Baseline Emissions from the Candidate Urban HAP 3-7
Spatial Allocation of Baseline Emissions of the
Candidate Urban HAP 3-7
40 Highest Priority Pollutants Identified by Exposure/Toxicity
Indicators Ranking 3-15
Priority HAP Identified by Studies in Urban Areas 3-18
HAP with Modeled Concentrations Higher than an RBC in
at Least 50 Urban Census Tracts 3-20
HAP Ranking Analysis for the Integrated Urban Strategy 3-22
Results of the Three Ranking Analyses 3-23
List of Urban HAP for the Integrated Urban Air Toxics Strategy 3-25
Area Source Categories Already Subject to
Regulation or Which Will Be Subject to Regulation 4-2
New Area Source Categories As Listed 4-3
1990 National Emission Estimates for Urban HAP Emitted from
Mobile Sources 4-8
Completed Rules from Section 112 of the CAA
(MACT Standards) 4-14
EPA Paradigm for Risk Assessment and Risk Management 5-3
Sources of Information for Hazard Identification 5-7
Summary of Major Differences Between EPA's 1986 Guidelines
(U.S. EPA, 1986b) and 1996 Proposed Guidelines for Carcinogen
Risk Assessment (U.S. EPA, 1996b) 5-13
Guiding Principles with Respect to Risk Descriptors 5-15
Status of Fiscal Year 1999 IRIS Activities for HAP 6-16
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National Air Toxics Program: The Integrated Urban Strategy
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Acronym List
AEGL acute exposure guidance level
AIHA American Industrial Hygiene Association
AIRS Aerometric Information Retrieval System
ARE acute reference exposure
ASPEN Assessment System for Population Exposure Nationwide
ATSDR Agency for Toxic Substances and Disease Registry
BCF bioconcentration factor
BMD benchmark dose
CAA Clean Air Act
CAS Chemical Abstract Services
CASAC Clean Air Scientific Advisory Committee
CEP Cumulative Exposure Project
CERCLA Comprehensive Environmental Response, Compensation, and Liability Act
CFR Code of Federal Regulations
CHAD Consolidated Human Activity Database
CMAQ Community Multi-Scale Air Quality
C/MSA consolidated metropolitan statistical area
CO carbon monoxide
CWA Clean Water Act
DNA deoxyribonucleic acid
DOT Department of Transportation
BMP ACT Environmental Monitoring for Public Access and Community Tracking
EPA Environmental Protection Agency
EPCRA Emergency Planning and Community Right-to-Know Act
ERPG emergency response planning guideline
ES Executive Summary
FIFRA Federal Insecticide, Fungicide and Rodenticide Act
FR Federal Register
GACT generally available control technology
GIS geographic information systems
GLC ground-level concentration
HAP hazardous air pollutant
HAPEM Hazardous Air Pollutant Exposure Model
HASTE Houston Area Source Toxic Emissions
HC hydrocarbon
HEAST Health Effects Assessment Summary Tables
HEC human equivalent concentration
HI hazard index
HQ hazard quotient
IEM Integrated Exposure Methodology
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National Air Toxics Program: The Integrated Urban Strategy
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Acronym List (Continued)
I/M inspection and maintenance
IRIS Integrated Risk Information System
ISC3 ' Industrial Source Complex
km kilometers
K,,w octanol-water partition coefficient
LCA Life Cycle Analysis
LOAEL lowest-observed-adverse-effect level
LOG level of concern
LIDAR Light Detecting and Ranging
MACT maximum achievable control technology
MEASURE Mobile Emissions Assessment System for Urban and Regional Evaluation
MMT methylcyclopentadienyl manganese tricarbonyl
MOU memorandum of understanding
MPCA Minnesota Pollution Control Agency
MPO Metropolitan Planning Organizations
MRL minimal risk level
MSA metropolitan statistical area
MTBE methyl tertiary butyl ether
MWC municipal waste combustor
MWI municipal waste incinerator
NAAQS national ambient air quality standard
NAC National Advisory Committee
NERL National Exposure Research Laboratory
NESHAP national emission standards for hazardous air pollutants
NHAPS National Human Activity Pattern Survey
NHEXAS National Human Exposure Assessment Survey
NOAEL no-observed-adverse-effect level
NOX nitrogen oxide
NTI National Toxics Inventory
PAH polycyclic aromatic hydrocarbons
PAMS Photochemical Assessment Monitoring Stations
PBPK physiologically based pharmacokinetic (model)
PBT persistent, bioaccumulative, and toxic
PCB polychlorinated biphenyls
PCDD polychlorinated dibenzo-p-dioxin
PCDF polychlorinated dibenzofuran
PM paniculate matter
PMX particulate matter (x microns or smaller)
PNGV Partnership for a New Generation of Vehicles
POM polycyclic organic matter
PPA Pollution Prevention Act
-Vll-
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National Air Toxics Program: The Integrated Urban Strategy
Report to Congress
Acronym List (Continued)
PSI pollutant standard index
QSTR quantitative structure-toxicity relationship
RBC "- risk-based concentration
RED risk-based dose
RCRA Resource Conservation and Recovery Act
RDDR regional deposited dose ratio
REL reference exposure level
RfC reference concentration
RfD reference dose
RFG reformulated gasoline
RMP Risk Management Program
SAB Science Advisory Board
S AR structure-activity relationship
SARA Superfund Amendments and Reauthorization Act
SIC Standard Industrial Classification
TCDD 2,3,7,8-tetrachlorodibenzo-p-dioxin
TCDF 2,3,7,8-tetrachlorodibenzofuran
TEAM Total Exposure Assessment Methodology
TEF toxic equivalency factor
TMDL total maximum daily load
TNRCC Texas Natural Resources Conservation Commission
TRI Toxics Release Inventory
TRIM Total Risk Integrated Methodology
TSCA Toxic Substance Control Act
TSD treatment, storage, and disposal
UF uncertainty factors
U.S. United States
U.S.C. United States Code
VMT vehicle-miles of travel
VOC volatile organic compounds
WMPT Waste Minimization Prioritization Tool
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National Air Toxics Program: The Integrated Urban Strategy
Report to Congress
Executive Summary
On July 19, 1999, we published a notice in the Federal Register entitled "National Air
Toxics Program: The Integrated Urban Air Strategy" (Strategy) that outlined the U.S.
Environmental Protection Agency's (EPA's) plans for addressing cumulative health risks in
urban areas'. The Strategy presented our plan for future actions to reduce emissions of air toxics
and improve our understanding of the health risks posed by toxics in urban areas.
Section 112(k) of the Clean Air Act (CAA) requires the EPA Administrator to submit
two Reports to Congress on actions taken under the CAA that reduce the risk to public health
posed by the release of hazardous air pollutants (HAP) from area sources. This Report to
Congress (Report), originally due in 1998, was prepared to meet the first part of that
requirement. In addition, it expands on much of the information provided in the Strategy, such as
the methodology for developing the emissions inventory, identifying the 33 urban HAP and
identifying the area source categories that will be subject to regulation. Furthermore, this Report
summarizes existing information on risk assessments that have been conducted in various urban
areas. These studies were performed by EPA and various States over the last several years.
Taking into consideration the uncertainties and limitations of each study, these assessments
provide useful information on the potential nature and magnitude of exposures and health risks in
urban areas. Finally, this Report also provides a very detailed discussion of 13 research needs to
address in achieving the goals of the Strategy. These needs were identified in the following
areas: exposure assessment, health effects, dose-response assessment, risk assessment, risk
characterization and risk management. In addition, Chapter 6 of this Report provides a summary
of ongoing EPA activities to address those needs.
Section 112(k) also requires EPA to identify specific metropolitan areas that continue to
experience high risks to public health as the result of emissions from area sources. Since we
have only recently begun to work toward implementing the Strategy, we are unable to identify in
this first Report the metropolitan areas that continue to experience high risks to public health as
the result of emissions from areas sources. However, in the next few years, as we make progress
toward the goals of the Strategy, we will be better able to identify those metropolitan areas with
high risks due to air toxics.
The following sections provide an overview of the Strategy and describe the four
components of the Strategy and explain their role in achieving its goals. The four components
are: Standard Setting Activities, National and Local Initiatives, Air Toxics Assessments, and
Education and Outreach. These components also form the framework of our National Air Toxics
Program. Finally, Chapter 1 of this Report summarizes the contents of each chapter and their key
points. Important health and other general information about each one of the 33 urban HAP is
provided in the Appendix.
]64 FR 38705. National Air Toxics Program: The Integrated Urban Strategy (Notice). July 19,1999.
ES-1
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National Air Toxics Program: The Integrated Urban Strategy
Report to Congress
Overview of the Strategy
The Strategy presents a framework for further reducing HAP emissions from all types of
sources found in urban areas, including major industrial sources, smaller stationary sources, and
cars and trucks. Air toxics can pose special threats in urban areas because of the large number of
people and the variety of sources that emit HAP. Individually, some of these sources may not
emit large amounts of toxic pollutants. However, all of these pollution sources combined can
potentially pose significant health threats. We are also concerned about the impact of toxics
emissions on minority and low income communities which are often located close to industrial
and commercial urbanized areas. Accordingly, there are three goals for the Strategy:
1. Reduce, bv 75 percent, the incidence of cancer associated with air toxics from both large
and small industrial/commercial sources. This is relevant to all HAP from both major and
area stationary sources in all urban areas nationwide. Reductions can be the result of
actions by Federal, State, local and/or Tribal governments achieved by any regulations or
voluntary actions.
2. Substantially reduce noncancer health risks (e.g.. birth defects and reproductive effects)
associated with air toxics from small industrial/commercial sources. This includes health
effects other than cancer posed by all HAP. Reductions can be the result of actions by
Federal, State, local and/or Tribal governments achieved by any regulations or voluntary
actions.
3. Address disproportionate impacts of air toxics hazards across urban areas, such as those
in areas known as "hot spots." and minority and low-income communities in urban areas.
This will necessarily involve consideration of both stationary and mobile source
emissions of all HAP, as well as sources of HAP in indoor air. We intend to characterize
exposure and risk distributions both geographically and demographically. This will
include particular emphasis on highly exposed individuals (such as those in geographic
"hot spots") and specific population subgroups (e.g., children, the elderly, and low-
income communities).
To accomplish these goals, the Strategy is comprised of four key components:
1. Standard setting activities addressing sources of air toxics at both the national and local
level;
2. Initiatives at both the national and local level to address specific pollutants (e.g., mercury)
and to identify and address specific community risks (e.g., through pilot projects);
3. Air toxics assessments (including expanded air toxics monitoring and modeling) to
identify areas of concern, to prioritize efforts to reduce risks, and to track progress; and
ES-2
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National Air Toxics Program: The Integrated Urban Strategy
Report to Congress
4. Education and outreach efforts to inform stakeholders about the Strategy and to get input
into designing programs to implement it.
Standard Setting Activities
This first component includes our regulatory tools and programmatic activities for source-
specific and sector-based standard setting, as well as those of States, local agencies, and Tribes.
These standards contribute to reductions in emissions of air toxics from major, area, and mobile
sources. This component includes activities such as selecting urban HAP, setting emission
standards, conducting studies, developing policies, and conducting enforcement and compliance
assistance activities. These actions result in emission reductions, as well as associated reductions
in risk.
The C AA includes certain specific requirements for the Strategy. First, we must identify
at least 30 HAP, "which, as the result of emissions from area sources, present the greatest threat
to public health in the largest number of urban areas" (CAA § 112(k)(3)(B)(i)). To select these
HAP, we evaluated the health effects information available for 188 HAP, estimated emissions
from all known sources using a variety of techniques, assessed available air quality monitoring
data, reviewed existing studies, and produced a list of pollutants based on the relative hazards
they pose in urban areas, considering toxicity, emissions, and related characteristics. From this
effort, we established a list of 33 urban HAP which pose the greatest threats to public health in
urban areas, considering emissions from major, area and mobile sources (see Exhibit ES-1). This
list includes not only those that are emitted from area sources, but reflects the integrated nature of
the Strategy by including those posing public health concerns in urban areas regardless of
emissions source type. Included among the 33 urban HAP are the 30 HAP with greatest
emissions contributions from area sources (i.e., the "area source HAP"). The remaining three
urban HAP (i.e., coke oven emissions, 1,2-dibromoethane and carbon tetrachloride) have less
significant emissions contributions from area sources. Under section 112(k), there are no
specific regulatory implications of listing these three HAP, but we'll use all 33 HAP in
prioritizing efforts to address risks.
Second, we're required to assure that sources accounting for 90 percent of the emissions
of identified area source HAP are subject to standards (CAA § 112(c)(3) and (k)(3)(B)(ii)). We
adopted a two-step process for selecting the source categories which will be subject to regulation
under the Strategy. First, we identified those area source categories that emit one or more of the
30 area source HAP that are already listed for regulation under the CAA. For each of those
source categories, we identified the percentage contribution to the total area source emissions for
each of the 30 area source HAP.
In the second step, we added area source categories that, based on inventory data,
contribute at least 15 percent of the national urban emissions of at least one of the 30 area source
HAP. We adopted this criterion to account for the uncertainties in our current emissions
inventory data. While we've been able to significantly improve our baseline emissions inventory
ES-3
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National Air Toxics Program: The Integrated Urban Strategy
Report to Congress
EXHIBIT ES-1
LIST OF URBAN HAP FOR THE INTEGRATED URBAN AIR TOXICS STRATEGY
("URBAN HAP LIST")
-. HAP
Acetaldehyde
Acrolein
Acrylonitrile
Arsenic compounds
Benzene
Beryllium compounds
1,3-butadiene
Cadmium compounds
Carbon tetrachloride*
Chloroform
Chromium compounds
Coke oven emissions*
1 ,2-dibromoethane*
1,2-dichloropropane (propylene
dichloride)
1 ,3-dichloropropene
Ethylene dichloride
( 1 ,2-dichloroethane)
Ethylene oxide
CAS No. +
75070
107028
107131
71432
106990
56235
67663
8007452
106934
78875
542756
107062
75218
HAP
Formaldehyde
Hexachlorobenzene
Hydrazine
Lead compounds
Manganese compounds
Mercury compounds
Methylene chloride
(dichloromethane)
Nickel compounds
Polychlorinated biphenyls
(PCBs)
Polycyclic organic matter (POM)
Quinoline
2,3 ,7,8-tetrachlorodibenzo-p-
dioxin (& congeners & TCDF
congeners)
1 , 1 ,2,2-tetrachloroethane
Tetrachloroethylene
(perchloroethylene)
Trichloroethylene
Vinyl chloride
CAS No. +
50000
118741
302012
75092
1336363
91225
1746016
79345
127184
79016
75014
+ Chemical Abstracts System number. *HAP with less significant contributions from area sources.
data, data gaps and uncertainty still remain. The list of source categories will be modified to
reach the 90 percent requirement by 2003.
As a result of this two-step approach, the Strategy identified and listed 29 area source
categories that emit significant amounts of one or more of the 30 area source HAP. Currently,
we have regulations under development or completed for 16 of these area source categories. We
ES-4
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National Air Toxics Program: The Integrated Urban Strategy
Report to Congress
expect to develop regulations for the remaining 13 area source categories over the next five
years. Exhibit ES-2 shows those area source categories, as listed in the Strategy, that contribute
to emissions of the 30 area source HAP, and are either subject to existing standards, or will be
subject to standards that are currently being developed. Exhibit ES-3 shows the area source
categories listed in the Strategy for the first time, as required in section 112(c)(3). These are the
area source categories that contribute at least 15 percent of the total area source emissions of at
least one of the 30 area source HAP.
EXHIBIT ES-2
AREA SOURCE CATEGORIES ALREADY SUBJECT TO STANDARDS
OR WHICH WILL BE SUBJECT TO STANDARDS
Chromic Acid Anodizing
Commercial Sterilization Facilities
Other Solid Waste Incinerators (Human/Animal
Cremation)
Decorative Chromium Electroplating
Dry Cleaning Facilities
Halogenated Solvent Cleaners
Hard Chromium Electroplating
Hazardous Waste Combustors
Industrial Boilers
Institutional/Commercial Boilers
Medical Waste Incinerators
Municipal Waste Combustors
Open Burning Scrap Tires
Portland Cement
Secondary Lead Smelting
Stationary Internal Combustion Engines
EXHIBIT ES-3
NEW AREA SOURCE CATEGORIES BEING LISTED
Cyclic Crude and Intermediate Production
Flexible Polyurethane Foam Fabrication
Operations
Hospital Sterilizers
Industrial Inorganic Chemical Manufacturing
Industrial Organic Chemical Manufacturing
Mercury Cell Chlor-Alkali Plants
Gasoline Distribution Stage I
Municipal Landfills
Oil & Natural Gas Production
Paint Stripping Operations
Plastic Materials and Resins Manufacturing
Publicly Owned Treatment Works
Synthetic Rubber Manufacturing
ES-5
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With respect to mobile sources, title n of the CAA provides several mechanisms to
achieve reductions in HAP. The most direct of these is section 202(1) which requires us to
identify the need for and consider regulations for control of HAP from motor vehicles and their
fuels. Those standards are to reflect the greatest degree of emissions reductions achievable
through the application of technology which will be available, taking existing standards,
availability and costs of the technology, noise, energy and safely factors into account. Section
202(1)(2) further specifies that, at a minimum, benzene and formaldehyde emissions must be
addressed.
The section 202(1)(2) proposal will identify the HAP emitted by motor vehicles and their
fuels, assess the reductions achieved by our current and recently proposed title n regulations, and
evaluate the appropriateness of additional motor vehicle and fuel controls. With regard to
control strategies, several of the existing emission control programs developed under section
202(a) (motor vehicle controls) and section 211 (fuel controls) of the CAA already limit many
HAP emissions from motor vehicles and their fuels, hi our assessment of whether additional
action is appropriate under section 202(1)(2), we'll consider the impacts of these programs, our
recent and ongoing regulatory activities (such as our recent final rulemaking for new light-duty
"Tier 2" emission standards and gasoline sulfur controls2 and our recent proposal for heavy-duty
engine and vehicle standards and on-highway diesel fuel sulfur controls3), and such other mobile
source programs as are relevant to mobile source air toxics controls.
As we review existing regulations for a number of motor vehicle and nonroad engine
categories, the Strategy's goal of reducing disproportionate air toxics risks will be considered, hi
addition, we envision that work done in the early stages of implementing the Strategy, such as
improving monitoring and inventories, will help us compare options related to the various
emissions sources in urban areas and control authorities to provide the best relative reduction of
risks to the urban public. To the extent possible, we will consider costs in the development of
regulations aimed at reducing those risks. Capital costs, fuel costs and incremental labor costs to
operate equipment are some but not all of the factors that may be considered in assessing the cost
effectiveness of a particular control strategy.
Overall, in meeting the Strategy's goals, we'll consider reductions in HAP resulting from
Federal actions both to address air toxics (e.g., maximum achievable control technology (MACT)
standards under section 112(d), residual risk standards, mobile source emission controls) and
attain the national ambient air quality standards (NAAQS) for particulate matter (PM) and ozone,
as well as State, local and Tribal measures. We'll consider cumulative risks presented by
exposures to emissions of all HAP from all sources in a given area. Further, consistent with the
2 65 FR 6698. Tier 2 Motor Vehicle Emission Standards and Gasoline Sulfur Control Requirements.
February 10, 2000.
3 65 FR 35430. Proposed Heavy-Duty Engine and Vehicle Standards and Highway Diesel Fuel Sulfur
Control Requirements. June 2,2000.
ES-6
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direction of section 112(k)(4) to encourage and support areawide strategies developed by State or
local air pollution control agencies, we'll work with State, local, and Tribal air pollution control
programs for additional progress toward these goals.
National and Local Initiatives
The second component of the Strategy involves local and community-based initiatives to
focus on multimedia and cumulative risks within urban areas. Developing the Strategy is a
challenge at the national level because urban air toxics problems vary significantly across the
country. Because of this variability, the Strategy is being approached as a partnership between
EPA and State, local and Tribal governments. These governments (including municipal offices
other than pollution control departments) have the most experience with local air pollution
issues, and can lend their expertise and knowledge to address and resolve air toxics concerns that
are unique to cities. Many of these governments also have existing air pollution control
programs that currently address, and can effectively continue to address, some or all of these
issues. In addition, these governments are often able to act much more quickly than we can to
address local concerns, which leads to less overall pollution, particularly in the areas where
pollution is of greatest concern.
At the Federal level, we can contribute Federal standards and requirements using our
authorities to develop and implement a national regulatory program. We also have the
knowledge base and expertise to evaluate, or to help other agencies evaluate, air pollution
problems. By integrating our relative strengths, we can provide a stronger, more efficient, and
more effective program to address toxic air pollution in urban areas. For example, as discussed
in Chapter 5 of this Report, once we've completed the initial assessment, we'll have a better
understanding of our status with regard to the risk reduction goals of the Strategy. This will
inform us about additional Federal activities needed to meet those goals, and what additional
State, local and Tribal activities are needed to complement these activities. Periodic assessments
will continue to inform us about needed programs over time.
Concurrent with the initial assessments, we plan to meet with our State, local and Tribal
partners. We'll be reviewing the goals and the various components of the Strategy and how they
interrelate. In particular, we'll focus on the assessment tools and their role in defining Federal,
State, local, and Tribal activities. These activities may include pilot projects to identify and
address risk and may rely on some of the assessment activities and tools described below.
Air Toxics Assessments
The third component of the Strategy discussed in this Report is the urban component of
national air toxics assessments (NATA). NATA will provide us with meaningful information
and allow us to describe progress that we've made in meeting our overall program and strategy-
specific goals. We'll identify the pollutants and sources that contribute to any failures in meeting
our risk reduction goals and provide information to support regulatory and policy decisions
needed to move us closer to meeting these goals. These activities rely on improving our base of
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knowledge (e.g., concerning health effects and exposure characteristics) and tools (e.g.,
emissions inventories, monitoring networks, and computer models), along with our plans for
their improvement and related research.
Historically, EPA's risk assessment and decisionmaking have focused on the likelihood
of health effects associated with exposure to individual environmental contaminants. In recent
years, our risk assessment emphasis has shifted increasingly to a greater consideration of multiple
pollutants, endpoints, pathways, routes of exposure, and holistic reductions of risks. This
complex analysis is often called "cumulative risk assessment." It describes who or what is at risk
of adverse effects and identifies sources and stressors considering several different routes of
exposure over varied timeframes. Assessing progress in reducing cumulative risks from HAP
will require us to move away from a focus on assessing reductions in tons per year emitted
toward a focus on estimating reductions in cancer and noncancer risks associated with lower
emissions.
In general, the choice of appropriate risk assessment approaches will be influenced by
both the availability of data to support exposure assessment, and the level of detail and resolution
needed to support the purpose of the assessment. Possible approaches span a wide range, from
simple weighting adjustments of emissions data or ambient concentrations, to detailed
multipathway risk assessments. Our assessment approaches will be iterative in nature to take
advantage of emerging science, new data, and improved tools that become available as future
assessments are performed. Beginning in early 2000, we'll conduct an initial set of assessments
that will be based on final, updated emissions data for the 1990-93 and 1996 time periods and the
best available methods and tools.
We'll tailor each assessment to the purpose(s) it is to serve (e.g., measuring progress
against the 75 percent estimated cancer incidence reduction goal). Accordingly, assessments will
vary in scope, level of refinement, and, thus, data and resource requirements. The scope of each
assessment will generally be defined by the following characteristics:
The number of HAP to be evaluated (all 188 or some subset);
Types of sources included (area, major, mobile);
Spatial resolution (e.g., aggregation of results on the national, State, or urban scale); and
Pathways and media to be evaluated (inhalation and air only or multipathway and
multimedia).
Further, for each assessment, we will specify an appropriate approach for estimating
progress toward our risk reduction goals since it will not be possible to directly measure
reductions in cancer incidence or noncancer risks attributable to HAP emissions. Alternative
approaches will range from rough approximations to more precise risk estimates, depending on
data and resource requirements.
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Our risk assessment science has been extensively peer-reviewed, is widely used and
understood by the scientific community, and continues to expand and evolve as scientific
knowledge advances. We intend to use the most current and appropriate risk estimation methods
to track progress under the Strategy.
Education and Outreach
The fourth component of the Strategy, communicating about risks through education and
outreach to the public, ensures that the activities we undertake are responsive to stakeholder
concerns. Over the course of implementing the Strategy, we plan to work with State, local, and
Tribal governments and other stakeholders on developing the national assessments of the risks
from air toxics and the materials to communicate the findings with the public. We will include
State, local and Tribal authorities, and in particular mayors, in planning activities to assess and
address local air quality concerns and plan pilot project activities under the Strategy.
We will also explore the formation of groups such as roundtables and panels to involve
communities, small businesses and other stakeholders, including representatives from
universities and hospitals. These groups will explore issues related to rulemaking coordination,
risk assessments, and the process of defining roles and responsibilities for Federal and State,
local and Tribal agencies in implementing the Strategy. In addition, many of the activities
identified in the Strategy will require public notice and comment, which will provide further
opportunities for stakeholder input as the various activities are developed. We'll also continue to
use the established Integrated Urban Air Toxics Strategy website on the Internet to update the
public on ongoing activities and opportunities to participate in implementation of the Strategy.
This will include updates on rule development, assessment activities, and progress toward
meeting all of the Strategy goals.
As noted above, we're required by the CAA to provide two Reports to Congress on
actions taken to reduce the risks to public health posed by the release of HAP from area sources.
The CAA also requires that the reports identify specific metropolitan areas that continue to
experience high risks to public health as the result of emissions from area sources. This
document is our first Report to Congress. The second report is required to be submitted by 2002.
We also expect to report to the public about air toxics emissions trends and air quality in urban
and other areas in our annual Air Quality and Emissions Trends Reports.
Research Needs
The Strategy describes the process we'll use for identifying the various risks that may be
present in an urban environment. Part of that process is to determine gaps in our scientific
information and to identify the tools we'll need to assess urban risks and to implement the risk
reduction elements of the Strategy. Chapter 6 of this Report describes the activities and research
needed to assist in our assessment and management of risks in urban environments and to
improve risk assessment and risk management of air toxics from all emission sources.
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We're also developing an Air Toxics Research Strategy which will build on the research
needs presented in this Report, as well as other research strategies that our Office of Research
and Development has prepared that address specific air toxics research issues (e.g., the draft
Mercury Research Strategy, the draft Human Health Risk Assessment Research Strategy, and the
Ecological Research Strategy). The Air Toxics Research Strategy will identify the key scientific
questions that need to be answered for risk assessment and management of air toxics from all
emission sources and describe the research needed to answer them and, thereby, guide our
research efforts.
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1. Introduction
Since the enactment of the CAA Amendments of 1990, we have made considerable
progress in reducing emissions of air toxics from major stationary sources through regulatory,
voluntary and-other programs. Our efforts to characterize, prioritize and address the impacts of
HAP on the public health and the environment have resulted, or are projected to result, in large
reductions in HAP emissions. However, the pollution sources addressed by our efforts so far
account for only part of the air toxics problem.
Recently, EPA announced a Strategy that aims at reducing the health risks associated with
air toxics exposures affecting populations in urban areas. In addition to addressing specific
statutory requirements for area sources as outlined in section 112(k), the Strategy has the
following goals:
Attain a 75 percent reduction in incidences of cancer attributable to exposure to HAP
emitted by stationary sources in urban areas nationwide;
Attain a substantial reduction in public health risks posed by HAP emissions from area
sources in urban areas nationwide;1 and
Address disproportionate impacts of air toxics hazards across urban areas.
By integrating activities and programs under different parts of the CAA, we expect to
address more effectively the aggregate exposure to air toxics in areas where emissions and risks
are most significant.
This Report responds to a requirement in section 112(k)(5) of the CAA that calls for EPA
to submit a Report to Congress:
On actions taken under this subsection and other parts of this Act to
reduce the risk to public health posed by the release of hazardous
air pollutants from area sources. The reports shall also identify
specific metropolitan areas that continue to experience high risks to
public health as the result of emissions from area sources.
Even though this Report is being released shortly after the publication of the Strategy, it
provides further details on many of its key areas. For example, this Report contains a more
detailed discussion of the research needs to be addressed as part of the Strategy. Also, the
emissions inventory and methodology for the selection of the urban HAP are discussed more
thoroughly here. Since the Strategy has not been implemented yet, we're unable, in this Report,
works.
'Examples of area sources include hospital sterilizers, dry cleaners, and small publicly owned treatment
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to identify specific metropolitan areas that continue to experience high risks to public health.
Nevertheless, we are providing, in this Report, a summary of recent risk-based assessments in
various urban areas. These assessments provide useful information on the potential nature and
magnitude of exposures and health risks in urban areas.
The following sections will provide a glimpse of the main issues discussed in each
chapter of this Report. Also, the Appendix gives key information about each of the urban HAP.
1.1 Characterization of Urban Air Pollution (Chapter 2)
The urban environment is very unique since the combination of high population densities
and large concentrations of commercial activity provide the conditions conducive to high
exposures and health risks as a result of the emissions of air toxics. Hazardous air pollutants are
emitted from thousands of sources ranging from small commercial facilities to large industrial
sources and also mobile sources. As the ambient concentrations of HAP in urban areas result
from a combination of different sources (e.g., area, major2, and mobile3) emitting many of the
same pollutants, we need to consider contributions from all types of sources in order to achieve
the reductions envisioned by Congress. The Strategy, described in detail in this Report, is that
part of the overall air toxics program that specifically focuses on the urban environment. The
Strategy will consider contributions from area, major, and mobile sources of HAP in addressing
reductions in public health risks.
Chapter 2 provides general information on our current understanding of the urban
environment and presents a summary of risk analyses that have been conducted over the past 10
years. Although it is not possible to draw any specific conclusions on current health risks, the
data that are available today support our concern that potential problems exist in urban areas and
suggest that we should continue our efforts to study the urban environment and to implement the
Strategy this Report presents.
1.2 Emissions Inventory and Selection of the Urban Pollutants (Chapter 3)
Chapter 3 presents two very important components of the Strategy. The first is the
baseline emissions inventory for 40 candidate HAP used to identify the final list of urban HAP.
The baseline inventory quantifies the emissions of the candidate urban HAP and identifies the
source categories that emit them. The second is the ranking methodology used to identify the
final list of 33 priority urban HAP which are judged to present the greatest threats to public
health in the largest number of urban areas.
2Major stationary sources are sources that emit more than 10 tons per year of any one HAP or 25 tons per
year of a combination of HAP. Examples include chemical plants, oil refineries, aerospace manufacturers and steel
mills.
3Mobile sources include motor vehicles (e.g., cars and trucks), and off-road equipment (e.g., construction
equipment and lawn mowers) and their fuels.
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In developing the final HAP list, we estimated emissions from all known sources using a
Variety of techniques, evaluated available health effects information for the 188 HAP, assessed
available air quality monitoring data, reviewed existing studies, and produced a list of pollutants
based on the relative hazards they pose in urban areas, considering toxicity, emissions, and
related characteristics. From this effort, we established a list of urban HAP which pose the
greatest threats to public health in urban areas, considering emissions from major, area and
mobile sources. Among these urban HAP are a subset of 30 HAP with the greatest emissions
contributions from area sources (the "area source HAP"). The analyses leading up to the
selection of these priority urban HAP are the focus of this chapter.
1.3 Regulatory Programs and Activities to Reduce Air Toxics Emissions
(Chapter 4)
Chapter 4 presents the list of area source categories that were identified in the Strategy
and explains how we intend to ensure that, as required, we reach the goal of addressing the
source categories that represent 90 percent of the emissions of each of the 30 area source HAP.
Also, this chapter describes the regulatory options that will be considered in order to address air
toxics from area sources. The role of mobile sources is also noted in this chapter, and the current
and future programs are described. Finally, a very important component of the Strategy is
described in this chapter - the role of State, local and Tribal programs in helping us address air
toxics and achieve the desired goals.
Chapter 4 describes the regulatory approaches to enable the emission reductions
necessary to achieve the goals of the Strategy. We plan to pursue a tiered approach that will
consider three standard-setting processes. The specific process selected for a particular source
category will depend on the criteria outlined below:
Tier 1 - Maximum achievable control technology (MACT) standard process;
Tier 2 - Source category-specific generally available control technology (GACT)
standard process; and
Tier 3 Flexible GACT process.
The Strategy outlined a timeframe for the completion of area source standards, as shown
in the time line below:
2004 - Promulgate the area source standards newly listed in the Strategy; we'll attempt to
meet this demanding schedule as expeditiously as practicable;
2006 - Promulgate some additional area source standards to meet the 90 percent
requirement;
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2009 - Promulgate all remaining area source standards necessary to meet the 90 percent
requirement; and
2012 - Expected compliance under all standards.
We'll prioritize the order in which we regulate source categories to address those posing
the greatest risks first.
Mobile sources and their role in the air toxics problem are also discussed in Chapter 4.
Several of our existing emission control programs limit HAP emissions from mobile sources,
primarily through the regulation of hydrocarbon (HC), oxides of nitrogen (NOX) and particulate
matter (PM) emissions. We achieve mobile source controls through a range of programs under
various sections of the CAA, including motor vehicles controls, emission standards for nonroad
engines and vehicles and urban bus standards. In addition, section 202(1)(2) of the CAA directs
us to set standards for air toxics emissions from motor vehicles or their fuels, or both. Some of
the current and future regulations and programs aimed at reducing HAP emissions from mobile
sources are highlighted in this chapter.
1.4 Assessment of Progress Toward the Goals (Chapter 5)
The discussion of our assessment activities in this chapter first focuses on how we
generally intend to assess progress in meeting the goals of the Strategy. We then discuss in more
detail our methods and tools for estimating health risks and describe more specifically how we
intend to apply these risk assessment methods and tools in assessing progress and in supporting
implementation of the Strategy.
As we move from a focus on emissions reductions to a focus on estimated risks
reduction, we note that Agency risk assessment and decisionmaking have historically focused on
the likelihood of health effects associated with exposure to individual environmental
contaminants. In recent years, our risk assessment emphasis has shifted increasingly to a greater
consideration of multiple pollutants, endpoints, pathways and routes of exposure, and integrated
reduction of risks. This more complex assessment is often called "cumulative risk assessment,"
defined according to who or what is at risk of adverse effects, from identifiable sources and
stressors, through several routes of exposure over varied timeframes. While various integrated
approaches are now being used within the Agency, we realize that there are significant gaps in
methods, models and data that limit our ability to assess cancer and noncancer risks associated
with cumulative exposure to mixtures of pollutants having different endpoints. Progress toward
more refined assessments of cumulative risks will depend upon the pace and evolution of our
policy and guidance on cumulative risk and the underlying research.
We've identified four basic approaches that we plan to use for various assessments to
evaluate the progress of the Strategy in reducing estimated risks. Each of these approaches uses
the same dose-response information, but relies on different types of data to represent exposures.
The four basic approaches that we intend to use are:
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Emissions or ambient concentration weighting;
Comparisons between ambient concentrations and risk-based concentrations (RBCs);
Comparisons between estimated exposures and RBCs; and
Quantitative estimates of carcinogenic risks for individuals and populations.
Each of these approaches is discussed in Chapter 5.
1.5 Research Needed to Address Knowledge Gaps (Chapter 6)
The purpose of Chapter 6 is to describe the types of scientific information and related
research needed to better inform future risk assessment and risk management judgments that will
be made in carrying out the Strategy. The research needs presented in this chapter are
categorized into both short-term (less than five years) and long-term (greater than five years).
These needs are organized around the risk assessment/risk management paradigm, first
promulgated by the National Academy of Sciences in 1983. The needs are listed below:
Exposure Assessment Information Needs
Need 1. Improved ambient monitoring methods, characterization, and network design to
support a national ambient air toxics monitoring network.
Need 2. Improved area source emissions estimation methodologies and spatial allocation
methods.
Need 3. Methodologies that allow for identification and speciation of important HAP and
their combustion and transformation products.
Need 4. A more accurate nonroad mobile source emissions characterization.
Need 5. Improved characterization of air toxics from trucks and improvement of modal
emissions modeling capabilities for all vehicle classes.
Need 6. Development of source-based urban-scale air quality models for the urban HAP.
Need 7. An understanding of the distribution of human exposures (including susceptible
subpopulations) and the pathways by which HAP reach humans.
Health Effects Information Needs
Need 8. Use alternative sources of human health effects data (chronic and acute) for urban
HAP to develop and update dose-response assessments.
Need 9. Development of statistical and mode of action methods for developing acute and
chronic dose-response assessments.
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Risk Assessment and Risk Characterization Information Needs
Need 10. Improved risk assessment methods for mixtures.
Need 11. - Development of better information for more effective techniques for
communicating the results of health risk assessments for urban HAP.
Risk Management Information Needs
Need 12. Identification of processes contributing to the HAP emissions from area source
categories, and listing of control options and pollution prevention alternatives for
these processes.
Need 13. Identification of pollution prevention alternatives for HAP emissions from mobile
sources.
Each of these needs for further research are discussed in Chapter 6.
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2. Characterization of Urban Air Pollution
2.1 Introduction
The urban environment is unique in many ways. In urban areas, you will find a mix of
chemicals and their sources in close proximity to diverse populations, leading to large numbers
of people being exposed to the emissions of many HAP from many sources. While urban
exposures to some pollutants may be fairly similar across the country, studies in a number of
urban areas indicate that exposures and associated risks may vary significantly from one urban
area to the next. Recognizing this, Congress instructed us to develop a strategy for air toxics in
urban areas that includes specific regulatory actions addressing the large number of smaller,
stationary sources (i.e., area sources), and which also contains broader risk reduction goals
encompassing all stationary sources. Specifically, section 112(k)(l) of the CAA states:
The Congress finds that emissions of hazardous air pollutants from area sources may
individually, or in the aggregate, present significant risks to the public health in urban
areas. Considering the large number of persons exposed and the risks of carcinogenic
and other adverse health effects from hazardous air pollutants, ambient concentrations
characteristic of large urban areas should be reduced to levels substantially below those
currently experienced.
As the ambient concentrations of HAP in urban areas result from a combination of
different sources (i.e., area, major, and mobile) emitting many of the same pollutants, we need to
consider contributions from all types of sources in order to achieve the reductions envisioned by
section 112(k). The Strategy presented in the July 19,1999 Federal Register (U.S. EPA, 1999a),
and discussed in this Report, is a part of our overall national effort to reduce toxics but with a
specific focus on the urban environment. The Strategy will consider contributions from area,
major, and mobile sources of HAP in addressing reductions in public health risks.
This chapter is intended to provide general information on our current understanding of
the air quality in the urban environment, to present a summary of risk analyses that have been
conducted over the past 10 years, and to provide the basis for our continuing support for an urban
program that will enhance our understanding of the urban environment and provide the strategy
for protecting the health of the public.
2.2 What Do We Know About HAP?
Section 112(b) of the CAA identifies 188 chemicals as HAP1. They include pollutants
like benzene, perchloroethylene, methylene chloride, heavy metals like mercury and lead,
polychlorinated biphenyls (PCBs), dioxins, and some pesticides. More than half of the HAP are
known or suspected to be human carcinogens. In addition, many are known to affect the
'Caprolactam was delisted on June 18, 1996 (61 FR 30816)
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respiratory, neurologic, immune, reproductive, or developmental systems, particularly for more
susceptible or sensitive populations, such as children. Hazardous air pollutants are also known to
cause adverse effects in many species (e.g., toxicity in fish or reproductive decline in bird
species), including endangered species. These environmental effects may impact individual
species within a single level of the food chain or the entire ecosystem where multiple species are
affected.
Health concerns result from both short- and long-term exposures. Some health problems
occur very soon after a person inhales a toxic air pollutant (i.e., from a short-term exposure).
These immediate effects may be serious, such as life-threatening lung damage, or they may be
minor. Health problems which are usually associated with long-term exposures may develop
slowly over time or may not appear until many months or years after a person's first exposure to
the toxic air pollutants (e.g., cancer). Depending on their characteristics (e.g., vapor pressures
and atmospheric transformation rate), HAP may disperse locally, regionally, nationally, or
globally and may deposit in the environment and in some cases, bioaccumulate in the food chain.
2.3 What Do We Know About HAP Emissions?
Hazardous air pollutants are emitted from a variety of stationary sources of varying sizes
and from mobile sources. Emissions data, along with specific information about the emitting
sources (e.g., the height and location of the emissions release points, size of emitting facility,
local meteorology), may be used as inputs to computer models. These models generate estimates
of ambient HAP concentrations in areas surrounding a source. Although these concentrations are
not estimates of personal exposure and risk, an understanding of these emissions and their
sources is necessary when preparing a strategy for dealing with associated risks to public health
and the environment.
For this reason, we developed the National Toxics Inventory (NTI). The NTI contains
emissions data for major, area and mobile sources. The data for the NTI have been gathered
from EPA (i.e., MACT development data and the Toxic Release Inventory, or TRJ2), State, and
2Section 313 of the Emergency Planning and Community Right-To-Know Act (EPCRA) and section 6607
of the Pollution Prevention Act (PPA) mandate a publicly accessible database containing information on the release
and other waste management activities of toxic chemicals by facilities that manufacture, process, or otherwise use
them. The EPCRA specifically requires manufacturers to report releases of more than 600 designated toxic
chemicals to the environment. The reports are submitted to the EPA and State governments. The EPA compiles
these data in an on-line, publicly accessible national computerized TRI. More information about the TRI database
is available at the following website: http://www.epa.gov/opptintr/tri/.
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EXHIBIT 2-1
HAP BASELINE NTI
EMISSIONS BY SOURCE
Area sources
Mobile sources
Major sources
Adapted from Trends Report (EPA, 1998)
Representative of 1990 - 1993 period
local studies and databases. A baseline year NTI3
has been developed and estimates emissions at
the county level. According to this inventory,
approximately 8.1 million tons of air toxics were
released annually (during the 1990 to 1993
timeframe) to the air nationwide with
approximately 6 million tons being released
annually into urban areas4. Exhibit 2-1 provides a
breakdown of the total, national emissions by
source.
Although the level of specificity of this
inventory is insufficient for drawing conclusions
about population exposure levels in individual
urban areas versus rural areas, these data show
that the largest emissions are
found in those States which are
highly industrialized and contain
some of the largest urban areas in
the country. Exhibit 2-2 (taken
from 1997 Trends Report (EPA,
1998)) illustrates the distribution
of HAP baseline emissions by
State. While these national-level
emission estimates are useful for
describing general trends, they do
not necessarily reflect the specific
situation that may exist in specific
urban areas where a wider variety
of HAP are emitted. This is
particularly important because
some pollutants which
individually would not be
expected to present harm, may
work together as a mixture resulting in a potential for harm. Thus, depending on exposure levels
EXHIBIT 2-2
HAP EMISSIONS BY STATE BASED ON 1993 NTI
B HAP E>-tiB«rra gnaw ihan -&7/_>>S tenant
I l*iAP Enna'm tdwoon 77.OCC - 1/,DCO Irrayr
Im*P f-ma&ksn* Kiss llan TTSXn tnnay
3The baseline NTI that we have compiled over the past few years is representative of the years 1990-93.
4In estimating the amount of emissions from urban areas, we have totaled emissions from all U.S. counties
that include a metropolitan statistical area with a population greater than 250,000 or for which more than 50 percent
of the population has been designated "urban" by the U.S. Census Bureau. For a more detailed description of
emissions allocation among urban and rural areas, see the technical support document for the emissions inventory
which is available through the public docket (Docket No. A-97-44).
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and characteristics of the pollutants, multiple pollutant exposures which may be more prevalent
in urban populations may pose increased public health risks.
An updated version of the NTI containing emission data from 1996 is currently being
developed. This 1996 NTI will be our first effort to estimate HAP emissions from all sources on
a national scale and to associate with them source-specific parameters necessary for modeling.
Important modeling parameters include location and facility characteristics which describe the
emission points (e.g., stack heights, stack exit velocities, emission temperatures). This new
inventory will have greater utility for assessing trends in emissions, for providing data in
sufficient detail to perform regional, urban, and local level air quality and exposure modeling
assessments, and to monitor progress on risk reductions.
Emissions data such as the NTI provide useful estimates of emissions in outdoor air, but
they do not reflect the levels of HAP that exist in many indoor air environments. It is estimated
that most people spend as much as 80 to 90% of their time indoors5. This is of particular concern
because over the past several decades, exposure to indoor air pollutants is believed to have
increased due to a variety of factors, including the construction of more tightly sealed buildings,
reduced building ventilation rates (to save energy), the increased use of synthetic building
materials and furnishings, and the increased use of chemically formulated personal care products,
pesticides, and household cleaners. Our current lack of understanding of the nature of indoor
sources of HAP and our limited information on the movement of air between the outdoor and
indoor environments leave a gap in our ability to more completely characterize human exposures,
especially in urban areas6.
2.4 What Do Monitoring Data Tell Us?
Monitoring data provide information about the ambient levels of HAP in specific areas
and generally represent a snapshot of what HAP are present. These data, like modeled ambient
concentration data, may provide information about the potential for exposure and risk. When
monitoring data are used, however, the ability to identify the particular emitting source may be
lost unless the placement of the monitor allows for the detection of HAP contributions from
uniquely identifiable sources. Where the source or sources contributing to the monitored HAP
levels are not known, the monitored HAP levels may be considered to be a background
concentration7. In these cases, background concentration data may provide a comparison and/or
5An analysis of human activities published in 1996 reported that people spend as much as 69% of their
time in personal residences with an additional 18% of time being spent in other indoor environments (EPA, 1996).
^More information on indoor air quality may be obtained at the following website: http://www.epa.gov/iaq.
7The concentration of HAP present in the ambient air that is not solely attributable to a specific or
identifiable source being studied. For example, a monitor may detect HAP emissions from stationary, mobile, or
nonanthropogenic sources while the source being modeled (i.e., the source of the emissions data being used) is a
stationary source.
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a context concentration for ambient HAP levels estimated by modeling. In other cases,
background concentration data for a specific HAP may be added to the ambient HAP levels
estimated by modeling to account for known HAP sources not considered in the modeling
analysis. This may be done for HAP such as formaldehyde because of its ability to be formed by
the direct chemical transformation8 from other HAP in the air (see Section 2.6 of this Report for
more detailed discussion of transformation).
Currently, there is no national ambient air quality monitoring network designed to
measure the ambient levels of HAP in the environment. The data we have available nationally
come from monitoring that is done under programs like the Photochemical Assessment
Monitoring Stations (PAMS) program, the PM2 5 monitoring network, and from the many
voluntary State monitoring programs. The ambient air monitoring information collected by
States in certain metropolitan areas provides us with a limited understanding of HAP ambient
concentrations in urban areas. Data collected during the 1990's demonstrate elevated
concentrations of several HAP in urban areas across the country. For example, a limited
evaluation of the subset of HAP monitored indicate the presence of HAP in some cities which,
when evaluated cumulatively, is suggestive of upper bound estimates of additional, lifetime
cancer risks at or above 1 in 10,0009. Comparisons of estimated concentrations to RBCs can
provide indicators of a potential public health problem but should not be considered a
characterization of actual health risks.
2.5 What Do We Know About Urban Populations?
A unique feature of urban areas is the proximity of many stationary and mobile sources
and their pollutants to each other and to the populations which live or work in these areas.
According to a 1997 report on population (U.S. Department of Commerce, 1997), approximately
212 million people (including 57 million children) or 80% of the estimated 1996 U.S. population
live in metropolitan areas. This estimate represented a gain of 13 million people in these areas
since the 1990 census estimate. Given (as described earlier) that the largest levels of HAP
emissions are found in those States which contain some of the largest urban areas, we seem to
have mixtures of HAP and increasingly high density populations existing together in urban areas.
The issue becomes complex when other population factors such as age, socio-economic
status, proximity to emitting sources, decreased health and nutrition status, and lifestyles are
considered because it is known that these factors may lead to increased sensitivity and
An air contaminant may undergo a chemical change in the atmosphere as it either breaks down or reacts
with other chemicals. The pollutants that are formed as a result of this transformation process may be more or less
toxic than the pollutants originally released.
9The technical support documentation for this assessment analysis is available from the public docket
(Docket No. A-97-44) and includes a presentation of ambient monitoring data in 17 cities for a variety of HAP.
Also presented are the upper bound estimates of excess cancer risks associated with continuous lifetime exposures
at those concentrations.
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susceptibility to the effects of HAP exposures. Within the general population, children, for
example, are likely to have additional susceptibility and vulnerability to HAP exposures because
of their daily activities, their immature or developing metabolic systems, or their developing
organ systems. In addition, the poverty factor (over 20% of the urban population consists of
children in poverty (U.S. Department of Commerce, 1997)) increases their vulnerability because
they are more likely than other children to lack sufficient nutrition and access to health care.
In conducting an assessment that considers the population (i.e., an exposure assessment),
models are used to characterize population exposures based on ambient concentration data
(derived from modeling or monitoring). Specific population exposure factors such as the
location of various populations, population demographics, and group activity patterns10 when
coupled with HAP toxicity information provide a clearer picture of how, when, and for how long
people are exposed to HAP and what their potential risks may be. These are a few of the many
aspects that are considered when evaluating public health risks from HAP in urban areas.
2.6 Characterization of Air Toxics in Urban Areas
As discussed above, different types of information may be useful for characterizing the
urban environment. In this Report, we have focused on nine risk-based assessments performed
by EPA and various States over the past ten years. Although some general similarities are
evident across these assessments, the identity and concentration of air toxics may vary
significantly from one city to the next depending on the particular sources present (or dominant),
the substances emitted, the local meteorology, and other factors. It should be noted that most of
these studies were based upon the situation that existed in urban environments up to ten years
ago. Given our current, national information, the situation is likely to have improved. That
notwithstanding, the summaries contribute to our understanding of the potential nature and
magnitude of exposures and health risks in specific urban areas and to the pollutants and sources
contributing to those exposures and risks.
To put these assessments in perspective, it is useful to first discuss some of the
uncertainties that were inherent in these assessments because of the lack of information at the
time or because of the way these assessments were designed. We can evaluate uncertainties .from
the perspective of what we don't know or what wasn't considered in the analysis. For example,
most of these assessments did not consider risks from endpoints other than cancer, pathways
other than inhalation, or exposures other than long-term. The potential exposure to HAP for
which we have little or no health data was assumed to have resulted in no adverse health effects.
These uncertainties are not quantifiable but are our reason to err on the side of conservatism
when it comes to interpreting the different assessments. The other side of the uncertainty
question (i.e., what we do know now that we didn't know then) may have quantifiable effects.
'°The movement of people through different daily micro-environments as they participate in various
activities. For example, being in an indoor or outdoor environment, or riding in a car are a few of micro-
environments to consider in an exposure assessment.
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One HAP, 1,3-butadiene, was identified as a very common urban HAP responsible for much of
the estimated risk seen in these assessments. Currently, we are reevaluating the cancer potency
value, and it is likely that the potency value will decrease (i.e., the potency will likely be lower
than what was used in these assessments). This is important to keep in mind because many of
the assessments highlighted this HAP as being a major contributor to risk levels11.
Uncertainty is also present when various policy assumptions are used in deriving cancer
risk estimates. In most of these assessments (as well as many current screening assessments),
measurements and estimates of air concentrations are used, with the assumption of a lifetime
exposure to these concentrations, to calculate upper-bound estimates of an individual's lifetime
increased cancer risk from each pollutant. Upper-bound estimates are used in order to avoid
underestimating the true value. The true value may, however, be lower than the estimate and
may, in fact, be zero. The upper-bound estimates for each HAP are summed to obtain a worst-
case estimate of individual lifetime increased cancer risk resulting from exposure to the mixture
of HAP. For each of the studies described below, these worst-case estimates were on the order of
a 1 in 10,000 chance of getting cancer for someone exposed continuously over a 70-year
lifetime12. For substances that are not thought to cause cancer, air concentration estimates are
compared to concentrations considered unlikely to be harmful. These rough worst-case estimates
are used to identify those HAP posing the greatest likelihood of harm. For these nine
assessments, it must be kept in mind that other HAP which may have been present in the urban
air, and for which toxicity information was insufficient for the risk assessments, were excluded
from these calculations.
Additionally, not all possible HAP were considered in these assessments because HAP
selected usually met one or more of the following conditions: they were known or suspected to
be present in urban air, they were suspected to be important contributors to health risk based on
knowledge of their toxicity (most urban air studies to date have focused primarily on pollutants
either known to cause cancer in humans or for which test data are less conclusive yet provide an
indication of a potential to cause cancer), and/or there were available data on their emissions or
ambient concentrations. Pollutants that have been commonly studied in urban areas include
arsenic, benzene, 1,3-butadiene, cadmium, carbon tetrachloride, chromium, ethylene dichloride,
formaldehyde, methylene chloride, perchloroethylene, polycyclic organic matter (POM) (which
The review and revision of data (resulting in revised unit risk and reference values) for the HAP in these
studies, (e.g., 1,3-butadiene) and for the other HAP not included in these studies is an ongoing process. It is likely
that the results of the studies described here would be different had these results been reevaluated. Future
assessments will have the benefit of the most current health effects data.
12As described in Chapter 5 of this Report, our assessment approach will be generally iterative in nature, so
as to take advantage of emerging science, new data, and improved tools that become available at the time future
assessments are performed, (e.g., with better emissions and exposure data, our exposure estimates will be more
central tendency than upper bound). The resulting risk characterizations in these future assessments should reflect
this shift in data quality.
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include polycyclic aromatic hydrocarbons and certain other chemicals that have multiple benzene
rings that are emitted as products of incomplete combustion), and trichloroethylene. Each of
these pollutants has been evaluated in multiple major studies of urban air, including the nine
assessments discussed below. Benzene and formaldehyde were evaluated in all nine of the
studies.
These assessments relied on source inventories that were created much earlier than the
assessments. Although a variety of sources were identified and assessed in different urban areas,
no attempt was made to identify all of the possible, specific sources of emissions. The particular
emission sources of concern can vary widely from one city to the next, and many of these
assessments concentrated only on what were thought to be the largest sources or only on one type
of source (e.g., area sources). Today's inventories have reduced the potential uncertainty in this
area because more source data are available and have been included in the recent NTI (discussed
previously). These data which include area, major, and mobile source data will be used in future
urban risk assessments.
Emission estimates (i.e., inventories) do not consider that some HAP may disperse over
great distances (mercury, for example, may disperse globally). This type of HAP dispersion or
long-range transport would be of particular concern for HAP that have longer half-lives or which
may persist in the environment for a longer time. In the case of persistent HAP, re-volatilization
or resuspension of a deposited HAP may continue the transport of that HAP to more distant
locations. When developing an emissions inventory (i.e., a list of sources emitting HAP of
interest or concern), it is not always possible to consider sources that are too distant from the
geographic areas of interest. This may lead to an underestimate of the ambient HAP
concentrations predicted by modeling (dispersion models typically limit the ambient
concentration estimates calculated to a 50 kilometer (approximately 30 mile) radius around an
identified source). This is less of an issue when monitoring data are used as the basis for the
ambient HAP concentrations because monitors detect HAP regardless of their sources or their
distance from the monitor. The inventories developed for the urban assessments discussed below
did not consider the long-range transport of the HAP of interest into the geographic areas of
study.
The inventories developed for these assessments, also, did not consider the potential
effects of atmospheric transformation. An air contaminant may undergo a chemical change in the
atmosphere as it either breaks down or reacts with other chemicals. The pollutants that are
formed as a result of this transformation process may be more or less toxic than the pollutants
originally released. Just as some contaminants may degrade to less harmful chemicals,
sometimes relatively innocuous airborne chemicals may combine with other chemicals in the
atmosphere to form HAP (e.g., the formation of formaldehyde (a HAP) from the chemical
reaction among the components of "smog" and isoprene, a less harmful chemical). Trans-
formation in the atmosphere may occur as the chemicals are dispersed and transported from an
emitting source. If the transformation process is not considered or only partially considered (by
adding some "background value," as some of the urban assessments did), the significance of this
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on the final result must be part of the evaluation process when considering the results of these
assessments.
None of the urban assessments discussed below considered specific sub-populations (i.e.,
populations that may be more susceptible or vulnerable to HAP exposure) in their calculations of
potential risks. In addition, these assessments, with the exception of the Mobile Vehicle Study,
did not project changes in those aspects of daily lives that will continue to change the profile of
emissions and exposures especially in urban areas. For example, the number of miles traveled by
commercial and private vehicles nationally from 1990 to 1996 increased by approximately 310
billion miles (an average increase of 52 billion (2.5%) vehicle miles traveled (VMT) per year)
(U.S. Department of Transportation, 1998). If the change in the U.S. population during this time
is considered (248.7 to 265.3 million people, respectively (U.S. Department of Commerce,
1997)), the increase in VMT is not due solely to a population increase but to an increase in the
number of miles "each person" traveled. This becomes an important factor when the overall
results of many of the urban assessments point to mobile sources and their HAP as contributing
to potential urban area risks.
In general, for each of the assessments discussed below, outdoor HAP concentrations
(estimated using computer modeling projections or ambient air monitoring) were used to
represent potential human exposures. When combined with simplifying assumptions that can
lead to either under- or overestimates of risk, researchers were able to reach conclusions about
the chemicals, and in some cases the air pollution sources, that seem to contribute the most to
risks from urban air pollution. In these assessments (e.g., benzene, 1,3-butadiene, and
formaldehyde were consistently shown to be most responsible for the higher risk estimates), the
studies identified all three major source categories (area, major and mobile sources) as
contributing emissions and potential risks in urban areas, and they presented estimates of
increased individual lifetime cancer risks from air toxics from multiple sources across the studies
that ranged from 3 in 1,000 to 2 in 1,000,000 (with a median of 1 in 10,000) (although the true
risks could be higher or lower13). While providing useful information on the potential nature and
magnitude of health risks in urban areas, these assessments are limited by the lack of exposure
information and by the incompleteness of our knowledge regarding the range of health effects
associated with any additional HAP that may be found in urban environments. The nine
assessments listed in Exhibits 2-3 and 2-4 are summarized below.
The design of each of the studies discussed included assumptions described as conservative or worst case. In these
cases, the incidence values presented within the context of each study may overestimate the true incidence. Conversely, the
limitations of the study designs and assumptions (i.e., these studies did not consider pathways of exposure other than inhalation,
exposures other than long term, risks from other HAP present in these study areas or their potential synergistic interactions) leave
open the possibility that the incidence values presented may underestimate the true risk.
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EXHIBIT 2-3
RISK-BASED ASSESSMENTS COVERING URBAN AREAS
Risk-based Assessments
U.S. EPA, 1989. Analysis of Air Toxic Emissions, Exposures, Cancer Risks and Controllability
in Five Urban Areas. This study was designed to define the multisource, multipollutant nature
of the urban air toxics problem and determine what control measures can best be employed to
mitigate the problem.
Engineering-Science, 1990. The Transboundary Air Toxics Study: Final Summary Report.
Risk assessment to evaluate the source types and pollutants which contribute to increased cancer
risk from air pollution in the Southeast Michigan/Windsor-Samia area.
MPCA, 1992. Estimation and Evaluation of Cancer Risks from Air Pollution in the
Minneapolis/St. Paul Metropolitan Area. Study by the Minnesota Pollution Control Agency to
analyze sources of HAP suspected or known to cause cancer, and to estimate the health risk
from exposure to these pollutants.
U.S. EPA, 1993b. Staten Island/New Jersey Urban Air Toxics Assessment Project: Summary of
the Project Report. Assesses risk to Staten Island residents from ambient air pollutants and
generates an inventory of major, area and mobile sources to qualitatively examine sources of
high risk and high observed concentrations.
U.S. EPA, 1993a. Motor Vehicle-Related Air Toxics Study. Summarizes what is known about
motor vehicle-related air toxics.
U.S. EPA, 1994. A Screening Analysis of Ambient Monitoring Data for the Urban Area Source
Program. Summarizes currently available ambient monitoring data sets for HAP from various
urban areas in the U.S. and estimates the risks associated with these HAP.
ENSR, 1995a, b, c. Arizona Hazardous Air Pollution Research Program. Risk assessment to
determine which HAP and sources should be the focus of future research and control strategies
in Arizona.
TNRCC, 1996. Houston Area Source Toxics Emissions Project. Risk assessment to determine
which HAP from area sources should be focused on for future research and control strategies in
Houston.
Woodruff etal., 1998. Cumulative Exposure Project. Assessment which compared modeled
ambient air concentration estimates with health benchmarks for 148 HAP nationwide.
Abbreviated
Name
Five City Study
Transboundary
Study
Twin Cities Study
Staten Island
Study
Motor Vehicle
Study
Ambient
Monitoring Study
Arizona Study
HASTE Study
CEP
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EXHIBIT 2-4
OVERVIEW OF ASSESSMENTS
Study"-
Five City Study
Transboundary
Twin Cities Study
Staten Island Study
Motor Vehicle Study
Ambient Monitoring
Study
Arizona Study
HASTE Study
CEP
Approach
Hazard
Assessment
Ambient
Monitoring
No. Air
Contaminants
Studied
23
57
29
40
4"
195C
163d
40
148
Location
5 unspecified cities
Southeast Michigan/Windsor-
Samia area
Minneapolis/St. Paul
metropolitan area
Counties in NJ and NYa
U.S. locations
40 U.S. locations
Phoenix, Tucson, Casa
Grande, and Payson, AZ
Harris County, TX
National assessment
Health Effects
Evaluated
Cancer
Cancer
Cancer
Cancer,
Noncancer
Cancer
Cancer,
Noncancer
Cancer,
Noncancer
Cancer,
Noncancer
Cancer,
Nnnranrer
a Middlesex and Union Counties in New Jersey and Staten Island in New York for area and mobile sources, with
the addition of Monmouth, Essex, and Hudson Counties in New Jersey and Brooklyn (Kings County) in New York
for major sources.
b Study included four HAP and three mixtures (diesel and gasoline particulates and gasoline vapors).
c Monitoring data available for 195 air contaminants, but assessment focused on 93 HAP for which health effects
data were available.
d Of the 163 possible contaminants, 25 chemicals of interest were selected for each of the four regions.
Five City Risk Assessment
This assessment, published in 1989,
was done to help characterize the
multisource, multipollutant nature of the
urban environment (U.S. EPA, 1989). A
base year emissions inventory was
compiled for each of five, unspecified
cities from a number of different data
sources and included inventories
representing point, area, and mobile source
emissions. The base year nominally
represents 1980 but selected source updates
Five City Study
Time Period Covered: 1980 - 1987
Top HAP Contributing to Predicted HAP-
Related Cancer Risk: POM, 1,3-butadiene,
formaldehyde, benzene, and chromium
Individual Lifetime Cancer Risk Estimates:
Ranged from 2 x 10"4 to 7 x 10 "* (two to ten excess
cancer cases per year across the five cities)
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were included so that the inventory was actually more reflective of the 1980 to 1985 timeframe.
Emissions and source data were modeled to estimate annual average ambient HAP
concentrations for all 23 HAP included in this assessment. Monitoring data for formaldehyde
were included in order to calculate estimates of formaldehyde ambient concentrations that were
due to atmospheric transformation14. The ambient data for all HAP were then converted to
estimates of individual, lifetime cancer risks and incidence by applying the cancer unit risk
factors that were available at that time. The individual lifetime cancer risks ranged from 2 x 10"4
to 7 x 10"4 and provided an estimate of the multisource, multipollutant contribution to exposure
for the entire study area. This assessment did not consider routes of exposure other than
inhalation nor endpoints other than cancer.
Transboundary Study
Transboundary Study
This assessment was initiated to . . . _ . , A0. , .0.
... , Time Period Covered: 1980-1989
prepare an emissions inventory that through
Top HAP Contributing to Predicted HAP-
Related Cancer Risk: Formaldehyde, coke oven
emissions, 1,3-butadiene, carbon tetrachloride,
chromium, POM, dioxins
Individual Lifetime Cancer Risk Estimates:
9 x 10~5 or five cancer cases per year over total study
area
risk assessment would help define the
relative contributions of various source
types to the risk estimated in the urban
transboundary area (Southwest Michigan/
Windsor-Sarnia area) (Engineering-
Science, 1990). The pollutants chosen were
"generally substances known to be
atmospherically deposited in this region,
substances known to pose carcinogenic risk
or other substantial human health risk, or both." Of the 57 pollutants chosen, inventories for 42
were identified. These inventories were not designed to cover all possible sources but rather only
the largest contributors to overall emissions for each of the pollutants. They did consider area,
point, and mobile sources. Only data between the years 1980 and 1989 were considered with the
target year being 1985. Background concentrations and local ambient concentrations due to
long-range transport were assumed to be zero, with two exceptions. The background
concentration levels for formaldehyde and carbon tetrachloride were assumed to be 2.2yUg/m3 and
O.SjUg/m3, respectively. These background concentration estimates were combined with modeled
ambient concentration estimates for these HAP.
The individual, lifetime excess cancer risks in this study was 9 x 10"5. This translates into
an estimated total cancer incidence of approximately 373 cases over 70 years or five cases per
year. Over 90% of these resulted from exposure to seven pollutants: formaldehyde, coke oven
emissions, 1,3-butadiene, carbon tetrachloride, chromium, POMs, and dioxin; with more than
50% being attributed to formaldehyde and carbon tetrachloride alone. The contribution of the
additional "background" concentrations to these latter results was not discussed, but the added
14Modeled ambient concentrations were subtracted from ambient values derived from monitoring to yield
that portion of the ambient concentration due to the atmospheric transformation of other chemicals to formaldehyde.
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background may have played a role in their higher contribution to overall incidence. No attempt
was made to include other routes of exposure or effects other than cancer in this assessment.
Twin Cities Study
Time Period Covered: Completed in 1992
Top Air Contaminants Contributing to Cancer
Risk: Diesel, gasoline, and wood-stove paniculate
emissions, formaldehyde, benzene, 1,3-butadiene
Individual Lifetime Cancer Risk Estimates:
2x10" (2 cancer cases per year per million over
study area)
Twin Cities Study
The purpose of this assessment was
to analyze sources of HAP suspected or
known to cause cancer and to estimate the
cancer risks resulting from exposure to these
HAP (MPCA, 1992). Emission inventories
were developed for point, area, and mobile
sources, and modeled to estimate the
ambient concentrations of 29 pollutants and
three different POM mixtures (diesel, wood-
stove, and gasoline particulates). This
assessment developed estimates of increased
lifetime individual and population risks in the Minneapolis/St. Paul metropolitan area, but did
not estimate maximum risks. The results yielded an estimated individual lifetime cancer risk of 2
x 10"4 over the entire study area. This may result in an estimated two excess cancer cases per
year per million residents. Overall, 61% of the excess incidence may be attributed to road
vehicles which contributed gasoline arid diesel particulates (including POMs) as well as
formaldehyde, benzene, and 1,3-butadiene. Wood stoves and fireplaces were also an important
source is this area, accounting for 17% of the incidence. It was concluded that mobile sources
and area sources were the dominant contributors to risk in this assessment, but it should be noted
that the assessment area did not include some of the major point sources that are present near the
study area. Noncancer endpoints, risks due to background concentrations, or risks due to routes
of exposure other than inhalation were not considered in this study.
Staten Island Study
This ambient monitoring-based
assessment estimated the increased risk
of cancer and noncancer effects in
Middlesex and Union Counties in New
Jersey, and in Staten Island (Richmond
County) in New York (U.S. EPA,
1993b). Monitoring data were collected
from October 1987 to September 1989.
A total of 40 pollutants were monitored
but only 20 had adequate lexicological
data to use for the risk assessment. The
study found that lifetime cancer risk ^^^^^^^^^^^^^^^^^^^^^^
estimate was approximately 1 x 10 "* or
one to two excess cancer cases per year per million population. As in other studies, only
Staten Island Study
Time Period Covered: October 1987 - September 1989
for ambient air (plus July 1990 - March 1991 for indoor
air)
Top HAP Contributing to Risk: Benzene, arsenic,
chromium, nickel, cadmium, formaldehyde
Individual Lifetime Cancer Risk Estimates: 1 x 10"
(1 excess cancer case per year per million)
Noncancer Effects: HI > 2 for both respiratory and
hematopoietic effects
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inhalation risk was considered. This study did include an evaluation of noncancer effects as well.
A hazard index (HI)15 of two was estimated for the respiratory tract as the target (chromium and
nickel) and also for the blood (hematopoietic) system (benzene).
Motor Vehicle Study
Time Period Covered: 1990 projected to 2010
HAP Studied: Benzene, 1,3-butadiene,
formaldehyde, acetaldehyde, diesel particulates,
gasoline particulates
Estimated Cancer Deaths Per Year or Incidence:
For year: 1990 2000 2010
Benzene
Formaldehyde
1,3-Butadiene
Acetaldehyde
70
44
304
5
35
21
176
3
35
22
204
3
Motor Vehicle Study
In 1993, EPA published the
assessment of risks due to motor vehicles
and their fuels beginning in 1990 and
projecting out to 2010 (U.S. EPA,
1993 a)16. The assessment focused on the
emissions of benzene, formaldehyde, 1,3-
butadiene, acetaldehyde, and a group of
mixtures (diesel and gasoline particulates
and gasoline vapors) and on the assessment
of carcinogenic risk. It used exposure to
carbon monoxide (CO) as a tracer for toxic
exposures and used the relationship
between CO emission factors and toxic
emissions factors to estimate toxic
emissions. Monitoring data were used to evaluate the modeling results, and modeled
concentrations were adjusted to match the upper end of the monitored data. This assessment
focused on eleven urban areas and two rural areas, but the results were extrapolated to the entire
Nation using population data beginning in 1990. From 1990 to 2000 (projections), predicted
cancer incidence or deaths decreased for all HAP. During the years 2000 to 2010, the projected
estimates associated with 1,3-butadiene increased. Increases in the cancer incidence projected
for those later years were attributed to projected increases in the number of VMT for those later
years. It was also shown that for each HAP studied, the urban incidence accounted for over 80%
of the total (i.e., 80% of the total number of cancer deaths was due to exposure levels in urban vs.
rural areas).
15The sum of hazard quotients (HQs) for multiple chemicals where the HQ is the ratio of a level of
exposure for a single substance to a reference level (e.g., a reference concentration) for that chemical derived from a
single exposure. An HQ or HI greater than one usually suggests that additional, more refined, analysis may be
warranted.
16It is important to note that since the completion of this study, EPA has promulgated or proposed a
number of programs that are expected to significantly reduce air toxics emissions in the future, including our
reformulated gasoline (RFG) program, the national low emission vehicle (NLEV) program, Tier 2 motor vehicle
emissions standards and gasoline sulfur control requirements, and our recently proposed heavy-duty engine and
vehicle standards and on-highway diesel fuel sulfur control requirements. As discussed in Chapter 4 of this Report,
EPA is updating estimates of motor vehicle toxic emissions and exposure (EPA, 1999b).
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Ambient Monitoring Study
Time Period Covered: 1986 - 1993 (individual
studies varied from a few months to multiple years)
Air Contaminants Studied: 195 detected, 93 with
health reference values: 1,3-butadiene, benzene,
formaldehyde, acrolein, 1,2-dibromoethene, and
manganese were more consistently ranked among the
top with respect to health concerns
Individual Lifetime Cancer Risk Estimates:
1,3-butadiene: 2 x 10 '3 to 5 x 10"4
benzene: 2 x 10" to 1 x 10'5
formaldehyde: 1 x 10"4 to 2 x 10'5
Noncancer Concern: Acrolein, 1,2-dibromoethene,
manganese
Ambient Monitoring Study
This assessment summarizes the
analyses of ambient monitoring data
obtained from 16 monitoring studies
some of which were collecting data since
1987. They represented over 40 urban
areas and 195 air contaminants (U.S.
EPA, 1994). Risk was calculated for
only 93 contaminants (most of which are
listed as HAP in section 112(b) of the
CAA) for which health effects data
required for risk assessments were
available. For each site, a long-term
average concentration was calculated and
then applied to health reference values to
estimate lifetime excess cancer risks and
potential noncancer health effects for
each. Because the data were derived from monitoring studies rather than modeling, no
discussion of potential sources was included in the report. No estimates of population risks were
made nor were routes of exposure other than inhalation considered.
With respect to cancer risks, 1,3-butadiene possessed the highest estimated individual risk
among all pollutants. Estimates for benzene and formaldehyde also ranked consistently near the
top. Acrolein, 1,2-dibromoethene, and manganese exhibited exceedances of noncancer reference
values more consistently than other contaminants. However, there were gaps in the data
presented. For example, not every contaminant was detected in every area due to variations in
the methodologies used in the different studies. The data, however, do provide a snapshot view
of urban areas with respect to contaminant concentrations and their potential to pose health risks
of concern.
Arizona Study
This assessment examined cancer and noncancer risks posed by air pollutants in four
areas of Arizona (Phoenix, Tucson, Casa Grande, and Payson) and was designed to evaluate the
existing risk to public health and to provide options and recommendations for programs to
control releases (ENSR, 1995a, 1995b, 1995c). These regions were assumed to represent a large
fraction of the State's population and were characteristic of many of the types of communities in
the State. Monitoring of the selected HAP was done primarily in residential neighborhoods.
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About 25 HAP of "greatest concern"
were selected for each region. Half of the
estimated cancer risks for air pollutants was
caused by 1,3-butadiene. Other significant
contributors included benzene and
formaldehyde. Acrolein was identified in all
four regions as the HAP most likely to pose
health risks other than cancer. Smaller
likelihoods of noncancer risks were attributed
to acetaldehyde, benzene, and manganese.
Motor vehicles were found to be the largest
contributor to estimates of cancer risks from
HAP in three of the four areas. Non-
inhalation pathway risk was determined not
to be of significance in any region studied.
Arizona Study
Time Period Covered: 1990 - 1995
Top HAP Contributing to Concern:
1,3-butadiene, benzene, formaldehyde, acrolein,
acetaldehyde, manganese, arsenic
Lifetime Cancer Risk Estimates:
1 to 5 x 10^ (two to seven excess cancer cases
per year per million)
Noncancer HI: 6 to 15 for all endpoints
The urban centers, Phoenix, and to a lesser extent, Tucson, were found to have higher
estimates of cancer risk from HAP than the two areas that are more rural. Although emission
reduction mechanisms were expected to decrease the risk estimates in the near future, it was
stated that increases in population growth along with increases in motor vehicle use in these
urban areas would begin to erode any potential gains. The estimates of individual lifetime
increased cancer risks from air pollutants in all study areas ranged from one to 5 x 10^. The total
HI for noncancer risks, calculated for young children, was six to fifteen for all endpoints. The HI
for respiratory effects was greater than one in all regions. Other HI greater than one were found
for neurological and blood effects but not across all regions studied.
HASTE Study
This project was conducted in three
phases: development of an emission inventory,
modeling of the inventory, and a risk analysis
(TNRCC, 1996). Only area sources of HAP
were studied. Health reference concentrations
(RfCs), when available, were used to compare
against the ground-level concentrations (GLCs)
estimated by modeling, for 87 air contaminants
for cancer and noncancer effects. With the
exception of acrylonitrile, benzene, 1,3-
butadiene, ethylene dibromide, ethylene oxide,
2-nitropropane, and vinyl chloride, the
estimated cancer risks for each of the
remaining air contaminants was less than 1 x 10"6. Individual lifetime cancer risks for the seven
ranged from 2 x 10~6 to 2 x 10"5. The acrolein GLC was the only one which exceeded its RfC (5
fold).
HASTE Study
Time Period Covered: 1995 - 1996
Contributors to Predicted Cancer Risk:
Acrylonitrile, benzene, 1,3-butadiene, ethylene
dibromide, ethylene oxide, 2-nitropropane, vinyl
chloride
Contributors to Noncancer Risk:
Acrolein (HQ = 5)
Individual Lifetime Cancer Risk Estimates:
2x10-* to 2xlO-5
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Cumulative Exposure Project -,-, 4 . .
(CEP) CEPAnalVSlS
Time Period Covered: 1990
The CEP is a recent effort by the EPA
to model ambient HAP concentrations on a
national scale (Woodruff et al., 1998). The
CEP suggests that HAP exposures are
. . ., ... ethylene dichloride, formaldehyde, 1,3-butadiene
prevalent nationwide, and that, in some
Top HAP Contributing to Cancer Risk:
Benzene, bis(2-ethylhexyl)phthalate, carbon
tetrachloride, chloroform, ethylene dibromide,
Top HAP Contributing to Noncancer Risk :
Acrolein
locations, concentrations are significantly
higher than the concentrations associated
with a one-in-one million excess cancer risk
(SAI, 1998; Woodruff et al., 1998)17. The
estimated outdoor concentrations, based on
1990 emission estimates, for 119 of the 148 HAP modeled in more than 60,000 census tracts
nationwide were compared to RBCs. The results suggest that HAP exposures are prevalent
nationwide, particularly in urban areas. For 75% of the HAP modeled, the average estimated
concentrations in urban areas were greater than the overall national average concentrations. The
emissions of three HAP (benzene, formaldehyde and 1,3-butadiene) appear to contribute to
concentrations above the associated one-in-one million excess cancer RBCs in at least 90% of
the census tracts. Estimated concentrations are generally higher in urban areas, and
concentrations of 28 HAP were greater than their RBCs in a larger proportion of urban areas as
compared to rural areas. In a smaller number of locations (both urban and rural), concentrations
of certain HAP were estimated to be more than a factor of 100 greater than the corresponding
RBCs (Woodruff et al., 1998). Estimated exceedances seen in this assessment suggest potential
public health problems especially in urban areas.
2.7 Why Is The Urban Strategy Needed?
The overall findings of these nine assessments may be summarized as follows:
Benzene, 1,3-butadiene, and formaldehyde were consistently shown to be most
responsible for the higher risk estimates;
The studies identified all three major source categories (area, major and mobile sources)
as contributing emissions and potential risks in urban areas; and
Estimates of increased cancer risks for air toxics from multiple sources across the studies
ranged from 3 in 1,000 to 2 in 1,000,000 with a median of 1 in 10,000.
The estimated ambient concentrations were then compared to risk-based concentrations (termed
benchmarks by the authors) intended to represent either continuous exposure levels associated with a one-in-a-
million upper bound estimate of excess lifetime cancer risk, or continuous lifetime exposure levels associated with
no significant risks of adverse noncancer effects (e.g., EPA's Inhalation RfC).
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In addition, because many of these emission sources are area or mobile sources, their emissions
are likely to be released at ground level where people are more likely to be exposed to them. The
prevalence of minority and low income communities in urban industrial and commercial areas,
where ambient concentrations of HAP may be greater, increases the likelihood of elevated HAP
exposures among these subgroups. The potential for air toxics in urban areas, either directly or
indirectly, to contribute to elevated health risks among these and other subgroups (especially
children, the elderly and persons with existing illness or other potential vulnerabilities)
demonstrates the need to assess risk distributions across urban populations in order to address
disproportionate impacts of HAP.
As discussed earlier, each of these studies was limited in its scope and design (e.g.,
considered cancer effects from inhalation exposures only), and the results must be considered in
the context of conditions which existed up to ten years ago. Thus, many were performed prior to
the implementation of control strategies (including vehicle and fuel additive regulations, (e.g.,
HD2004 and Tier 2) and emission standards for numerous source categories) and do not reflect
the progress made in reducing emissions from air toxics through regulatory, voluntary, and other
programs at the State and Federal levels. For example, section 112(d), MACT standards
(adopted to date) are projected to yield yearly emission reductions of approximately 1.5 million
tons of HAP from stationary sources. Additional emission reductions are expected as the
remaining MACT standards are promulgated. Additionally, automobile emissions which
accounted for 20% of the total emissions of HAP in the baseline inventory mentioned earlier,
decreased by approximately 258,000 tons per year between the years 1993 and 1996 (U.S. EPA,
1998), possibly as result of regulations requiring the use of reformulated fuels which may have
contributed to the decreases seen in benzene emissions. Future assessments will be needed to
determine the impact of these reduced emissions on potential air toxics-related health risks.
In the meantime, these assessments adequately support our concern that a potential
problem exists in urban areas, and that we should continue with our efforts to study the urban
environment and to implement the urban strategy described earlier in the Federal Register (U.S.
EPA, 1999a) and presented again in this Report.
2.8 References
Engineering-Science. 1990. The transboundary air toxics study, final summary report. Prepared
for U.S. EPA Region V, Air and Radiation Division. Fairfax, VA. December.
ENSR. 1995a. Arizona hazardous air pollution research program final report volume 1:
approach. Document number 0493-013-900. Phoenix, AZ. August.
ENSR. 1995b. Arizona hazardous air pollution research program executive summary.
Document number 0493-013-920. Phoenix, AZ. December.
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ENSR. I995c. Arizona hazardous air pollution research program volume 2: findings. Document
number 0493-013-920. Phoenix, AZ. December.
Minnesota Pollution Control Agency (MPCA). 1992. Estimation and evaluation of cancer risks
from air pollution in the Minneapolis/St. Paul metropolitan area. March.
Systems Applications, Inc. (SAI). 1998. Modeling cumulative outdoor concentrations of
hazardous air pollutants: final technical report. Prepared by SAI Division of ICF Kaiser
International. Prepared for U.S. Environmental Protection Agency. February.
Texas Natural Resources Conservation Commission (TNRCC). 1996. Houston area source
toxic emissions (HASTE) project, health effects evaluation. TNRCC Office of Air
Quality/Toxicology and Risk Assessment Section, Austin, TX. February.
U.S. Department of Commerce. 1997. Population profile of the United States. Current
population reports, special studies P23 194. Economic and Statistics Administration,
Bureau of the Census, Washington, DC.
U.S. Department of Transportation. 1998. Traffic volume trends, December 1997. Federal
Highway Administration report, publication number FHWA-PL-98-004.
U.S. EPA. 1989. Analysis of air toxic emissions, exposures, cancer risks and controllability in
five urban areas, volume I: base year analysis and results. Office of Air Quality Planning
and Standards, Research Triangle Park, NC. EPA-450/2-89-012a. July.
U.S. EPA. 1993a. Motor vehicle-related air toxics study. Office of Mobile Sources, Ann Arbor,
ML EPA-420/R-93-005. April.
U.S. EPA. 1993b. Staten Island/New Jersey urban air toxics assessment project, summary of the
project report. U.S. EPA Region 2, New York, NY. EPA-902/R-93-002. January.
U.S. EPA. 1994. A screening analysis of ambient monitoring data for the urban area source
program, final report. Office of Air Quality Planning and Standards, Research Triangle
Park,NC. EPA-453/R-94-075. October.
U.S. EPA. 1996. Analysis of the national human activity pattern survey (NHAPS) respondents
from a standpoint of exposure assessment. EPA/600/R-96/074. July.
U.S. EPA. 1998. National air pollutant emissions trends update, 1970-1997.
EPA-454/E-98-007. December.
U.S. EPA. 1999a. National air toxics program: the integrated urban strategy; notice. Federal
Register 64:38705. July 19.
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U.S. EPA. 1999b. Analysis of the impacts of control programs on motor vehicle toxics emissions
and exposure in urban areas and nationwide (volumes I and II). Prepared for U.S. EPA
by Sierra Research, Inc. and Radian International Corporation/Eastern Research Group.
EPA 420-R-99-029 and EPA420-R-99-030. November 30.
Woodruff, T.J., D.A. Axelrad, J. Caldwell, R. Morello-Frosh, and A. Rosenbaum. 1998. Public
health implications of 1990 air toxics concentrations across the United States. Envr.
Health Persp. 106(5):245-251.
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3. Emissions Inventory and Selection of the Urban Pollutants
3.1 introduction
Section 112(k)(3) of the CAA directs EPA to identify at least 30 HAP which, as the result
of emissions from area sources, present the greatest threat to public health in the largest number
of urban areas. In the Strategy, we identify 33 HAP ("urban HAP") to meet this requirement.
The Appendix of this Report details the physical properties, sources of exposure, health hazards,
and other pertinent information for each of the 33 urban HAP.
In developing the final HAP list, we estimated emissions from all known sources using a
variety of techniques, evaluated available health effects information for the 188 HAP, assessed
available air quality monitoring data, reviewed existing studies, and produced a list of pollutants
based on the relative hazards they pose in urban areas, considering toxicity, emissions, and
related characteristics. From these efforts, we established the list of urban HAP which pose the
greatest threat to public health in urban areas, considering emissions from major, area and mobile
sources. Among these urban HAP are a subset of 30 HAP with greatest emissions contributions
from area sources (the "area source HAP").
The first step we took toward developing both an emissions inventory and a HAP ranking
analysis was in 1997 when we conducted an initial screening analysis using a preliminary
methodology. In addition to identifying HAP for which we separately conducted a public review
of our emissions inventory information, this evaluation provided us with the opportunity for peer
review of our preliminary methodology, hi the peer review, outside experts reviewed the ranking
methods and data used and offered suggestions on how the methodology could be used and
improved to select the priority urban HAP. The draft emissions inventory for the HAP identified
by the initial screening analysis was also made available for public comment. This was the first
of two public comment opportunities for the emissions inventory.
hi the sections below, the results of the final analyses are described in detail. The initial
analyses are mentioned, as appropriate, primarily to give you a sense of how the final analyses
were developed in response to public comment and improvements made to the methodologies.
hi section 3.2 of this chapter, the methods and data sources used to develop the baseline
emissions inventory are described. The baseline inventory quantifies the emissions of the
candidate urban HAP and identifies the source categories that emit them. The limitations of the
inventory are also discussed, and the final emissions estimates presented, hi section 3.3, the
ranking methodology is described; the final selection criteria and the list of urban HAP are
presented in section 3.4. References are provided in section 3.5.
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3.2 Baseline Emissions Inventory for
the Integrated Urban Air Toxics
Strategy
One of the building blocks of the Strategy
is the baseline emissions inventory. The
inventory is critical in order to evaluate our
progress toward meeting the goals of the Strategy
as described in Chapter 1. Specifically, the
emissions inventory will help:
Identify source categories that will be
subject to regulations under the Strategy,
as explained in more detail in Chapter 4;
Evaluate progress toward the goal of
assuring those source categories are
subject to standards;
Evaluate progress toward the goal of
reducing by 75 percent the incidence of
cancer associated with air toxics across all
urban areas; and
Evaluate progress toward the goal of
substantially reducing noncancer health
risks associated with air toxics across all
urban areas.
To identify the required source categories
and to measure our progress toward the other
goals listed above, we developed a baseline
emissions inventory of HAP emissions
approximating emissions during the years 1990 to
1993. We believe the intention of the CAA is
that reductions occur from 1990 levels because
that was the year the CAA was amended to
include these requirements. However, since there
were very limited data for 1990, the inventory
spans a longer period of time. We believe that this is an appropriate timeframe because these
years represent HAP emissions prior to implementation of any MACT source category standards.
The baseline inventory contains emissions estimates for major, area, and mobile sources of the
188 HAP and segregates according to whether the sources are located in urban or rural areas. A
Review of the Urban HAP Inventory
The Draft 1990 Emission Inventory of
Forty Section 112(k) Pollutants was made
available on EPA's World Wide Web site in
1997 for review by individuals within and
external to the EPA (i.e., trade organizations,
environmental advocacy groups, academic
experts, and the general public). In addition,
EPA contacted individuals representing trade
organizations, industry, and environmental
groups by letter to announce the availability
of the inventory and to solicit review
comments.
The technical comments related to
development of the inventory were
summarized in the EPA document Public
Comments Received About Technical Aspects
of the 1990 Emission Inventory of Forty
Pollutants in the Section 112(k). This
document can be obtained from the EPA's
website: http:// www.epa.gov/ttn/uatw/
urban/112kfac.html.
A few sections of the draft inventory were
revised based on new data provided by the
reviewers. The updated inventory was then
made available for public review for the
second time on September 14, 1998 as part of
the draft integrated urban strategy. During
this public review, a significant amount of
new data were provided which greatly
improved our facility-specific estimates for a
number of important source categories. All of
the changes made to the inventory subsequent
to the September 14, 1998 release are
reflected in the information presented in this
document.
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subset of the baseline inventory is information collected and publicly reviewed for 40 candidate
HAP to support the analysis of the Strategy, and an additional two HAP developed to support the
section 112(c)(6) efforts.
This section summarizes how the baseline emissions inventory was developed for each of
the candidate urban HAP. The first inventory of 40 HAP, which was a product of the screening
analysis described earlier, was the starting point for more intensive and refined inventory efforts.
The final inventory estimates presented below in section 3.2.2 are the result of revisions made
after two public comment opportunities as described in the accompanying sidebar.
3.2.1 Development of the Baseline Inventory
The national estimates of the HAP
included in the NTI are calculated using
existing information; no source testing or
industry surveys were conducted specifically
for the purposes of generating the inventory.
Existing emissions inventory data are obtained
from a variety of State and local databases and
EPA programs (such as the TRI, standards
development programs, and other studies
required by the CAA). Sometimes, emissions
information is available from direct
measurement of emissions at a source. For
logistical and financial reasons, direct
measurement, or stack testing, is usually
performed only at large point sources and is
far less common than the use of emission
factors.
Documentation of the Inventory
For complete documentation of the inventory,
the reader is encouraged to refer to the 1990
Emissions Inventory of Forty Section 112(k)
Pollutants, Supporting Data for EPA's
Proposed 112(k) Regulatory Strategy, Final
Report (U.S. EPA, 1999a). The Final Report
presents: emission estimates for each HAP by
source category; estimates of total national
emissions for each source category; separate
urban and rural emission estimates; specific
documentation for the subject pollutants of each
source category; the input data used to calculate
emissions; and the algorithms used to estimate
national emissions. The Final Report can be
obtained from the EPA's Internet Web site
(www.epa.gov/ttn/uatw/urban/l 12kfac.html).
Many of the national emissions
estimates in the inventory (primarily for area
and mobile sources) were developed by applying an emission factor, or series of factors, to
activity data which are representative of source categories nationally. Emission factors are one
way to estimate emissions of various chemicals for a particular source category. To estimate
emissions, these factors were combined with information about the activity levels of a source, '
such as the production capacity of the facility, the number of hours of operation, or the amount of
fuel consumed. Emissions for each source category were then allocated according to whether
they are emitted by major or area sources.
The baseline NTI that was used in developing the Strategy is the first one compiled. New
NTI base year inventories will be compiled every three years (1996,1999,2001, etc.). Although
the inventory development methodology described below applies in general to all emissions
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inventories, the baseline and 1996 NTIs do differ in the level of detail they contain. Unlike the
baseline NTI, which includes emissions estimates from all counties by source category and
pollutant, the 1996 NTI will contain facility- and location-specific information that places
individual facilities within those counties and makes the emissions data suitable as input to
computer dispersion models that predict ambient air concentrations. The 1996 NTI data set was
compiled in cooperation with State and local agencies which submitted data they have gathered
during facility permitting and other regulatory activities.
Many estimates presented in the NTI (primarily for area and mobile sources) were
developed by using an emission factor in combination with appropriate activity data. The
emission factors were evaluated for age of the information, completeness and whether the data
adequately represent current practices. The EPA made judgments about the overall quality of the
information, and acceptable data were used to develop composite emission factors for use in the
national estimates.
The availability and overall quality of the activity data vary by source category. Most of
the activity data were obtained from published business/manufacturing sources, governmental
statistics publications, and background information from EPA regulatory programs. Other
sources of activity data were industrial trade associations, the Department of Transportation and
the Department of Energy's Energy Information Administration.
For many source categories, multiple methods were available to develop emission
estimates with some methods being preferable to others. The preferred approach was to use
national emissions estimates from existing inventories previously prepared by EPA.
For pollutants where no EPA, State or local agency inventory was available, other sources
of information were used. In general, other sources of information were prioritized in the
following order.
1. National estimates available from other reference sources that were judged to be
reasonable, complete, and well documented. These estimates were used directly in the
inventories. Examples of these sources include air toxics inventories compiled by
individual State or local agencies, various regulatory projects for different source
categories, and Reports to Congress (e.g., the Utility Air Toxics Study). Estimates
obtained from such programs were generally accepted as the best available data for the
inventory. These estimates are based on recent test data, control information,
representative modeling scenarios, and input from informed industry and government
experts and are considered to be of higher quality than estimates derived through the use
of an overall emission factor and associated activity data.
2. Inventory data from TRI. These data sources received lower priority based on the
evaluation criteria. The TRI contains national inventory data only for sources that meet
certain reporting criteria, and the emission calculation methods cannot be confirmed.
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While considered a relatively low-priority reference source, TRJ data provide a significant
amount of emissions data for sources that might be missed completely by other inventory
compilation methods.
3. Calculated emission estimates. Emissions were calculated if national emissions estimates
were not directly available from a preferred reference source, and emission factors and
activity level data for a source category could be identified. The greatest influence on the
quality of these calculated estimates is the validity of the emission factor(s) used (in terms
of absolute accuracy), as well as representativeness for the processes to which they were
applied. The activity data also affect the quality of an emissions estimate; however, many
standardized and credible references for activity data preclude any large margin of error
being associated with the activity level.
Sometimes, data are available about the composition of emissions from a source category.
This type of information, called a speciation profile, is a list of HAP on a percentage basis
that are the constituents of the emission plume. Thus, if the total concentration of the
plume is known, it can be multiplied by the speciation profile to determine the
concentration of the various HAP which comprise the mixture. In this analysis, suitable
speciation profiles were not available for most source categories in the inventory and
were generally not used. Significant limitations were identified which limited the use of
the speciation profiles, particularly the poor representation of source categories and the
age of the data on which most profiles are based. However, there were some exceptions.
For example, mobile source categories emissions were calculated by first estimating total
HCs or particulates, then deriving the toxic components by using HAP profiles. In the
case of these mobile source categories, this approach is deemed to provide high quality
emissions estimates.
3.2.2 Baseline Inventory Results
Exhibit 3-1 summarizes the baseline inventory estimates developed for each candidate
urban HAP. Total national emissions for each HAP are presented, and emissions are reported for
major, area, and mobile sources. These data are also illustrated in Exhibits 3-2 and 3-3.
Because there are multiple programs investigating HAP emissions in the United States,
emissions data and source activity data are continually changing and improving. The data
presented in this section reflect emissions estimates that have been developed according to the
input data and assumptions described above. The estimates are applicable for a specific time
period and may not necessarily agree with the national estimates from other published estimates
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EXHIBIT 3-1
BASELINE EMISSIONS INVENTORY ESTIMATES FOR EACH OF THE
40 CANDIDATE URBAN HAP (1990 - 1993)
HAP
Benzene
Formaldehyde
Acetaldehyde
Tetrachloroethylene
Methylene Chloride
Trichloroethylene
1,3-Butadiene
Acrolein
Styrene
Chloroform
1 ,3-Dichloropropene
Methyl Chloride
Carbon Tetrachloride
1 ,4-Dichlorobenzene
Ethylene Dichloride
Lead Compounds
Manganese Compounds
Vinyl Chloride
Ethylene Oxide
Acrylonitrile
Coke Oven Emissions
Polycyclic Organic Matter as 7-PAH
Nickel Compounds
Chromium Compounds
bis(2-Ethylhexyl)phthalate
1 ,1 ,2-Trichloroethane
1 ,2-Dichloropropane
Arsenic Compounds
1 ,1 ,2,2-Tetrachloroethane
Methylene Diphenyl Diisocyanate
Vinylidene Chloride
Mercury Compounds
Cadmium Compounds
Ethyl Acrylate
Ethylene Dibromide
Acrylamide
Quinoline
Baseline
National Total
(tons)
390,000
350,000
140,000
130,000
100,000
75,000
72,000
68,000
54,000
23,000
20,000
6,400
5,500
5,100
4,200
3,300
2,800
2,700
2,600
2,600
1,800
1,300
1,200
930
810
740
660
280
260
240
220
210
200
160
51
35
26
Baseline
Major Sources
(tons)
36,000
32,000
21,000
22,000
85,000
61,000
4,000
750
31,000
22,000
34
6,300
5,400
735
4,100
1,500
2,100
2,100
1,200
2,100
1,800
250
740
490
740
740
630
220
51
160
170
120
160
140
50
32
24
Baseline
Area Sources
(tons)
74,000
140,000
51,000
100,000
19,000
14,000
20,000
55,000
3,200
600
20,000
89
110
4,400
100
540
650
570
1,300
440
0
1,000
400
390
68
5
23
65
206
82
48
71
38
20
0.50
3.3
1.6
Baseline
Mobile Sources
(tons)
280,000
180,000
66,000
0
0
0
48,000
12,000
20,000
0
0
0
0
0
0
1,200
52
0
0
0
0
48
95
54
0
0
0
2.8
0
0
0
12
0.31
0
0
0
0
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EXHIBIT 3-1 (Continued)
BASELINE EMISSIONS INVENTORY ESTIMATES FOR EACH OF THE
40 CANDIDATE URBAN HAP (1990 - 1993)
HAP
Hydrazine
Beryllium Compounds
Dioxins/Furans as 2,3,7,8-TCDD TEQ
TOTAL
Baseline
National Total
(tons)
20
12
3.2e-03
1,468.344
Baseline
Major Sources
(tons)
18
9.5
2.2e-03
348.854
Baseline
Area Sources
(tons)
1.1
2.6
9e-04
509.414
Baseline
Mobile Sources
(tons)
0
0.02
1e-04
609,454
EXHIBIT 3-2
SOURCES OF BASELINE EM ISSIONS
FROM THE CANDIDATE URBAN HAP
35%
24%
41%
EXHIBIT 3-3
SPATIAL ALLOCATION OF BASELINE
EM ISSIONS OF THE CANDIDATE
URBAN HAP
67%
33%
due to differences in base years, emission factors and activity data, and calculation assumptions.
It should be recognized that some of the data presented here will likely change as more
information and improved estimation approaches are developed.
3.2.3 Allocating Emissions Between Locations and Source Types
For purposes of selecting the priority urban HAP, the emission estimates were further
refined in two ways. First, the emissions were allocated to either urban or rural areas so that it
could be determined which pollutants were potentially the most significant in the largest number
of urban areas. Second, the pollutants were allocated by source type including major sources,
area sources and mobile sources. The statutory language of section 112(k) focuses on area
sources, but as explained earlier, the Strategy will combine a number of statutory requirements
for both stationary and mobile sources to address the urban air toxics problem in the most
efficient and effective way. The subsections below describe these analyses.
Urban/Rural Source Allocations
Section 112(k) of the CAA specifically addresses HAP that "present the greatest threat to
public health in the largest number of urban areas." However, the CAA does not provide a
definition of "urban." In other sections of the CAA, urban areas with populations greater than
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250,000 are singled out for air monitoring, although the possibility of monitoring other urban
areas is also mentioned.
Statistical data from the Bureau of the Census were used to spatially allocate emissions
on an urban and rural basis (U.S. Bureau of the Census, 1990). The Bureau of the Census has
designated urban and rural areas within every county in the United States based on population
density and total population. For this analysis, using population data and urban/rural
designations for 1990, every county in the United States was classified as either urban or rural
according to the following definitions:
Urban counties are defined as those which include a metropolitan statistical area (MSA)
with a population greater than 250,000, or those counties that do not have an MSA with a
population greater than 250,000, but more than 50 percent of the county population has
been designated by the Bureau of the Census as "urban." These counties include areas
with one or more central places and adjacent, densely settled, surrounding urban fringe
areas. The urban fringe consists of contiguous territory having a density of at least 1,000
persons per square mile.
Rural counties do not have an MSA with a population greater than 250,000 and the
Bureau of the Census designates more than 50 percent of the county population as
"rural."
For the purpose of defining "urban" and "rural" for the Strategy, if more than 50 percent
of the population was classified as rural, then that county was classified "rural." All remaining
counties were classified as "urban."
Emissions were assigned to counties by various methods. In some cases, such as with
TRI estimates and data obtained from regulatory programs studies, emissions could be assigned
to the actual county. Where facility-specific data were not available, emissions were assigned to
individual counties using surrogate approaches. Examples of these surrogate approaches include
proportioning national level emissions to counties based on population, proportioning emissions
from some industrial sectors to counties based on employment estimates, and assigning
emissions from forest fires to counties based on forested acres.
Major/Area Source Allocation
The national emission estimates for stationary source categories were also allocated
according to whether the emitting source category was classified as "major," "area," or could be
classified partially as both. According to section 112(a) of the CAA, a "major source" is any
stationary source (including all emission points and units located within a contiguous area and
under common control) of air pollution that emits or has the potential to emit, considering
controls, 10 tons or more per year of any single HAP or 25 tons or more per year of any
combination of HAP. An "area source" is any stationary source of HAP that does not qualify as
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a major source. The allocation of emissions for each source category on a major/area source
basis will be helpful in evaluating the effects of existing and future regulatory programs on
emissions reductions.
The major/area allocation proportions were derived in a variety of ways. The primary
goal was to determine whether emissions from a category were predominantly emitted from
major or area sources so that sources accounting for 90 percent of the aggregate area source
emissions of each pollutant can be identified. The rationale used to make the major/area source
determinations varied depending on available information. The EPA report Documentation for
Developing the Initial Source Category List, which was used to identify major source categories
for standards development purposes, was a key reference (U.S. EPA, 1992). In some cases, the
accepted way that a source category is typically inventoried served as a guide for the
classification (e.g., residential wood burning is always assessed as an area source). In other
cases, technical analyses were conducted using actual and representative model plant data to
determine typical facility sizes and emissions. With the above information, the percentage of
facilities in a category likely to exceed the 10 or 25 ton-per-year HAP thresholds could be
estimated. Engineering judgment was used to assign an allocation in cases where data were
limited.
3.2.4 Limitations of the Emissions Inventory
In the development of emissions inventories, the quality of the final estimates varies
considerably among the different source categories. The data for some source categories will
have greater uncertainty and limited information especially if those categories have not been a
priority for previous evaluations of emissions. Despite these uncertainties, we feel that the
baseline inventory represents the best available data set for the 1990 to 1993 timeframe, and that
it meets the inventory needs of the Strategy at this time, and the 1996 NTI will represent
significant improvement because of its facility-level detail. Future NTI base year inventories are
expected to continue to improve in quality as data collection and estimation methodologies
improve. This section discusses some of the limitations of the data used to develop the
inventory.
Consistency of Emissions Estimation Methods Within and Among Source
Categories
Because the NTIs, regardless of base year, are compiled in part by the collection of data
from other primary references (e.g., individual States, TRI, regulatory development programs,
etc.), the methods for developing those estimates vary. For example, TRI emissions are self-
reported by individual facilities. Those facilities may estimate their emissions via different
technical approaches (e.g., mass balance versus stack testing) or report emissions on different
bases in scope or time (actual versus potential, or daily versus annual emissions), hi developing
the NTI, we have made assumptions to allow us to standardize all of these reported emissions to
develop emissions on an 'actual annual' emissions basis.
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Emissions Inventories Continue to be Revised Over Time
Because there are multiple programs investigating HAP emissions in the U.S., emissions
data and source activity data are continually changing and improving. To develop emission
factors, extensive information about the different types of industrial processes is required.
Research is always ongoing to update the emission factors so they reflect the most current
knowledge about the industrial sources. Because estimating emissions requires making various
assumptions, the estimates are applicable for a specific time period and may not necessarily agree
with the national estimates from other published estimates due to differences in base years,
emission factors and activity data, and calculation assumptions. It should be recognized that
some of the data presented in the baseline inventory used in developing the Strategy are likely to
change as more information and improved estimation approaches are developed.
Source Category Specific Limitations
hi some cases, categories are known or suspected to emit candidate urban HAP, but it was
not possible to develop emission estimates. At this time, the relative magnitude of these sources
is unknown. The majority of this type of uncertainty is in emissions from chemical
manufacturing facilities, hi the baseline inventory, these emissions are reported in the baseline
NTI as "unspeciated organic HAP." These emissions data were collected to develop the MACT
standard for this industry and could not be speciated into the individual chemical compounds.
Thus, the emissions estimates for benzene and the other HAP that may be included in the
emissions from this source category may be underestimated.
Old or Limited Data
As described earlier, some of the emissions estimates in the NTI are based on calculations
made using emissions factors and activity data. We consider some of these estimates to be of
very high quality (e.g., mobile source estimates that are based on recently developed emissions
factors, VMT, and criteria pollutant inventory data). However, for some source categories,
primarily in the area source sector which has not been the focus of previous HAP studies,
emissions are based on emission factors that are either old (i.e., from the 1980's) and/or very
limited in terms of coverage. This means that for some source categories, a very limited number
of data points were available to characterize an entire category.
Assumptions Required to Divide Emissions into Urban Versus Rural Counties and
Major Versus Area Sources
As described in more detail below, for the sake of the Strategy, we had to allocate
emissions by urban/rural and major/area splits. These distinctions required some technical
assumptions. The major/area distinctions are generally a function of how the emissions estimates
were derived. For example, a facility reporting emissions of one HAP in an amount greater than
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10 tons would definitely be a 'major' source, but a similar facility that reports less than 10 tons
may not be major unless other HAP are emitted as well.
For urban/rural designations, the distinction was simple if we knew the actual location of
a facility within a county that has been designated as urban or rural using U.S. Census Bureau
data. This was not so simple when no location was known, particularly for area sources. For
example, if the area source category emissions were calculated for the entire Nation and then
spatially allocated to urban and rural counties using a surrogate (e.g., population), an individual
county's emissions may be skewed high or low, even though the national emissions estimate is
accurate.
3.3 Ranking the Urban Hazardous Air Pollutants
This section describes the ranking analyses used to select the priority urban HAP. The
analyses are described in more detail in an EPA technical support document (U.S. EPA, 1999b).
As with the emissions inventory, the first step we took toward ranking the pollutants was the
development of an initial screening methodology. While the final ranking used to identify the
priority urban HAP is similar to that of the screening analysis, the methodology was revised to
address the comments of the January 1998 peer review panel and public comments. The analysis
was rerun using updated emissions, monitoring and toxicity information that became available in
the interim. The accompanying text box describes the screening analysis and its peer review.
The purpose of these analyses was to identify which of the 188 HAP "present the greatest
threat to public health" in urban areas. In order to use the available data in the most robust
manner, we conducted three ranking analyses, each of which is described below. First, we
ranked the HAP by combining indicators of toxicity and exposure into four risk-related ranking
indices and then produced an overall ranking by combining each of the individual indices (i.e.,
the Exposure/Toxicity Indicators Ranking Analysis). Second, we reviewed a number of
previously conducted risk or hazard assessments concerning HAP in urban areas and produced a
list based on the results of these assessments (i.e., the Risk Assessment/Hazard Ranking Studies
Analysis). Third, we used information provided by EPA's CEP which compares modeled
ambient concentrations of HAP in urban areas with health-based benchmarks (i.e., the CEP
Ranking Analysis). Each of these analyses have various limitations, but by assembling and
assessing this variety of analyses and types of information, a weight of evidence approach was
taken to provide a more sound identification of urban HAP than would be possible from a single
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analysis. The three separate analyses
and types of information are described
below along with their strengths and
limitations.
Limitations Shared By All
Three Ranking Analyses
The ranking analyses are
uncertain because there are
gaps and uncertainties
associated with the health
effects, monitoring and
emissions data for the 188
HAP.
Although all three ranking
analyses used ambient
concentration data in the same
form, none considered
personal exposure. Personal
exposure, which includes
physiological and behavioral
factors that vary with
individuals, may vary
substantially from ambient
concentrations.
Only HAP having both
toxicity data and emissions or
ambient concentration data
could be ranked. This could
lead to overlooking potentially
high-risk pollutants because of
sparse data.
Initial Screening Analysis and Peer Review
The screening analysis for the initial HAP ranking used various
types of information combined in five different rankings to
assess the relative potential health risks posed by each of the
188 HAP. For each method, contributions from major, area,
and mobile sources were considered. This approach accounted
for risks from multiple sources and minimizes the impact of
missing information for individual sources. The selection
process for the candidate HAP as well as the methods and data
used in the screening analysis are explained in detail in an EPA
document, "Prioritization of HAP for the Urban Air Toxics
Study - Peer Review Draft" (U.S. EPA, 1997a), which is
available in the Urban Strategy Docket.
A technical review panel was convened on January 21, 1998 to
review the preliminary methodology used to select the candidate
list of HAP. Nine scientists from academia, government
agencies and an EPA/industry-supported research institute
participated as panel members. The panel was charged with
reviewing the ranking methodology for scientific accuracy,
objectivity, technical quality and validity. Reviewers were also
asked to comment on the general approach taken, the individual
ranking methods, the results of the ranking and other technical
aspects of the ranking method such as uncertainties and data
gaps, which were presented in the draft EPA report (U.S. EPA,
1997a).
In general, the reviewers agreed that the information available at
the time of the review had been appropriately incorporated into
the ranking approaches, and that the ranking results were
systematically evaluated and integrated. The various ranking
methods seemed to complement each other in that one method
filled in data gaps that the other ranking methods may have
missed. Overall, the ranking methodology appeared to result in
the highest rankings for pollutants with the most potential to
cause human health risks and lower rankings for those less
likely to be priorities. However, the reviewers expressed
concern that data gaps and the use of arbitrary cutoffs to select a
predetermined number of pollutants could result in some
priority pollutants being left off the list. The reviewers also
suggested that EPA explain how massing or uncertain data could
affect the ranking, that the analysis be updated periodically with
new science as appropriate, and that the reasons for selecting
each pollutant be illustrated more clearly. (The complete set of
written comments by the peer reviewers may be obtained from
the Urban Strategy Docket (A-97-44)).
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3.3.1 Exposure/Toxicity indicators Ranking Analysis
The first analysis ranked HAP by combining surrogates for toxicity and exposure into
risk-related ranking indices. By considering short-term inhalation hazards and hazards posed by
ingestion of HAP with a potential to accumulate in foods, this analysis complemented the other
two ranking analyses described below, both of which considered only long-term inhalation
hazards or risks.
The surrogates for toxicity were the RBC for inhalation and the risk-based dose (RED)
for ingestion. These are calculated by selecting a specified risk level (e.g., 1 in 1,000,000 excess
cancer risk) and calculating exposure concentration or dose of the HAP which will cause the risk
level to be exceeded, assuming the relevant acute or chronic exposure conditions. For effects
other than cancer, the RBC or RBD is the chronic RfC (or similar value from another source). If
available, the EPA's inhalation RfC was chosen as the chronic noncancer RBC. If an RfC was
not available for a HAP, then a comparable value was obtained from another agency, such as the
minimal risk level (MRL) developed by the Agency for Toxic Substances and Disease Registry,
or the reference exposure level (REL) developed by the State of California Environmental
Protection Agency. Similarly, the EPA's reference dose (RfD) was the first choice for the
noncancer RBD. Acute RBCs were set equal to risk management exposure guideline levels (e.g.,
Acute Exposure Guideline Levels (U.S. EPA, 1997b)) for mild, transient or no effects from short
exposure periods, when available.
For HAP categorized as "known," "probable," or "possible" human carcinogens, rankings
were done separately for two risk levels. In the first case, the RBC or RBD was set at an
exposure associated with a one in one million upper-bound predicted lifetime cancer risk, or the
RfC/REL for noncancer effects (whichever was lower). In the second case, the RBC or RBD
was set at an exposure associated with a one in ten thousand upper-bound predicted lifetime
cancer risk, or the RfC/REL (whichever was lower). Two risk scenarios were selected because if
the cancer risk level was preset at only one in one million upper bound lifetime cancer risk, the
list of 30 substances selected likely would be dominated by carcinogens. This would in effect
give cancer preference over noncancer effects because the amount of pollutant needed to trigger
the one in one million cancer risk level would almost always be lower than the amount needed to
trigger the risk level based on noncancer effects. Thus, the lower of the cancer or noncancer
RBCs and RBDs is selected under two different risk scenarios to ensure that noncancer effects
are given appropriate consideration in the ranking.
Surrogates for exposure included measured ambient concentrations and emission
estimates from mobile, major and area sources. The Exposure/Toxicity Indicators ranking is
necessarily based on databases which are not complete and contain information that varies in
quality. While we believe that these databases contain the best available information, there is
still substantial uncertainty in this analysis. The results should be considered estimates of the
relative potential hazards of the various HAP and not a quantitative estimate of risks.
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Normalized Scores
A normalized score is prepared by listing the
score for each pollutant and dividing each score
by the value of the highest score. By
normalizing the scores, the magnitude of the
differences between the scores of each pollutant
is preserved. In addition, because each index is
normalized in the same way, each is given equal
weight, or importance, in the analysis.
Four separate ranking indices - three
of which had two separate risk scenarios (case
1 and case 2) as noted above - were prepared
for each HAP. The pollutants were ranked on
a normalized scale. To obtain the final
ranking, the normalized scores from each
index for each pollutant were averaged. The
average normalized value for each pollutant
was then ranked in order from highest to
lowest. (If a score was not available for a
pollutant in a given index, the value was
treated as "missing," not zero, so as not to
lower the average value.)
Toxicity is inversely related to the value of the RBCs and RBDs. For example, the more
toxic the HAP, the lower the concentration at which health effects would be realized.
Consequently, the more toxic HAP would have lower RBCs and/or RBDs. In contrast, the
relative concern for exposure increases with increasing ambient measures or emissions (i.e.,
surrogates for exposure). Therefore, higher emissions (or ambient concentrations) are of greater
concern than lower emissions. In order to rank the HAP by toxicity and exposure, the exposure
surrogate is divided by the RBC (or RBD), as illustrated by the following equation:
Exposure Surrogate/RBC = Ranking Index
The ranking indices are used to estimate the relative concern for public health. The four
indices are:
Index 1: Ambient/Acute. This index was intended to rank HAP by relative short-term
inhalation hazard. The ambient acute index for each HAP was calculated by dividing the
95th percentile 24-hour concentration of the database of 24-hour urban area ambient
concentrations by the RBC for acute inhalation exposure.
Index 2: Ambient/Chronic. This index was intended to rank HAP by relative long-term
inhalation hazard. The ambient chronic index for each HAP was calculated by dividing
the average ambient long-term concentration for the urban areas monitored by the chronic
RBC. This was done separately for case 1 (RBC set at 1 x 10~6 upper bound cancer risk or
the RfC, whichever was lower) and case 2 (RBC set at 1 x 10"4 upper bound cancer risk or
the RfC, whichever was lower).
Index 3: Emission/Chronic/Inhalation. This index was intended to rank HAP by
relative long-term inhalation hazard. The emissions-based chronic inhalation index for
each HAP was calculated by dividing the national urban emissions estimate by the RBC
for chronic inhalation exposure. The emissions estimates were obtained from the
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baseline NTI (U.S. EPA, 1998a). As with the ambient chronic index, this was done
separately for case 1 (RBC set at 1 x 10"6 upper bound cancer risk or the RfC, whichever
was lower) and case 2 (RBC = 1 x 10"4 upper bound cancer risk or the RfC, whichever
was lower).
Index 4: Emission/Chronic/Oral. This index was intended to rank HAP by relative
potential for oral toxicity and food-chain bioaccumulation. The emissions-based chronic
oral index for each HAP was calculated by multiplying the national urban emissions
estimate by the HAP's bioconcentration factor (BCF) and then dividing by the oral RED
for chronic oral exposure. As with the other chronic indices, this was done separately for
case 1 (RBD set at 1 x 10"6 upper bound cancer risk or the RfD, whichever was lower)
and case 2 (RBD = 1 x 10"4 upper bound cancer risk or the RfD, whichever was lower).
With the exception of radionuclides, each HAP was carried through the index
calculations even if health benchmark, emission, or ambient data were not available. We believe
that this presentation will allow readers to see data gaps more clearly and will serve as a guide for
future efforts to prioritize data collection for the air toxics program. The results of the
Exposure/Toxicity Indicators ranking are shown in Exhibit 3-4.
EXHIBIT 3-4
40 HIGHEST PRIORITY POLLUTANTS IDENTIFIED BY
EXPOSURE/TOXICITY INDICATORS RANKING
Acetaldehyde
Acrolein
Acrylonitrile
Arsenic compounds
Benzene
Bromomethane
(methyl bromide)
1,3 -Butadiene
Cadmium
compounds
Carbon tetrachloride
Chloroform
Chloroprene
Coke oven emissions
Chromium compounds
1 ,2-Dibromomethane
1 ,4-Dichlorobenzene
1 ,3-Dichloroethane
1 , 1 -Dichloroethylene
1 ,3-Dichloropropene
Dioxin (2,3,7,8-TCDD)
Ethylene oxide
Formaldehyde
Heptachlor
Hydrogen chloride
Hydrazine
Lead compounds
Manganese
compounds
Mercury compounds
Methylene chloride
Napthalene
Nickel compounds
2-Nitropropane
PCBs
POM
Propylene dichloride
Quinoline
1 , 1 ,2,2-Tetrachloro-ethane
Tetrachloroethylene
Trichloroethylene
Vinyl chloride
Xylene
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Data Sources for the Exposure/Toxicity Indicators Ranking
In order to rank each of the HAP in the indices described above, data on health-based
reference values, ambient air quality measurements, emissions, and bioconcentration factors were
collected. Each of these are described below.
Health-Based Reference Values. Dose-response assessments for health effects of HAP
were obtained from various sources, and prioritized according to: (1) applicability, (2) conceptual
consistency with EPA risk assessment guidance, and (3) level of review received. The
accompanying text box lists in priority order the health-based reference values which were used
in this analysis. For dose response estimates that are currently under review or being revised, we
reviewed current information to determine how potential changes to dose-response estimates
might affect the outcome of the analysis1. The Technical Support Document contains additional
details regarding these reference values (U.S. EPA, 1999b).
Estimates of Exposure. The second major part of the HAP ranking indices (the first part
being the dose-response data described above) was information on exposure. Actual data
describing human exposure to HAP are limited and lack the comprehensive geographic,
temporal, and multicontaminant coverage that this ranking exercise required. Therefore, we
chose to base the ranking on exposure surrogates - data related to, but not identical with,
exposure. The two types of exposure surrogates chosen were long- and short-term ambient air
quality measurements from urban areas, and estimated annual emissions of HAP from major,
area, and mobile sources in urban areas.
The ambient air quality data set used in this analysis was created by combining all
available monitoring data from EPA's Aerometric Information Retrieval System (AIRS) and
Toxics Data Archive (12/31/97 version) databases for the 188 HAP. The analysis was restricted
to data from 1990 through 1997, for 24-hour sampling intervals only from counties designated as
"urban 1" or "urban2." A minimum of 20 observations during a year were required for inclusion
of that year's data, and for volatile and semi-volatile compounds it was further required that at
least five observations were from the spring or summer and five from the fall or winter.
Concentration data that were below the method detection limit were used as reported in the
calculations, while data values designated only as "below detection limits" (i.e., without a
reported concentration) were assumed to be present at one-half the detection limit (instead of
'For example, in the case of 1,3-butadiene, we determined that the EPA's Integrated Risk Information
System (IRIS) risk estimate is no longer an appropriate basis from which to extrapolate human risk, and the updated
assessment has progressed to the point where it is appropriate for use here. Use of this new assessment, however,
does not affect the presence of 1,3-butadiene on the urban HAP list. In the case of vinyl chloride, we've chosen to
use the Agency consensus assessment currently in IRIS rather than a draft assessment that may yet change
significantly. However, we've confirmed that using the draft assessment for vinyl chloride wouldn't change its
status on the final urban HAP list.
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Data Sources and Health-Based Reference
' Values Used in the Exposure/Toxicity
Indicators Ranking Analysis
For chronic exposure (cancer and noncancer
reference values, in order of preference):
1.
2.
3.
4.
5.
EPA IRIS
Agency for Toxic Substances and Disease
Registry (ATSDR) MRLs
EPA Health Effects Assessment Summary
Tables (HEAST)
California EPA inhalation unit risks
EPA estimates of cancer risk from oral
exposure converted to inhalation units (IRIS
or HEAST)
For short-term exposure (noncancer effects):
omitting the observation). For HAP having
fewer than 10 percent of observations above the
detection limit, the data were omitted
altogether.
For input to the chronic exposure
indices, selected ambient air quality data were
first averaged arithmetically for each year, by
HAP and monitoring site. The annual average
concentrations from 1990 to 1997 for each site-
pollutant combination were next averaged
across years. Finally, the resulting multiyear
average concentrations were averaged across
monitoring sites into a single national long-term
average concentration for each HAP for which
data met the selection criteria.
To simulate acute exposure for each
HAP, the 95th percentile concentration of the
database of 24-hour ambient concentrations at
all locations was selected. We judged-that this
concentration represented a reasonable
maximum short-term exposure.
The second type of data used in this
ranking analysis as a surrogate for exposure was
the estimated emissions of HAP from major,
area, and mobile sources in urban areas (U.S.
EPA, 1998b).
Bioconcentration Data. Measured and
estimated BCFs for HAP were obtained from
EPA's draft Waste Minimization Prioritization
Tool (WMPT). The BCF provides an estimate of how much a pollutant will accumulate in
tissues and be concentrated throughout the food web (U.S. EPA, 1998c).
Limitations of the Exposure/Toxicity Indicators Ranking
In addition to the general limitations of all three ranking analyses, the Exposure/Toxicity
Indicators ranking relied heavily on emissions data. Emissions-based indices do not consider
dispersion or transformation of HAP and are, therefore, likely to be less reliable surrogates for
exposure than are ambient concentrations. As a result, there are two limitations of this analysis:
1.
3.
4.
5.
6.
7.
National Advisory Committee (NAC)
Guideline Level (1-hr Level I)
NAC Acute Exposure Guideline Level (1-hr
Level II)
California EPA acute RELs
American Industrial Hygiene Association
(AIHA) Emergency Response Planning
Guidelines (ERPG) (1-hr Level I)
AIHA ERPG (1-hr Level IT)
10 percent of National Institute for
Occupational Safety and Health
Immediately Dangerous to Life or Health
levels
ATSDR acute MRL
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(1) the ranking is relative rather than absolute, and (2) the results cannot be inferred as
quantitative risk estimates.
3.3.2 Risk Assessment/Hazard Ranking Studies in Urban Areas
Much of the current information that has been collected to characterize urban air toxic
exposures and potential risks comes from 14 major studies in urban areas. These studies were
conducted by EPA and various State air pollution control agencies. All 14 included emissions
inventory analyses, although seven studies also included air monitoring data. Eleven of the
studies had a risk assessment component, while three studies were hazard rankings only and did
not have a risk assessment component. The number of pollutants studied varied from 11 to 34.
Most studies focused on carcinogens, but six of the 14 also assessed noncancer risks. Eleven of
the 14 studies included major, area and mobile sources, and three evaluated area sources only.
These 14 studies were reviewed to determine which pollutants contributed the most to the
total risk or hazard reported for the study area. For example, if the total excess cancer risk was
estimated to be three cases per year and pollutant X contributed 0.3 cases per year, then pollutant
X would receive a score of 0.10 because it accounted for 10 percent of the risk. This was done
for each pollutant in each study. The scores for each pollutant were then added together, and the
pollutants ranked from the highest aggregate score to the lowest. Two rankings (one for cancer
as an endpoint and one for noncancer effects) were produced for the 11 studies that included
major, area, and mobile sources. Similarly, two rankings were produced based on the three
studies of area sources only. We used these four HAP rankings to select 27 HAP that appeared
to contribute substantially more risk or hazard than the rest. The 27 HAP identified from this
analysis are shown in Exhibit 3-5.
EXHIBIT 3-5
PRIORITY HAP IDENTIFIED BY STUDIES IN URBAN AREAS
Acrolein
Acrylonitrile
Arsenic compounds
1,3-Butadiene
Benzene
Cadmium compounds
Carbon tetrachloride
Chloroform
Chromium compounds
Coke oven emissions
Cyanide compounds
Ethylene dichloride
Ethylene oxide
Formaldehyde
Glycol ethers
Hexane
Lead compounds
Manganese compounds
Methylene chloride
2-Nitropropane
Nickel compounds
POM
Tetrachloroethyene
Trichloroethylene
Toluene
Vinyl chloride
Xylene
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In addition to the general limitations shared by all three analyses, the urban studies
summarized in this hazard ranking analysis studied only 11 to 34 HAP, substantially less than the
188 HAP listed in section 112 of the CAA. Thus, it is possible that high-risk HAP may have
been overlooked. Despite these limitations, however, these studies represent high quality
analyses which identified priority pollutants in a variety of urban areas in the United States. As a
result, the analysis of these studies was a critical component of the overall ranking methodology
and HAP selection process.
3.3.3 CEP Ranking Analysis
The third ranking analysis was based on EPA's CEP, initiated in 1994, with the objective
of using existing data and methods to evaluate the combined exposures to multiple pollutants
through three different routes of exposure - air, food and drinking water. In the air toxics
component (the only component completed), long-term air concentrations of HAP (but not
personal exposure) are estimated on a national scale (SAI, 1998).
In the CEP, the Assessment System of
Population Exposure Nationwide (ASPEN) Sources ^Emissions Data
model was used with preliminary estimates of ^ ^ CEpj emssions from manufacturing point
1990 HAP emissions (see text box) to predict
long-term average concentrations at the census
tract level for 148 HAP. For some pollutants,
modeled concentrations were augmented with
estimates of background levels that were
intended to represent contributions from
natural sources as well as historic emissions of
persistent pollutants. The estimated ambient
concentrations were then compared to RBCs
sources are represented by data from the 1990
TRI. For the other five source categories, the
CEP estimates HAP emissions by applying
speciation profiles to inventories of VOC and
PM. Speciation profiles were specific to
industries or industrial processes. They
provided estimates, on a percentage basis, of the
amount of individual chemical constituents that
comprise VOC or PM emissions.
(termed benchmarks by the authors) intended ^^^^^^^^^^^^^^^^^^^^^^^
to represent either continuous exposure levels
associated with a one in one million upper bound estimate of excess lifetime cancer risk, or
continuous lifetime exposure levels associated with no significant risk of adverse noncancer
effects (e.g., EPA's inhalation RFC) (Caldwell et al., 1998). As stated earlier, estimated
concentrations greater than RBCs should be viewed as indicators of a potential health problem
and not as a characterization of health risks.
As we wanted to focus the analysis on modeled concentrations resulting from controllable
sources, and we are currently using updated RBCs which, in some cases, differ from those used
in the CEP analysis, we took some additional steps. Prior to using this analysis as part of our
final methodology, we repeated the analysis for the subset of HAP for which concentrations had
been augmented with background concentrations or for which the health reference values needed
to be updated. For this small re-analysis, we used the modeled concentrations resulting only
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from current area, major and mobile sources (i.e., without addition of a background value) and an
updated set of RGBs.
From these analyses, we identified those HAP for which the modeled concentrations
exceeded RBCs in the greatest number of urban census tracts. There were 36 HAP for which
modeled concentrations were greater than an RBC in at least 50 urban census tracts (see Exhibit
3-6). These 36 HAP are those of greatest potential concern based on our use of the CEP
modeling analysis.
EXHIBIT 3-6
HAP WITH MODELED CONCENTRATIONS HIGHER THAN
AN RBC IN AT LEAST 50 URBAN CENSUS TRACTS
Acetaldehyde
Acrolein
Acrylamide
Acrylonitrile
Arsenic and compounds
Benzene
Benzotrichloride
Beryllium and compounds
1,3 -Butadiene
Cadmium and compounds
Carbon tetrachloride
Chloroform
Chromium VI and compounds
1 ,2-Dibromomethane
1 ,4-Dichlorobenzene
1,2-Dichloropropane (Propylene dichloride)
Ethylene dichloride (1,2-dichloroethane)
1 ,3-Dichloropropene
2,3,7,8-Tetrachlorodibenzo-p-dioxin(&
congeners & TCDF congeners
Ethyl acrylate
Ethylene oxide
Formaldehyde
Heptachlor
Hexachlorobenzene
Hexachlorocyclopentadiene
Hydrazine
Lead and lead compounds
Manganese and compounds
Methylene chloride (Dichloromethane)
Nickel and compounds
PCBs
Quinoline
1 , 1 ,2-Trichloroethane
Tetrachloroethylene (Perchloroethylene)
Trichloroethylene
Vinyl chloride
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Limitations of the CEP
In addition to the general limitations of all three ranking analyses, the modeling
performed for this analysis was subject to the following uncertainties and limitations:
The ASPEN model, as it had been run, may under- or over-estimate some HAP. Such a
tendency could then lead to an under- or over-estimation of the number of census tracts
with air concentrations higher than an RBC.
This analysis prioritized HAP according to how frequently a modeled air concentration
was higher than an RBC; how much higher was not examined. Thus, a HAP whose
modeled concentration is slightly higher than the RBC in many census tracts would be
listed as a higher priority than a HAP whose modeled concentration is higher than the
RBC by a large margin in a smaller number of census tracts.
A majority of the RBCs were for cancer effects, rather than noncancer effects. This
reflects the fact that the cancer benchmarks set at a one in one million risk level are
generally much lower concentrations that the noncancer benchmarks. Consequently,
cancer as a health effect was emphasized over other health effects.
While we recognize certain limitations associated with this initial attempt at modeling
HAP concentrations nationwide, and its inappropriateness for use in drawing conclusions at
small geographic scales, this modeling effort is useful as a national screening tool.
3.4 Selection of the Urban Hazardous Air Pollutants
Exhibit 3-7 summarizes the three ranking methodologies and illustrates how the results of
these analyses were considered to produce one listing of priority urban HAP. Results for all three
ranking analyses are summarized in Exhibit 3-8.
For the final HAP list, we selected those HAP for which the baseline inventory data were
publicly reviewed (through EPA's public request in September 1997 for additional information
on 40 candidate compounds or during development of inventories for the specific HAP listed in
section 112(c)(6) of the CAA) and which had been either:
Identified by two of the ranking analyses (regardless of area source contribution), or
Identified by at least one of the three analyses and had an area source contribution to total
emissions of at least 25 percent.
Exhibit 3-9 summarizes the final integrated list. This list of 33 urban HAP includes not
only those with emissions from area sources, but reflects the integrated nature of the Strategy by
3-21
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National Air Toxics Program: The Integrated Urban Strategy
Report to Congress
EXHIBIT 3-8
RESULTS OF THE THREE RANKING ANALYSES
Contaminant
Tetrachloroethylene
Acrolein
Ethylene oxide
Chromium VI and
compounds
Nickel and compounds
Manganese and compounds
Formaldehyde
Vinyl chloride
Trichloroethylene
Cadmium and compounds
Methylene chloride
Acrylonitrile
Arsenic and compounds
1,3-Butadiene
Benzene
Chloroform
1 ,2-Dichloroethane
Carbon tetrachloride
1 ,3-Dichloropropene
Carcinogenic PAHs: 7-PAH
2,3,7,8-TCDD (dioxin)
Hexachlorobenzene
Risk
Assessment
Hazard
Ranking
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
CEP Urban
Analysis
(All Sources)
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
Exposure
Toxicity
Ranking
System
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
Ratio of
Area/Total
Emissions
81.4%
66.9%
53.0%
44.2%
33.0%
26.1%
23.7%
20.2%
19.3%
19.1%
17.7%
16.8%
16.4%
13.3%
11.2%
3.8%
2.9%
2.7%
99.8%
61.8%
23.5%
22.3%
Urban
Strategy
List3
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
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EXHIBIT 3-8 (Continued)
RESULTS OF THE THREE RANKING ANALYSES
Contaminant
PCBs
Acetaldehyde
Lead and lead compounds
Hydrazine, hydrazine sulfate
Quinoline
1 ,2-Dichloropropane
(propylene dichloride)
1 ,2-Dibromoethane
Coke Oven Emissions
1 , 1 ,2,2-Tetrachloroethane
Mercury and compounds
Beryllium and compounds
1 , 1 -Dichloroethylene
Ethyl acrylate
Acrylamide
1 , 1 ,2-Trichloroethane
Risk
Assessment
Hazard
Ranking
X
X
CEP Urban
Analysis
(All Sources)
X
X
X
X
X
X
X
X
X
X
X
Exposure
Toxicity
Ranking
System
X
X
X
X
X
X
X
X
X
X
Ratio of
Area/Total
Emissions
19.9%
18.8%
16.7%
8.0%
6.3%
3.6%
1.5%
0.0%
79.5%
34.5%
27.7%
19.3%
12.5%
9.1%
1.0%
Urban
Strategy
List"
X
X
X
X
X
0
o
o
X
X
X
"HAP to be used in selecting area sources for regulation under the Strategy are marked with an "X.!
for the Strategy, but not for area source selection, are marked with an "O."
HAP selected
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EXHIBIT 3-9
LIST OF URBAN HAP FOR THE INTEGRATED URBAN AIR TOXICS STRATEGY
Acetaldehyde
Acrolein "
Acrylonitrile
Arsenic compounds
Benzene
Beryllium compounds
1,3-Butadiene
Cadmium compounds
Carbon tetrachloride*
Chloroform
Chromium compounds
Coke oven emissions*
1 ,2-Dibromoethane*
1,2-Dichloropropane (propylene dichloride)
1 ,3-Dichloropropene
Ethylene dichloride
( 1 ,2-dichloroethane)
Ethylene oxide
Formaldehyde
Hexachlorobenzene
Hydrazine
Lead compounds
Manganese compounds
Mercury compounds
Methylene chloride (dichloromethane)
Nickel compounds
PCBs
POM
Quinoline
2,3,7,8-tetrachlorodibenzo-p-dioxin (&
congeners & TCDF congeners)
1 , 1 ,2,2-Tetrachloroethane
Tetrachloroethylene (perchloroethylene)
Trichloroethylene
Vinyl chloride
* These 3 HAP are identified mainly due to emissions from major sources, and therefore are not
considered urban area source HAP at this time.
including those posing public health concerns in urban areas regardless of emissions source type.
Included among the 33 urban HAP are the 30 HAP with greatest emissions contributions from
area sources (i.e., the "area source HAP"). The 3 HAP noted with an asterisk are listed mainly
due to major source emissions. Nonetheless, they are included in the Integrated Urban Air
Toxics Strategy (which considers emissions in urban areas from all source types) based on the
criteria presented in this chapter. Under section 112(k), there aren't any specific regulatory
implications of listing the other three HAP, and we'll use all 33 HAP in prioritizing efforts to
address risk.
It is important to note that the HAP list in Exhibit 3-9 was generated based on our best
estimates representing national baseline air toxics emissions and ambient concentrations for
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urban areas. For example, implementation of technology-based standards for coke ovens has
reduced the benzene, coke oven gases, and POM from these sources by 80 percent (or 1,408 tons
per year) since 1993. In addition, certain urban areas have reduced other benzene emissions by
as much as 30 or 40 percent. Much of this reduction is attributable to the implementation of
mobile source reformulated gasoline requirements. To ensure that we appropriately target
reductions of urban air toxics to support the protection of public health, it will be important to
reevaluate our priorities as we develop emissions estimates and obtain more comprehensive
monitoring information covering more recent years.
3.5 References
Caldwell, J.C., T.J. Woodruff, R. Morello-Frosch, and D.A. Axelrad. 1998. Application of
health information to hazardous air pollutants modeled in the Environmental Protection
Agency's Cumulative Exposure Project. Toxicology and Industrial Health, Vol.14, No. 3,
pp. 429-454.
Systems Applications, Inc. (SAT). 1998. Modeling cumulative outdoor concentrations of
hazardous air pollutants: final technical report. Prepared by SAI Division of ICF Kaiser
International. Prepared for U.S. Environmental Protection Agency. February.
U.S. Bureau of the Census. 1990. Summary tape file 1 A, 1990 decennial census of population
and housing. Washington, D.C.
U.S. EPA. 1992. Documentation for developing the initial source category list, final report.
EPA-450/3-91-030. Office of Air Quality Planning and Standards, Research Triangle
Park, North Carolina.
U.S. EPA. 1997a. Prioritization of HAP for the Urban Air Toxics Study - peer review draft.
Office of Air Quality Planning and Standards, Research Triangle Park, North Carolina.
December 29.
U.S. EPA. 1997b. National Advisory Committee for Acute Exposure Guideline Levels for
Hazardous Substances; notice. Federal Register 62:58839-58851. October 30.
U.S. EPA. 1998a. 1993 National Toxics Inventory, version 9702.
U.S. EPA. 1998b. Inventory of Emissions Estimates for HAP Emitted from MACT Source
Categories. Prepared by the Emission Factor and Inventory Group and the Emission
Standards Division, Research Triangle Park, North Carolina.
U.S. EPA. 1998c. Waste Minimization Prioritization Tool spreadsheet document for the RCRA
waste minimization PBT chemical list docket (#F-98-MMLP-FFFFF). Office of Solid
Waste and Emergency Response, Washington, D.C. Available on-line at
www.epa.gov/wastemin.
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U.S. EPA. 1999a. 1990 Emissions inventory of forty section 112(k) pollutants, supporting data
for EPA's proposed 112(k) Regulatory Strategy, final report. Office of Air Quality
Planning and Standards, Research Triangle Park, North Carolina. May 21.
U.S. EPA. 1999b. Ranking and selection of hazardous air pollutants proposed for listing under
section 112(k) of the Clean Air Act Amendments of 1990. Technical Support Document.
Office of Air Quality Planning and Standards, Research Triangle Park, North Carolina.
April 12.
U.S. EPA Docket A-97-44. Urban Air Toxics Strategy.
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4. Regulatory Programs and Activities to Reduce Air Toxics
Emissions
4.1 Introduction
The Strategy describes many of the programs and regulatory activities that will help
achieve the goals of reducing cancer and noncancer risks. One of the key aspects described by
the Strategy is that national regulatory programs are but one of the many tools that we will use to
address emissions of air toxics. Other authorities and laws will, directly or indirectly, also allow
us to address these pollutants. Furthermore, by working collaboratively with State, local, and
Tribal governments, we will ensure that localized air toxics issues are addressed as well.
Section 4.2 presents the list of area source categories that were identified in the Strategy
and explains how we intend to ensure that, as required, we reach the goal of addressing the
source categories that represent 90 percent of the emissions of each of the 30 area source HAP.
Section 4.3 describes the regulatory options that will be considered in order to address air toxics
from area sources. The role of mobile sources is noted in section 4.4, and current and future
programs are described. Other emission sources which may be affected by the Strategy are
described in section 4.5, while other programs and authorities which may also account for
emissions reductions are described in section 4.6. A very important component of the Strategy is
described in section 4.7 - the role State, local, and Tribal programs will play in helping us
address air toxics and achieve the Strategy goals. References are listed in section 4.8.
4.2 List of Area Source Categories
Our selection of the area source categories was a two-step process. First, we identified
area sources that contribute to emissions of the area source HAP and that are subject to existing
standards or will be subject to standards that are currently being developed. These area source
categories have already been listed for regulation under the CAA. For each of these source
categories, we identified the percent contribution to the total area source emissions for each of
the 30 area source HAP. These source categories are provided in Exhibit 4-1. We have included
hazardous waste combustors1 on this list, despite the fact that information related to the
percentage contribution of emissions from this area source category was not known at the time
that the list was developed. Once we determine the percentage of urban area emissions from the
area source categories affected by this rule, their emissions will be counted toward the 90 percent
requirement for the appropriate HAP2.
The Hazardous Waste Combustor source category combines the following: hazardous waste incinerators,
hazardous waste-burning cement kilns, and hazardous waste lightweight aggregate kilns.
We have recently promulgated MACT standards for hazardous waste combustors (U.S. EPA, 1999a) and
will be using the support information for that rule to update our information on this source category.
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EXHIBIT 4-1
AREA SOURCE CATEGORIES ALREADY SUBJECT TO REGULATION
OR WHICH WILL BE SUBJECT TO REGULATION
Chromic Acid Anodizing
Commercial Sterilization Facilities
Other Solid Waste Incinerators (Human/Animal
Cremation)
Decorative Chromium Electroplating
Dry Cleaning Facilities
Halogenated Solvent Cleaners
Hard Chromium Electroplating
Hazardous Waste Combustors
Industrial Boilers
Institutional/Commercial Boilers
Medical Waste Incinerators
Municipal Waste Combustors
Open Burning Scrap Tires
Portland Cement
Secondary Lead Smelting
Stationary Internal Combustion Engines
In the second step, we added to the list those area source categories that contribute at least
15 percent of the total area source emissions of any of the individually-listed HAP. This criterion
was adopted to account for uncertainties in our current inventory data. Although the baseline
emissions inventory data have improved, data gaps and uncertainty still remain. By listing only
those additional sources contributing 15 percent of the area source emissions of at least one of
the area source HAP, we can be fairly certain that, despite the gaps in our inventory data, a listed
source category genuinely contributes to emissions of that HAP. Once listed, we counted the
percent contribution, even if less than 15 percent, to emissions of any other listed HAP because
once the source is subject to regulation, its emissions of any of the 30 listed HAP can be counted
toward the 90 percent goal for each of the listed HAP. Exhibit 4-2 includes those new area
source categories listed under section 112(c)(3) for the first time.
The result of these criteria for the source selection process is that the current list of 29
source categories does not, at this time, contain area source categories representing 90 percent of
the emissions of each individual HAP. The current list meets the 90 percent or greater
requirement for 11 of the 30 area source HAP3. For 10 other HAP, the list accounts for at least
80 percent of the emissions4, and for ethylene dichloride the list accounts for approximately 78
percent of the emissions. Improved inventory data may demonstrate that the current list of area
sources already meets the 90 percent requirement for some of these HAP. For the remaining
HAP on the list, less than 75 percent of their emissions are accounted for in the list of source
3l,l,2,2-tetrachloroethane, 1,2-dichloropropane, POM, acetaldehyde, acrolein, benzene, dioxins/furans,
ethylene oxide, formaldehyde, quinoline, and tetrachlorethylene.
4l,3-butadiene, 1,3-dichloropropene, acrylonitrile, beryllium compounds, chloroform, hydrazine, mercury
compounds, methylene chloride, trichloroethylene, and vinyl chloride.
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EXHIBIT 4-2
NEW AREA SOURCE CATEGORIES AS LISTED
Cyclic Crude and Intermediate Production
Flexible Polyurethane Foam Fabrication
Operations
Hospital Sterilizers
Industrial Inorganic Chemical Manufacturing
Industrial Organic Chemical Manufacturing
Mercury Cell Chlor-Alkali Plants
Gasoline Distribution Stage I
Municipal Landfills
Oil & Natural Gas Production
Paint Stripping Operations
Plastic Materials and Resins Manufacturing
Publicly Owned Treatment Works
Synthetic Rubber Manufacturing
categories: arsenic compounds, cadmium compounds, chromium compounds,
hexachlorobenzene, lead compounds, manganese compounds, nickel compounds and PCBs.
It's important to clarify that we still intend to meet our statutory obligation to list area
sources accounting for 90 percent of the emissions of each of the 30 area source HAP. We have
chosen to complete this list in stages by keeping the option to add or delete source categories
from the list as we gather more and improved data. This first stage lists those area sources that
we are reasonably confident add real contributions to the total area source emissions of a
particular area source HAP. We anticipate to begin evaluating the source categories for the HAP
for which we haven't reached a 90 percent emission reduction, including the six metal HAP,
PCBs, and hexachlorobenzene, when we conduct an initial risk assessment by the end of 2000
(discussed in Chapter 5 of this Report). That initial assessment will use the updated 1996 NTI.
We'll use this information as part of our process to reevaluate the source categories listed in the
Strategy. Based on this updated information, we may decide to remove an area source category
listed here if, for example, the reason for the listing was inaccurate (e.g., faulty reporting to the
TRI) or if no urban area sources exist. We'll also use this assessment to evaluate area source
categories to be added and will complete the list by 2003.
4.3 Regulatory Activities for Area Sources
We plan to pursue a tiered approach that will consider three standard-setting processes.
The specific process selected for a particular source category will depend on the criteria outlined
below. We intend to determine which one of these approaches is most appropriate when we
conduct rulemaking. The three tiers of standard setting processes that will be considered are:
Tier 1 - MACT standards;
Tier 2 - Source category-specific GACT standards; and
Tier 3 - Flexible GACT.
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4.3.1 Tier 1 - MACT Standards
We'll develop MACT standards in accordance with section 112(d)(3) for those area
sources whose emissions pose the greatest threat to human health and the environment, and for
which the technology to achieve maximum reductions in HAP emissions is appropriate. Section
112(d)(3) requires the standards to reduce HAP emissions as much as is achievable, considering
the cost of these reductions, effects on health or the environment (other than air), and energy
requirements.
Section 112(d)(3) requires us to use a minimum statutory baseline ("floor") when setting
MACT standards. For new sources, the MACT standards for a source category or subcategory
must be at least as stringent as the emission control achieved in practice by the best controlled
similar source. The standards for existing sources can be less stringent than standards for new
sources, but they can't be less stringent than the average emission limitation achieved by the
best-performing 12 percent of existing sources (excluding certain sources) for categories or
subcategories with 30 or more sources, or by the best-performing five sources for categories or
subcategories with fewer than 30 sources.
We've issued MACT standards for area sources in previous cases. For example, in the
chromium electroplating national emission standards for hazardous air pollutants (NESHAP), we
developed MACT standards for area sources because of the high toxicity of chromium.
Similarly, in the Portland Cement NESHAP, we determined that MACT controls were
appropriate because of the quantity and toxicity of the HAP being emitted from area sources. In
addition, both of these source categories have numerous, widespread sources. We've also
determined in a recent rulemaking that air toxic emissions from area source hazardous waste
combustors present a threat of adverse effects to human health and, thus, will be required to meet
MACT controls.
4.3.2 Tier 2 - Source Category-Specific GACT Standards
While we may develop MACT standards for some area sources, we expect most sources
will be subject to GACT standards developed in accordance with section 112(d)(5). As with
MACT standards, GACT standards would be developed for a specific source category, but they
would be based on the use of GACT rather than MACT. This approach will be used to address
source categories that present a human health risk or environmental concern, but where GACT is
a more appropriate approach for reducing HAP emissions than MACT. To make these decisions,
we'll consider economic feasibility and other factors that could lead us to GACT.
4.3.3 Tier 3 - Flexible GACT Process
Considering the large number and diversity of area sources and limitations in the data and
information currently available for many of them, it may be appropriate to develop flexible
requirements that would apply to several area source categories where more flexibility is
appropriate (e.g., where there are very few area sources, they are confined to a limited geographic
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area, or they contribute to localized public health or environmental risks). Under this option, we
might develop general requirements, such as a process rule similar to the one developed under
section 112(g) of the CAA, which would be applicable to area sources in several source
categories. These general requirements could outline procedures for determining what
constitutes "generally available control technology." In this context, by following these
procedures, States, local governments, and Tribal agencies could elect to develop GACT for the
area sources. We would review these resulting standards to ensure they were developed
following the procedures contained within the general requirements and, if appropriate, we
would adopt the standards as GACT for these area sources.
We believe this approach presents several advantages. It could be implemented in a
manner that permits States, local and Tribal agencies to address cumulative risk posed by
exposures to HAP emissions from many different source categories. It also permits greater
flexibility in tailoring GACT to individual area sources or area source categories which may
contribute to an undue public health risk in a particular area. For example, a State, local or
Tribal agency could tailor GACT to a particular source by requiring potentially more stringent
controls when the source contributes emissions that, when aggregated with emissions from other
sources in the area, pose health risk concerns. They could also require less stringent controls
when the source is in an area where exposures to aggregated emissions don't present significant
concern.
To supplement our general requirements, we may choose to issue control technique
guidelines or alternative control technology documents to provide information on generally
available control technologies for controlling HAP emissions. The CAA gives us flexibility in
deciding which level of control to apply to a given source category. As long as the result of the
rulemaking is that sources use enforceable GACT or management practices, we have the
flexibility in choosing between the adoption of numerical emission limits and the promulgation
of other requirements that result in sources applying GACT.
4.3.4 Issues on the National Versus Local Scope of Area Source Standards
Section 112(k) requires that listed area source categories be subject to standards under
section 112(d). Section 112(d) standards are national standards that generally apply everywhere
in the country. Consistent with this approach, we expect, in general, to apply area source
standards developed under section 112(k) nationally; however, for those area source categories
where the standards only apply in urban areas, we'll look to the consolidated metropolitan
statistical area (C/MSA) boundaries as a starting point to define the urban area. Although we
used the "urban 1" and "urban 2" definitions5 for the development of the inventory to support the
HAP and the source category analysis, we believe the C/MSAs are more appropriate for defining
5"Urban 1" areas are those counties that have a population of more than 250,000. "Urban 2" areas are
counties where at least 50 percent of the population is considered to be urban.
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applicability of area source standards, because the C/MSAs better reflect the nature of population
density, commercial development, area growth, and air emissions that represent urban areas.
Although we generally believe that urban areas are those C/MSAs with populations of
more than 50,000, we recognize that the appropriate area in which standards should apply may
vary among area source categories. Consequently, we believe the determination of the
appropriate urban area size for where standards apply should be made separately for each
category.
4.3.5 Schedule for Area Source Standards
The Strategy outlined a timeframe for the completion of area source standards, as shown
in the time line below:
2004 - Promulgate the area source category standards listed in Exhibit 4-2; we expect to
meet this demanding schedule as expeditiously as practicable;
2006 - Promulgate some additional area source standards to meet the 90 percent
requirement;
2009 - Promulgate all remaining area source standards necessary to meet the 90 percent
requirement; and
2012 - Expected compliance under all standards.
We'll prioritize the order in which we regulate source categories to address those posing
the greatest risks first. This will be a part of our initial assessments which will be done in the
spring of 2000. We'll be developing standards between now and 2009. Compliance with these
standards is required within 3 years of promulgation. Therefore, compliance with all standards is
anticipated by no later than 2012.
4.4 Regulatory Activities for Mobile Sources
4.4.1 Urban HAP Emitted from Mobile Sources
There are hundreds of different compounds and elements that are known to be emitted
from passenger cars, on-highway trucks, and various nonroad equipment. Using emission
speciation data from several sources, we have determined that 15 of the compounds included in
the list of 33 urban HAP may be emitted from mobile sources6. These are listed in Exhibit 4-3,
6As part of the air toxics rulemaking currently under development pursuant to the requirements of section
202(1) of the CAA, described below, we will be preparing a more comprehensive list of air toxics emitted by motor
vehicles and their fuels.
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along with their absolute and relative contributions as determined by our baseline emissions
inventory.
The inventory estimates presented in Exhibit 4-3 are 1990 estimates. As we continue to
improve our inventories for urban HAP from mobile sources, these values may change. For
example, the 1996 NTI is incorporating new information based on improved data and methods.
Based on information in EPA's Integrated Risk Information System (IRIS) database, four
of the urban HAP listed in Exhibit 4-3 are VOCs considered to be known or probable human
carcinogens (acetaldehyde, benzene, 1,3-butadiene, and formaldehyde), and a fifth VOC,
acrolein, is considered to be a possible human carcinogen (U.S. EPA, 1999b). POM includes a
number of carcinogenic compounds such as benzo(a)pyrene. While 2,3,7,8-TCDD (& congeners
& TCDF congeners) has a very high potency, it is emitted in only trace amounts by mobile
sources (Truex et al., 1998; Gertler et al., 1997; U.S. EPA, 1998a). The eight remaining HAP
listed in Exhibit 4-3 are metals that may be contained in very small quantities in particulate
emissions from gasoline and/or diesel engines7.
4.4.2 Diesel Exhaust
Diesel exhaust is one of the pollutants under consideration for inclusion on a
comprehensive list of air toxics emitted by motor vehicles and their fuels in the section 202(1)
rulemaking, described below. Diesel exhaust was not included by Congress on the list of 188
HAP under section 112(b) of the CAA and consequently was not included in the group of
pollutants that were considered for inclusion on the urban HAP list. Because diesel exhaust
emissions come almost exclusively from mobile sources, we are investigating the health risks
associated with diesel exhaust and assessing its role in the urban air toxics problem as part of the
section 202(1) rulemaking process.
Diesel exhaust includes components in the gas and particle phases. Gaseous components
of diesel exhaust include at least one organic compound known to cause cancer in humans (e.g.,
benzene) while possible or probable human carcinogens and compounds causing noncancer
effects are also present in the gas-phase (e.g., formaldehyde, acetaldehyde, 1,3-butadiene,
These metals are arsenic compounds, beryllium compounds, cadmium compounds, chromium compounds,
lead compounds, manganese compounds, mercury compounds, and nickel compounds. It is worth noting that: (1)
hexavalent chromium, a known human carcinogen, is the carcinogenic compound of interest among chromium
compounds; (2) nickel has been classified as a known human carcinogen; (3) while lead in gasoline has been
phased-out for use in cars, it is still used in aircraft and in racing fuel; (4) recent studies have not been able to detect
mercury compounds in measurable amounts in light-duty gasoline or heavy-duty diesel mobile source emissions
(Ball, 1997; Truex et al., 1998); however, we are presently undertaking further study of mercury emissions from
vehicles, and the Ball (1997) and Truex et al. (1998) studies should not be viewed as conclusive; and (5) we are
investigating the potential health impact of manganese in fuels under our section 211 testing programs, described
below; and (6) while mobile source emissions of beryllium compounds and cadmium compounds are reported in our
baseline inventory, these emission estimates are derived from data that are more than 10 years old and thus may not
be representative of current emissions.
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EXHIBIT 4-3
1990 NATIONAL EMISSION ESTIMATES
FOR URBAN HAP EMITTED FROM MOBILE SOURCESf
HAP
Acetaldehyde
Acrolein
Arsenic compounds
Benzene
Beryllium compounds
1,3-butadiene
Cadmium compounds
Chromium compounds
Formaldehyde
Lead compounds
Manganese compounds
Mercury compounds
Nickel compounds
POMJ
2,3,7,8-TCDD (&
congeners & TCDF
congeners)
Mobile Source
Tons/year
65,535
12,315
3
281,170
0.02
47,822
0.31
54
177,031
1,199
52
12
95
48
0.0001
Total Emissions
Tons/year
137,476
67,901
284
390,615
12.15
71,870
203.34
927
350,617
3,270
2,846
208
1,245
1,318
0.0032
Percent Mobile
Source
Contribution
47
18
1
72
0.16
66
0.15
6
50
37
2
6
8
4
2.9844
fEmissions and percentages for most of these compounds are rounded to the nearest whole unit. However, due to
the small amount of emissions of beryllium and compounds and cadmium and compounds, these emissions
and percentages are reported to 2 decimal places. Similarly, values for 2,3,7,8-TCDD (& congeners &
TCDF congeners) emissions and percentages are reported to four decimal places.
% POM represents the 7-polycyclic aromatic hydrocarbons (7-PAH) group from the baseline emissions inventory.
acrolein). Because diesel exhaust is a mixture of particles and gases, the choice of a measure of
exposure (i.e., dosimeter) is important. The EPA believes that exposure to whole diesel exhaust
is best described, as many researchers have done over the years, by diesel particulate
concentrations expressed in units of mass concentration (e.g., ^g/m3). This does not imply that
mass is the only lexicologically important aspect of PM since other parameters such as particle
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number, particle size, surface area, and chemical composition can influence toxiciry. The choice
of this dosimeter implies that the contribution of the gaseous components and diesel particulate
constituents to toxicity are related by diesel particulate mass. This assumption is consistent with
historic practice, but can only be validated when there is a better understanding of the
lexicological mode of action for diesel exhaust.
While some gaseous components of diesel exhaust may play a role in the cancer hazard
attributed to diesel exhaust exposure, studies suggest that the particulate component plays a
substantial role in carcinogenicity and other noncancer effects. Diesel PM typically consists of a
solid core, composed mainly of elemental carbon, which has a coating of various organic and
inorganic compounds. The characteristically small particle size (on average 0.2 microns in
diameter) increases the likelihood that the particles and the attached compounds will reach and
lodge in the deepest and more sensitive areas of the human lung. Diesel PM may be influential
in contributing to potential human health hazards from long term exposure.
Our draft health assessment for diesel emissions identifies lung cancer and several other
adverse respiratory health effects (including respiratory tract irritation, immunological changes,
and changes in lung function) as possible concerns for long term exposure to diesel exhaust (U.S.
EPA, 1999c). The evidence for these health effects comes from occupational exposures and high
exposure animal studies. The draft health assessment finds that diesel exhaust is a likely human
carcinogen in the lung at environmental levels of exposure, and that exposure to diesel exhaust
can pose a noncancer health risk. The draft health assessment document is currently being
revised to address comments from a peer review panel of the Clean Air Scientific Advisory
Committee (CASAC) (U.S. EPA, 2000a) and will be reviewed by CASAC again in late 2000.
4.4.3 Mobile Source Emission Control Programs
We regulate mobile sources emissions through a wide range of programs under the
authority contained in several sections of the CAA. These include the motor vehicles provisions
contained in section 202(a), the fuel requirements contained in section 211, the nonroad engine
and vehicle provisions contained in section 213, and the urban bus standards contained in section
219. While many of our programs are designed primarily for control of criteria pollutants,
especially ozone and PM, they also achieve important reductions in air toxics through VOC and
HC controls. For example, vehicle- and engine-based control programs reduce benzene, 1,3-
butadiene, formaldehyde, and acetaldehyde that are produced during the combustion process
when there is incomplete combustion. Overall, vehicle- and engine-based HC controls have
dramatically reduced exhaust emissions of gaseous air toxics emitted by mobile sources.
Similarly, we have several programs that reduce diesel exhaust emissions from diesel engines
and equipment. Finally, our evaporative control programs are designed to further reduce
emissions of volatile air toxics due to engine design or faulty components that allow fuel vapors
to escape into the atmosphere.
We also address mobile sources air toxics through fuel requirements. Our fuel control
programs have resulted in significant reductions in the emissions of toxic substances from motor
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vehicles. The phase-out of lead in gasoline has essentially eliminated mobile sources emissions
of this highly toxic substance. More recently, the reformulated gasoline (RFG) program has
assisted areas of the country with the worst ozone problems to help improve their air quality. By
controlling fuel benzene content and vehicle emissions of air toxics, ozone-forming HC and NOX,
Phase I of the-RFG program has removed thousands of tons of air pollutants for the 17 States and
the District of Columbia currently participating in the program. Phase n of the RFG program
began on January 1, 2000 and contains even more stringent emissions reductions requirements
than Phase I.
In addition to vehicle and fuel control programs, we have established several programs to
make sure vehicle emission controls are functioning properly in actual use. At the national level,
vehicle manufacturers are required to install computerized diagnostic systems that alert drivers
and mechanics to malfunctioning emission controls. We also follow up with manufacturers by
performing selective engine testing as engines leave the assembly line to make sure they are
manufactured as designed and meet the mandatory exhaust emission limits. At the State level,
we have developed programs that States can adopt to require vehicle owners to have their
vehicles periodically inspected. In addition, we follow up on in-use performance by testing or
requiring that manufacturers test vehicles that have been in service.
In continuing our progress in controlling emissions from mobile sources, there are four
major recent and ongoing mobile source rulemaking activities that have the potential to achieve
additional reductions of health risks from air toxics. First, in October of 1999, we proposed to
reconfirm heavy-duty diesel engine emission standards for the 2004 model year and proposed
heavy-duty gasoline vehicle emission standards for the 2004 model year (U.S. EPA, 1999d).
Second, we recently promulgated stringent new "Tier 2" emission standards and gasoline sulfur
controls that will reduce NOX and HC emissions from light-duty vehicles and light-duty trucks8
(U.S. EPA, 2000b). The Tier 2 program also contains new PM limits that will reduce PM
emissions from the diesel versions of these vehicles. Third, we recently proposed heavy-duty
engine and vehicle standards for the 2007 model year and highway diesel fuel sulfur controls
beginning in 2006 (U.S. EPA, 2000c). The proposed diesel fuel sulfur controls would enable the
use of a new generation of emission control technologies for diesel engines to decrease diesel PM
and other emissions. Fourth, we are conducting a technology review, to be concluded in 2001,
for land-based compression ignition nonroad engines (U.S. EPA, 1998b).
4.4.4 Mobile Source Air Toxics Assessments and Controls
In addition to the general emission control provisions mentioned above, title n of the
CAA contains provisions that call more directly for reductions in HAP from motor vehicles and
their fuels. These provisions are contained in section 202(1) of the CAA. The first of these
requirements, outlined in section 202(1)(1), requires us to study the need for and feasibility of
8Chapter 3 of the Regulatory Impact Analysis for this rule assesses the impacts of the Tier 2 program on
air toxics (U.S. EPA, 1999e).
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controlling emissions of toxic air pollutants associated with motor vehicles and their fuels that
are otherwise unregulated under the CAA.
Pursuant to section 202(1)(1), in 1993 we released the Motor Vehicle-Related Air Toxics
Study (U.S. EPA, 1993). The study summarized information on emissions of toxic air pollutants
associated with motor vehicles and motor vehicle fuels, as well as estimated exposures and
potential risks. The study also provided predictions of cancer risks associated with continuous
lifetime exposure to motor vehicle emissions of several air toxics in the years 1990,1995,2000,
and 2010 under various control scenarios. We have recently updated the emissions and exposure
analyses done for the study to account for new information (U.S. EPA, 1999f). These analyses
include base scenarios for the years 1990,1996,2007, and 2020, and control scenarios in 2007
and 2020. We modeled toxics emissions and exposure for 10 urban areas (Atlanta, Chicago,
Denver, Houston, Minneapolis, New York, Philadelphia, Phoenix, Spokane, and St. Louis), and
nationwide. In addition, we developed emission estimates for 16 geographic regions. We
assessed emissions and exposure from benzene, formaldehyde, acetaldehyde, 1,3-butadiene,
methyl tertiary butyl ether (MTBE), and diesel PM. As part of our section 202(1)(2) proposal
(see below), we will outline the additional research and technical analysis we plan to conduct to
improve these analyses.
We have several activities already under way to improve our understanding of the risks
associated with exposure to mobile source air toxics. We are developing and updating
information on health effects for some pollutants on the urban HAP list with contributions from
mobile sources including, for example, our recent benzen.e cancer risk assessment (U.S. EPA,
1998c; U.S. EPA, 1985) and our draft 1,3-butadiene risk assessment (U.S. EPA, 1998d)9. We are
also continuing our research on health effects of diesel exhaust through the development of our
diesel health assessment document, and through the support of research efforts by organizations
such as the Health Effects Institute. We are developing models of mobile source emissions as
inputs for emissions inventory and dispersion modeling efforts such as the NTI and ASPEN (see
discussion in Chapter 6 of this Report). In addition, we seek to better characterize emissions and
exposures to HAPutants through research and testing efforts at EPA facilities such as the
National Exposure Research Laboratory, as well as the National Vehicle Fuel and Emissions
Laboratory. We also have programs requiring manufacturer-run fuel and fuel additive health
effects testing programs under section 21 l(b) of the CAA, including testing of various fuels
containing oxygenates, such as MTBE or ethanol, as well as research focused on the gasoline
additive, methylcyclopentadienyl manganese tricarbonyl (MMT), and tailpipe emissions of
manganese particulates10.
This assessment is currently being revised based on comments from the EPA Science Advisory Board
(SAB) and others.
The test requirements for fuels containing oxygenates include short and long term animal health effects
testing, as well as human microenvironmental exposure measurement studies to determine how much of certain
compounds we breathe in our everyday lives. The list of compounds includes, but is not limited to, air toxics such
as benzene, 1,3-butadiene, formaldehyde, and acetaldehyde. The MMT testing program includes pharmacokinetic
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Section 202(1)(2) of the CAA instructs us to set standards for HAP from motor vehicles
or their fuels, or both. Those standards are to reflect the greatest degree of emissions reductions
achievable through the application of technology which will be available, taking into
consideration existing standards, availability and costs of the technology, noise, energy, and
safety factors^ and leadtime. The CAA also specifies that, at a minimum, benzene and
formaldehyde emissions must be addressed. We are currently working on a proposal in
compliance with section 202(1)(2). As indicated above, we are not limiting our examination of
toxic emissions from motor vehicles and their fuels to benzene and formaldehyde; rather, we are
preparing a more comprehensive list of air toxics emitted by motor vehicles and their fuels for
consideration in the rulemaking.
4.5 Other Hazardous Air Pollutant Emission Sources
As discussed previously, section 112(k)(3)(B) of the CAA requires that we ensure that
area sources accounting for 90 percent of the aggregate emissions of each of the 30 area source
HAP are subject to standards. However, in achieving required reductions in cancer incidences,
section 112(k)(3)(C) permits us to consider reductions in public health risks resulting from
actions to reduce emissions from "all stationary sources and resulting from measures
implemented by the Administrator or by the States under this or other laws." Therefore, we'll
consider emission reductions from a combination of major and area sources in conducting risk
assessments to address this requirement.
These assessments will support regulatory efforts under the CAA and other authorities, as
necessary, to address the identified risk. For example, any reductions resulting from MACT, the
NAAQS, and other programs that achieve reductions in HAP can be included in the assessment
of reductions in risks. Therefore, if we determine that a source category or an individual source
is presenting a significant health risk, then we'll address it using the appropriate regulatory
authority. For example, if needed to provide an ample margin of safety to protect human health,
section 112(f) residual risk standards will be developed for source categories currently subject to
MACT. Additionally, if our analyses reveal a major source category that is currently unregulated
or unlisted but poses a public health risk, we'll list that source category under the authority of
section 112(c) and develop the necessary regulations under section 112(d), or we may address it
through other activities like pollution prevention or voluntary programs. Similarly, if a specific
source is contributing to a local risk problem, then the State, local or Tribal program may be
more appropriate for addressing that risk.
We also intend to coordinate our authorities in addressing cumulative risks posed by
exposures to aggregate emissions from multiple source types. For example, during the
development of the Strategy, many commenters raised concerns about the risks from airports to
the communities that surround them. Airports can be viewed as "mini-cities," which produce
testing of manganese compounds and characterization of manganese emissions from vehicles utilizing fuels
containing MMT.
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numerous pollutants from multiple sources and are governed by many different authorities.
We'll need to have an integrated plan to reduce air emissions and the many other environmental
impacts associated with aviation activities.
Although airports don't meet the definition of "area" or "major" source under section 112
of the CAA, we're involved with numerous efforts to better understand and reduce the
environmental impacts of aviation-related activities and their associated human health risks. For
example, we co-chair the EPA/Federal Aviation Administration Voluntary Aircraft Emissions
Reduction Initiative, a multistakeholder process designed to identify and evaluate technically
feasible and cost-effective voluntary measures to reduce aviation emissions. We're actively
involved in the International Civil Aviation Organization, which is the forum for evaluating and
establishing international aircraft engine standards. We're also participating with other
stakeholders in the development of the South Coast Ground Service Equipment memorandum of
understanding (MOU) in California to identify ways to achieve additional emissions reductions
from the commercial aviation community. Implementation of the MOU should yield emissions
reductions through increased use of cleaner engines, electrification, and alternative fuels. In
addition, we're developing a Green Airport Initiative to demonstrate innovative strategies for
reducing the environmental impacts of aviation-related activities at an airport undergoing
expansion. In April 1999, we released a report that assesses the current and potential impact of
aircraft emissions on local air quality at ten selected airports (U.S. EPA, 1999g). The regulatory
and voluntary actions under way for aviation will produce data that can inform the Strategy and
begin to address the environmental impacts of aviation-related activities and their associated
risks to the communities that surround them.
4.6 Other Programs and Authorities
We've already made progress in addressing air toxics emissions using existing programs.
To put the problem in perspective, we estimate that approximately 8.1 million tons of 188 HAP
were released in the United States in 1993 (U.S. EPA, 1998c). We've already issued at least 43
MACT and GACT standards and two section 129 standards with post-1993 compliance dates,
which will address many sources of these emissions. Exhibit 4-4 lists the MACT standards that
we have finalized as of June 2000. Emission controls for the Nation's cars, trucks and off-road
equipment, and standards for fuels add even more to these reductions. In this section, we'll
discuss the utility of these programs and others to achieve additional air toxics emissions
reductions.
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EXHIBIT 4-4
COMPLETED RULES from SECTION 112 of the CAA (MACT STANDARDS)3
Source Category
Dry Cleaning
Aerospace Industry
Chronium Electroplating
Commercial Sterilizers
Gasoline Distribution
Magnetic Tape
Off-site Waste and
Recovery Operations
Polymers & Resins I
Polymers & Resins IV
Secondary Lead Smelters
Wood Furniture
Electric Arc Furnace:
Stainless & Non-stainless
Steel
Flexible Polyurethane Foam
Production
Mineral Wool Production
Final Rule
Publication Date
(Citation)"
09/22/93
(58 FR 49354)
09/01/95
(60 FR 45956)
01/25/95
(60 FR 4948)
12/06/94
(59 FR 62585)
12/14/94
(59 FR 64303)
12/15/94
(59 FR 64580)
07/01/96
(61 FR 34140)
09/05/96
(61 FR 46906)
09/12/96
(61FR48208)
06/23/95
(60 FR 32587)
12/07/95
(60 FR 62930)
06/04/96
(61 FR 28197)
10/07/98
(64 FR 34853)
06/01/99
(64 FR 29490)
Source Category
Hazardous Organic
NESHAP (HON)
Asbestos
Coke Ovens
Degrease Organic Cleaners
Industrial Cooling Towers
Marine Vessel Loading
Operations
Petroleum Refineries
Polymers & Resins n
Printing/Publishing
Shipbuilding & Ship Repair
Chromium Chemicals
Manufacturing
Ferralloys Production
Generic MACT
Nylon 6 Production
Final Rule
Publication Date
(Citation)6
04/22/94
(59 FR 19402)
1 1/30/95
(60 FR 6 1550)
10/27/93
(58 FR 57898)
12/02/94
(59 FR 61 801)
09/08/94
(59 FR 46339)
09/19/95
(60 FR 48399)
08/18/95
(60 FR 43244)
03/08/95
(60 FR 12670)
05/30/96
(61 FR 27 132)
12/15/95
(60 FR 64330)
06/04/96
(61 FR 28197)
05/20/99
(64 FR 27450)
06/30/99
(64 FR 34853)
02/12/98
(63 FR 7 155)
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EXHIBIT 4-4 (Continued)
COMPLETED RULES from SECTION 112 of the CAA (MACT STANDARDS)3
Source Category
Oil & Natural Gas
Production, Transmission &
Storage
Pharmaceuticals Production
Polyether Polyols
Productions
Primary Aluminum
Production
Pulp & Paper (Non-
combust) MACT I
Steel Pickling - HCL
Process Facilities &
Hydrochloric Acid
Regeneration Plants
Wood Treatment MACT
Cyanuric Chloride
Production
Secondary Aluminum
Polymers & Resins in
Aerosol Can-Filling
Facilities
Final Rule
Publication Date
(Citation)"
06/17/99
(64 FR 32610)
09/21/98
(63 FR 50280)
06/01/99
(64 FR 29420)
10/07/97
(62 FR 52383)
04/15/98
(63 FR 18504)
06/22/99
(64 FR 33202)
06/04/96
(61FR28197)
02/12/98
(63 FR 7 155)
03/23/2000
(65 FR 15689)
01/20/2000
(65 FR 3275)
11/18/99
(64 FR 63025)
Source Category
Pesticide Active Ingredient
Production
Phosphoric Acid/ Phospate
Fertilizers
Portland Cement
Manufacturing
Primary Lead Smelting
Pulp & Paper Cluster Rule
(Non-chem) MACT ffl
Tetrahydrobenzaldehyde
Manufacture
Wood Fiberglass
Manufacturing
Lead Acid Battery
Manufacturing
Publicly Owned Treatment
Works (POTW)
Antimony Oxides
Manufacturing
Final Rule
Publication Date
(Citation)"
06/23/99
(64 FR 33549)
06/10/99
(64 FR 3 1358)
06/14/99
(64 FR 3 1897)
06/04/99
(64 FR 301 94)
03/08/96
(61 FR 9383)
05/12/98
(63 FR 26078)
06/14/99
(64 FR 3 1695)
06/04/96
(61FR28197)
10/26/99
(64 FR 57572)
11/18/99
(64 FR 63025)
"Current as of June, 2000.
b Citation identifies the Federal Register (FR) volume and page number (e.g., 58 FR 49354 can be found in FR
volume 58, page 49354).
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4.6.1 Federal Regulatory Activities - CAA Section 112 Authorities
Section 112 of the CAA provides several authorities for us to use in meeting our air
toxics goals. We've promulgated section 112(d) MACT and GACT standards that are projected
to reduce air toxics emissions by approximately one million tons per year once fully
implemented. Within the next ten years, as we complete more MACT and GACT standards, the
air toxics program is projected to reduce emissions of toxic air pollutants by well over 1.5
million tons per year. These nationwide emissions reductions will contribute significantly to
reductions needed in urban areas.
The need for section 112(f) standards, or "residual risk" standards, is under consideration
for some of the early source categories covered by MACT standards. Where justified, these
standards will address remaining public health and environmental impacts of HAP to ensure an
ample margin of safety to protect public health and, in consideration of other factors, to prevent
adverse environmental effects. Consistent with the requirements of the CAA, we'll consider
such evaluation for those area source categories for which GACT standards have been
promulgated.
The chemical accident prevention regulations ("Risk Management Program
requirements," or "RMP rule") were promulgated under section 112(r). These regulations
require owners and operators handling more than a threshold quantity of any substance on the list
of regulated toxic substances and threshold quantities for accidental release prevention (40 CFR
68.130) to develop risk management plans to prevent and address accidental releases. Eighteen
of these listed substances are HAP.
We've already received several requests for permits under the section 112(g) construction
and reconstruction rule. This rule applies to new or reconstructed major sources and requires
them to install MACT to reduce HAP emissions, hi addition, the section 112(i)(5) rule (early
reductions) provides incentives for sources to reduce emissions by up to 95 percent from 1990
levels prior to proposal of MACT for that source category. Approximately 27 title V permit
applications have been received, representing HAP reductions of over 6,800 tons.
Section 112 (n)(l)(A) requires us to conduct a study of the hazards to public health
reasonably anticipated to occur as a result of HAP emissions from fossil fuel-fired electric utility
steam generating units (i.e., utilities) and on the alternative control strategies for HAP emissions
which may warrant regulation. In addition, section 112 (n)(l)(A) requires us to regulate HAP
emissions from utilities if we find such regulation is appropriate and necessary after considering
the results of study. In February 1998, we published a report describing the results of the study
described above (U.S. EPA, 1998h). The primary components of the report are: (1) a description
of the industry, (2) an analysis of emissions data, (3) an assessment of hazards and risks due to
inhalation exposures to 67 HAP, (4) assessments of risks due to multipathway (inhalation plus
non-inhalation) exposures to 4 HAP (radionuclides, mercury, arsenic, and dioxins), and (5) a
discussion of alternative control strategies. The overall conclusion of the 1998 Utility Study is as
follows:
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Based on available information and current analyses, the EPA believes that mercury
from coal-fired utilities is the HAP of greatest potential concern and merits additional
research and monitoring. There are uncertainties regarding the extent of risks due to
mercury exposures, including those from utility emissions. Further research and
evaluation are needed to gain a better understanding of the risks and impacts of utility
mercury emissions. In addition, further research and evaluation of potential control
technologies and strategies for mercury are needed.
For a few other HAP, there are still some remaining potential concerns and uncertainties
that may need further study. First, the screening multipathway assessments for dioxins
and arsenic suggest that these two HAP are of potential concern (primarily from coal-
fired plants); however, further evaluations and review are needed to better characterize
the impacts of dioxins and arsenic emissions from utilities. Second, nickel emissions
from oil-fired utilities are of potential concern, but significant uncertainties still exist
with regard to the nickel forms emitted from utilities and the health effects of. those
various forms. The impacts due to HAP emissions from gas-fired utilities are negligible
based on the results of this study; therefore, the EPA feels that there is no need for
further evaluation of the risks of HAP emissions from natural gas-fires utilities (U.S.
EPA, 1998h).
We plan to make the regulatory determination in December 2000. In the interim, we are
collecting additional information on mercury emissions and potential control technologies as well
as conducting various analyses to increase our understanding of the impact of HAP emissions
(especially mercury) from utilities and the feasibility of reducing those emissions.
4.6.2 Other CAA Authorities
Other programs under the CAA also contribute to the reductions of HAP in urban areas.
For example, section 109 requires States to develop State implementation plans to attain
compliance with the NAAQS. Many of the activities that are designed to address criteria
pollutants (e.g., ozone, PM, and lead) and attain the NAAQS also achieve reductions in air
toxics. For example, many of the VOCs that form ozone are also air toxics, such as benzene and
1,3-butadiene. hi addition, some VOCs can react in the atmosphere to form HAP, such as
formaldehyde. Thus, controlling VOCs leads to reductions in air toxics. Similarly, compliance
with the PM standards will provide incidental, but potentially significant, reductions in HAP that
are either emitted in the form of PM or condense to form particles in the atmosphere. These
include POM, chromium, mercury, and other metals. In addition, lead is a criteria pollutant and
lead compounds are listed as a HAP, so reducing lead emissions through the lead NAAQS also
reduces HAP.
With regard to mobile sources, in addition to authority under section 202(1) to address
hazardous air toxics, other sections of title n that address mobile sources, including other parts of
section 202 (motor vehicles), section 211 (fuel requirements), section 213 (emission standards
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for nonroad engines and vehicles), and section 219 (urban bus standards), are resulting in
reductions in urban air toxics by limiting VOCs, oxides of nitrogen, and PM.
We've established section 129 performance standards for two source categories for
combustion sources. These are expected to result in over 50,000 tons per year in HAP
reductions, much of which may be in urban areas. Finally, Title IV, The Acid Rain Program, and
Title VI, Stratospheric Ozone Protection, also reduce or eliminate urban air toxics emissions.
4.6.3 Other Authorities, Laws, Rules, and Programs to Help Reduce HAP
Emissions
There are a number of other authorities, laws, rules, and programs that will help reduce
emissions of HAP and consequent exposures and risks. Some of these are discussed below.
We're currently evaluating the appropriateness of these statutes for controlling emissions of HAP
as described under section 112(k)(3) and intend to take further actions under these statutes as
appropriate.
As discussed previously, the Strategy involves collaboration between offices within the
air program to assess the risks from exposures to air toxics indoors and to assimilate non-
regulatory, voluntary programs developed to address those risks. Title IV of the Superfund
Amendments and Reauthorization Act.(SARA) provides EPA with the authority to perform
research and provide information to the public on the health problems associated with air
pollutants in the indoor environment.
Under the Toxic Substances Control Act (TSCA), chemicals produced or imported into
the United States are evaluated as to toxicity to human health and the environment. To prevent
adverse consequences of the many chemicals developed each year, TSCA requires that any
chemical that will reach the consumer marketplace be tested for possible toxic effects prior to
commercial manufacture. Any existing chemical that is determined to pose health and
environmental hazards is tracked and reported under TSCA. Procedures are also authorized for
corrective action under TSCA in cases of cleanup of toxic materials contamination. The TSCA
is a complementary authority to the CAA and has contributed to decreased emissions of several
HAP. For example, concern over the toxicity and persistence in the environment of PCB
compounds led Congress to include, in TSCA, prohibitions on the manufacture, processing, and
distribution in commerce of PCBs (TSCA section 6(e), 15 U.S.C. 2605(e)). In 1990, TSCA
authority was relied upon to eliminate chromium use in, and emissions from, comfort cooling
towers (i.e., industrial process cooling towers used exclusively for cooling, heating, ventilation,
and air conditioning systems).
There are several provisions of the Resource Conservation and Recovery Act (RCRA)
and its amendments which may yield reductions of urban air toxics. One impact evidenced in the
1990's was increased recycling and recovery of hazardous waste, including solvents which
through volatilization contribute to HAP emissions. Section 3004(n) of RCRA has been the
basis of a three-phased regulatory program to control air emissions from hazardous waste
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treatment, storage and disposal facilities. The third phase would address any risks remaining
after implementation of the control regulations issued in 1990 and 1994, which were estimated to
reduce organic emissions by more than one million tons per year. Any resulting reductions in
emissions and risk can be considered in assessing progress toward the 75 percent reduction in
cancer incidence from the baseline.
Under the Comprehensive Environmental Response, Compensation and Liability Act
(CERCLA), commonly known as Superfund, the clean-up of abandoned hazardous waste sites
may also reduce emissions of HAP. Where significant health risks from chemical releases to the
air have been identified at Superfund sites in urban areas, clean-up will reduce risks from urban
air toxics.
Under the Clean Water Act (CWA), controls on the discharge of pollutants to surface
water can also reduce the amount of HAP entering the environment. These controls may take the
form of national technology-based standards under the effluent guidelines program or site-
specific water quality-based controls to achieve State water quality standards, hi addition to
providing control by establishing discharge limitations on pollutants (including HAP) in the
wastewater, process changes made in order to comply with these limitations may also reduce
fugitive emission sources.
As part of the effluent guidelines program under the CWA, we've issued effluent
limitations for the Pharmaceuticals industry. Human health benefits from these guidelines
include reductions in excess cancer risk through inhalation. The regulatory impact assessment
prepared for these guidelines estimates that the number of excess cancer cases avoided per year
nationwide ranges from 0.02 to 0.35. These reductions are due to reductions in VOC emissions,
including 10 carcinogens (principally chloroform and methylene chloride). We can also point to
air toxics benefits from the effluent guidelines for the pulp, paper, and particle board industry.
These guidelines, coupled with the associated NESHAP, are expected to decrease background
emission of HAP by 139,000 megagrams (152,900 tons) annually".
If a water body isn't meeting water quality standards even after all technology-based
controls under the effluent guidelines program are in place, the State, local agency, or Tribe must
list the water as "water quality limited" and prepare a total maximum daily load (TMDL)
calculation that allocates the maximum amount of pollution, with a margin of safety, that the
water body can absorb from point and nonpoint (including air deposited) sources. A plan must
then be developed to implement the TMDL, which might include provisions to address air
sources under Federal or State (or local or Tribal) programs. We're conducting a pilot project in
two waterbodies to study models which can be used to identify the relative contributions of air
pollutants deposited from various air pollution sources. This project will also examine how
1 !63 FR 18504. National Emission Standards for Hazardous Air Pollutants for Source Category: Pulp and
Paper Production; Effluent Limitations Guidelines, Pretreatment Standards, and New Source Performance
Standards: Pulp, Paper, and Paperboard Category. April 15, 1998.
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Federal and State water programs can work together to reduce contamination of water due to air
deposition.
The Federal Insecticide, Fungicide and Rodenticide Act (FIFRA) provides Federal
control of pesticide distribution, sale, and use. Several HAP listed in CAA section 112(b) have
been used as pesticides. An EPA registration is required of all pesticides sold in the United
States and is intended to ensure that pesticide use, when in accordance with label specifications,
doesn't cause unreasonable harm to people or the environment. It's a violation of FIFRA to use a
pesticide in a manner inconsistent with its label. Registered pesticides classified as "restricted
use" may only be used by registered applicators who have passed a certification exam. This
restricted use requirement minimizes the number of persons having access to certain pesticides.
The FIFRA regulations may also reduce emissions and exposures by banning (canceling or
denying registration) or severely restricting pesticide use. Seven individual HAP and members
of three HAP compound groups have been banned or severely restricted in their use as pesticides.
Two other Federal laws discussed earlier in Chapter 2 of this Report, EPCRA and PPA,
while not directly regulating air emissions of HAP, may influence decisions regarding chemical
usage and storage and yield significant reductions in air toxics risks in urban areas. The goal of
EPCRA is to reduce risks to communities through informing communities and citizens of
chemical hazards in their areas. Sections 311 and 312 of EPCRA require certain facilities to
report the locations and quantities of chemicals stored at their facilities to State and local
governments. This information is used by State and local agencies in preparing for, and
responding to, chemical spills and similar emergencies.
Through EPCRA, Congress mandated that TRIs be made public. The TRI provides
citizens with information about potentially hazardous chemicals stored, manufactured and used
in their community. Section 313 of EPCRA specifically requires certain manufacturers and all
Federal facilities to report to EPA and State governments all releases of any of more than 600
designated toxic chemicals to the environment (including most of the 188 HAP). Each year,
more than 20,000 manufacturing facilities and 200 Federal facilities submit information to us on
the releases of chemicals to the environment. We compile these data in an on-line, publicly
accessible national database, which is a significant source of information regarding HAP
emissions. Reporting requirements for TRI became more comprehensive in 1991, highlighting
the importance of pollution prevention. In 1997, we added seven industry groups (i.e., metal
mining, coal mining, RCRA subtitle C treatment, storage, and disposal (TSD) and solvent
recovery, petroleum distribution, electricity generating, and chemical distribution). We believe
that for the manufacturing sector, this public spotlight on releases and other waste management
of toxic chemicals has led to reductions in their environmental release.
The passage of the PPA established an environmental hierarchy that establishes pollution
prevention as the first choice among waste management practices. Traditionally, much
environmental protection has involved controlling, treating or cleaning up pollution. Pollution
prevention, which eliminates or minimizes pollution at the source, is most effective in reducing
health and environmental risks because it: (1) eliminates any pollutant associated risks; (2)
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avoids shifts of pollutants from one medium (air, water or land) to another, which can result from
certain waste treatments; and (3) reduces the waste of natural resources. For waste that cannot be
avoided at the source, recycling is considered the next best option. A waste generator should turn
to treatment or disposal only after source reduction and recycling have been considered.
Pollution prevention strategies include redesigning products, changing processes, substituting
raw materials for less toxic substances, increasing efficiency in the use of raw materials, energy,
water, land, and other techniques. The EPA implements the PPA by promoting voluntary
pollution reduction programs, engaging in partnerships, providing technical assistance, funding
demonstration projects and incorporating cost-effective pollution prevention alternatives into
regulations and other initiatives.
In addition, we've developed the "Waste Minimization National Plan," a voluntary, long
term effort to reduce the quantity and toxicity of hazardous waste through waste minimization.
The plan was built on extensive stakeholder involvement and was released in 1994. The plan
focused on the following key objectives:
Prioritize pollution prevention efforts based on risk;
Promote source reduction over recycling;
Adopt a multimedia approach and prevent cross media transfers;
Provide flexibility in implementing pollution prevention activities;
Provide accountability and measure progress; and
Involve the public.
The plan calls for a 50 percent reduction in the presence of the most harmful persistent,
bioaccumulative, and toxic (PBT) chemicals in hazardous waste by 2005.
The starting point for selecting chemicals for the national waste minimization list is
EPA's Waste Minimization Prioritization Tool (WMPT), which is a software program that
provides a screening-level assessment of the potential chronic risks that chemicals pose to human
health and the environment based on their persistence, bioaccumulative potential, and human and
ecological toxicity. This software program contains full or partial PBT data for approximately
4,200 chemicals. The draft WMPT was released for public comment on June 23,1997 (U.S.
EPA, 1997). We made significant changes in response to public comment and published a
revised version on November 9,1998 (U.S. EPA, 1998i). The revised software, in conjunction
with a publicly reviewed methodology, was used to generate a draft list of 53 PBT chemicals,
which is now in the process of being finalized.
4.7 State, Local, and Tribal Activities
This section describes the role of State, local and Tribal authorities in developing and
implementing the Strategy.
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4.7.1 Why are State, Local, and Tribal Programs Integral to the Strategy?
The CAA requires that the Strategy achieve the risk reduction goals considering control
of emissions of HAP from all stationary sources, using measures implemented by EPA under the
CAA, or by the States under the CAA, or other laws. By providing for State reductions in
achieving the goals, Congress acknowledged that there are many State programs achieving HAP
emissions reductions and, therefore, reducing the chances for exposure and health risks,
including cancer. For example, before the CAA was amended in 1990, many State, local and
Tribal governments developed their own programs for the control of air toxics from stationary
sources. Some of these programs have now been in place for many years and, for some of the
source categories, they may have succeeded in reducing air toxics emissions to levels at or below
those required by the Federal standards. It's clear that Congress intended State and local
governments to be important partners in carrying out the mandates of the Federal air toxics
program, and the Strategy provides a mechanism to recognize the reductions made by them.
Because of the varied nature of the emissions sources, legislative structures, and other
factors, the State, local and Tribal government programs address air toxics in a number of ways.
For example, some programs have enacted technology standards for source categories that
require controls for specific HAP, much like the MACT program. Other programs apply a risk
standard that prohibits emissions that result in exceedances of a certain level of risk, or they use
an ambient air standard for air toxics that is based on threshold or exposure levels. Still others
may rely on reductions achieved through VOC, PM, or lead regulations developed under section
110 or subpart D of the CAA to meet NAAQS. Regardless of the approaches used to address air
toxics, State, local and Tribal governments have accomplished and continue to accomplish
reductions in HAP. As we proceed to implement the Strategy, we'll work with these
governments to better characterize these reductions in emissions and the resulting reductions of
public health risks, including risks of cancer.
Developing the Strategy at the national level is a challenge because urban air toxics
problems vary significantly across the country. Because of this variability, the Strategy works
best if approached as a partnership between EPA and State, local and Tribal governments. These
governments (including municipal offices other than pollution control departments) have the
most experience with local air pollution issues and can lend their expertise and knowledge to
address and resolve air toxics concerns that are unique to cities. Many of these governments also
have existing air pollution control programs that currently address, and can effectively continue
to address, some or all of these issues. In addition, these governments are often able to act much
more quickly than we can to address local concerns, which leads to less overall pollution.
At the Federal level, we can contribute Federal standards and requirements using our
authorities to develop and implement a national regulatory program. We also have the expertise
to evaluate, or to help other agencies evaluate, toxic pollution problems. By integrating our
relative strengths, we can provide a stronger, more efficient, and more effective program to
address air pollution in urban areas.
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4.7.2 What are the Objectives of State, Local, and Tribal Activities?
As indicated before, the Strategy will be a partnership between EPA and State, local and
Tribal governments to address the risks from air toxics in urban areas. Listed below are the
objectives that we've identified to guide the CAA taken by us and our governmental partners so
that those actions will be effective and efficient in achieving the goals of the Strategy:
Establish appropriate national measures, through guidance, policies and
rulemaking, which enable State, local and Tribal agencies to be full partners. Many
of the State, local and Tribal agencies may be unable to do more than the Federal laws
and rules require. These agencies could benefit from Federal rulemaking guidance in
addressing local issues. As the same time, we recognize the need for flexibility for these
agencies to identify and address the local issues. We need State, local and Tribal
agencies' help to reach the CAA's goals for healthy air, and they'll benefit by being able
to tailor the Strategy to their specific needs.
Provide flexibility for strong State, local and Tribal programs. Many of these
governments have developed their own air programs. In fact, during the development of
the Strategy, we received many comments requesting that the Strategy acknowledge
programs that are already in place. Those governments that have been proactive in
controlling air toxics can benefit by tailoring the Strategy to their own needs, or by being
able to implement a program earlier than we can.
Provide incentives for State, local and Tribal action. Since enabling through
standards, policies and guidance and providing flexibility can result in more effective and
earlier controls of urban HAP, it will be beneficial to State, local, and Tribal
governments, to EPA, and to the public to facilitate State, local and Tribal actions.
Set priorities among urban areas and source categories. Given the broad scope of the
Strategy and the time it may take to implement, it may be most effective to first identify
and address those areas and sources with the highest air toxics emissions or exposure
levels (including consideration of multipathway exposure where appropriate).
Provide information to the public on HAP and potential risk in urban areas. The
public benefits by having a sound basis to use in setting their pollution control priorities
and communicating their priorities to us. Providing information to the public is also our
responsibility, and an informed public will be better equipped to help us set priorities for
appropriate State, local and Tribal HAP control actions. This public outreach will include
not only information on exposure to air toxics, but also information on the link between
water quality and the deposition of air toxics.
Facilitate a focus on areas with disproportionate impacts and greatest risks. The
Strategy is intended to recognize the potential for disproportionate impacts of air toxics
hazards across urban areas. State, local and Tribal governments can be particularly
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effective in identifying and addressing disproportionate impacts of HAP. We'll work
with our regulatory partners to provide technical and policy guidance to help identify and
address disproportionate impacts from HAP, including consideration of multipathway
exposure as appropriate.
4.7.3 ~ How Can State, Local or Tribal Agencies Participate in the Strategy?
The Strategy needs to be a partnership between EPA and State, local and Tribal agencies
in order to focus on local urban air toxics concerns. But our relative roles may vary according to
the needs of particular urban areas and any limitations faced by State, local and Tribal
governments. With our regulatory partners, we'll discuss and explore options for how the State,
local and Tribal agencies should participate in developing and implementing the Strategy to
address public and other environmental issues related to air toxics.
We see a broad range of possibilities for State, local and Tribal agency participation. For
example, as indicated above, many regulatory agency programs are designed to implement
delegated Federal requirements. However, to provide additional flexibility, we may be able to
provide a Federal program that allows the agencies to either develop and substitute their own
requirements for an existing Federal program, or, if they wish, to simply adopt and implement a
risk reduction program designed by EPA. For example, we could promulgate a Federal rule
describing how we'd develop and implement a local risk reduction program. State, local or
Tribal agencies could then either develop and implement a program modeled on ours, or submit
an alternative program for our approval.
Alternatively, instead of promulgating a Federal rule setting out the details of an
acceptable risk reduction program, we could promulgate a set of minimum elements that any
local risk reduction program - whether implemented by EPA or a State, local or Tribal agency -
must contain. This would provide agencies with more flexibility to design and implement their
own risk reduction programs that we could approve.
The Federal role in developing additional risk reduction strategies for urban areas could
be smaller still. It may not be necessary for us to directly guide development of State, local and
Tribal programs. It may be enough for us to encourage them to meet the goals of the Strategy
and to provide necessary guidance. In the end, we (or the State, local or Tribal agency) would
still need to measure progress against the mandatory goals of the CAA. We might then need to
determine whether additional Federal action is warranted to meet the goals.
In evaluating and comparing the options we develop together, we and our regulatory
partners and other stakeholders will need to consider how well each option addresses our
objectives. We'll also need to consider such other issues as practicality of implementation,
resource burden at each governmental level, and possible adverse impacts on other Federal, State,
local or Tribal programs.
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4.7 A What Elements Should a State, Local or Tribal Program Contain?
No matter who develops and implements State, local or Tribal programs, they should
contain certain basic elements in order to meet the risk reduction goals of the Strategy. The
following list of elements should be considered:
Locally-focused assessments using existing information and sufficiently refined tools
capable of identifying significant contributors to urban risk, problem chemicals and
sources, and toxic "hot spots" within an urban area, and characteristics of at-risk
populations;
A process, regulatory or otherwise, to develop strategies aimed at reducing risks from
those sources;
Opportunity for public review of both the baseline assessment and the proposed risk
reduction strategies;
A process and schedule for implementing the risk reduction strategies;
Evaluation of whether the goals of the Strategy have been met;
Provisions to implement additional risk reduction strategies if the goals have not been
met; and
A process to encourage public participation.
At this point, this list is fairly general because we don't have enough information to more
fully develop this program structure. However, over the next couple of years, we'll be working
to further develop this aspect of the Strategy, to develop and use information from assessments
and other tools to guide our thinking, and to get input from our stakeholders. Also, we've started
to develop the framework for a number of pilot projects in several urban areas. These pilot
projects will help us initiate and facilitate a broad partnership effort to get a better understanding
of the local urban health risks from air toxics and to identify actions that can be taken to improve
local air quality.
4.8 References
Ball, J. C. 1997. Emission rates and elemental composition of particles collection from 1995
ford vehicles using the urban dynamometer driving schedule, the highway fuel economy
test, and the US06 driving cycle. SAE Paper 97FL-376.
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Gertler, A.W., Sagebiel, J.C., Dippel, W.A., and L.H. Sheetz. 1997. A study to quantify on-road
emissions of dioxins and furans from mobile sources: phase 2. Prepared by the Health
and Environmental Sciences Department, Energy and Environmental Engineering Center,
Desert Research Institute, Reno, NV. Prepared for the American Petroleum Institute
(API). API Publication Number 4642.
Truex, T.J., Norbeck, J.M., Smith, M.R., Arey, J., Kado, N., Okamoto, B., Kiefer, K., Kuzmicky,
P., and I. Holcomb. 1998. Final report: evaluation of factors that affect diesel exhaust
toxicity. Prepared by the Center for Environmental Research and Technology and the
Statewide Air Pollution Research Center, University of California, Riverside, CA, and the
Department of Environmental Toxicology, University of California, Davis, CA. Prepared
for the California Air Resources Board, Contract No. 94-312. June 25.
U.S. EPA. 1985. Interim quantitative cancer unit risk estimates due to inhalation of benzene.
Prepared by the Office of Health and Environmental Assessment, Carcinogen Assessment
Group, for the Office of Air Quality Planning and Standards, Washington, DC.
U.S. EPA. 1993. Motor vehicle-related air toxics study. Office of Mobile Sources, Ann Arbor,
MI. EPA/420/R-93/005. April.
U.S. EPA. 1997. Notice of availability of waste minimization software and documents. Federal
Register 62:33868. June 23.
U.S. EPA. 1998a. The inventory of sources of dioxin in the United States. Office of Research
and Development, Washington DC. External Review Draft. EPA/600/P-98/002Aa.
April.
U.S. EPA. 1998b. Control of emissions of air pollution from nonroad diesel engines. Federal
Register 63:56968. October 23.
U.S. EPA. 1998c. Carcinogenic effects of benzene: an update. National Center for
Environmental Assessment, Washington, DC.
U.S. EPA. 1998d. Health risk assessment of 1,3-butadiene. EPA/600/P-98/001A. February.
U.S. EPA. 1998e. Study of hazardous air pollutant emissions from electric utility steam
generating units, final Report to Congress, vol. 1 and 2. EPA/453/R-98/004a (vol. 1) and
EPA/453/R-98/004b (vol. 2). February.
U.S. EPA. 1998f. Notice of availability of draft RCRA waste minimization PBT chemical list.
Federal Register 63:60332. November 9.
U.S. EPA. 1999a. NESHAPS: Final standards for hazardous air pollutants for hazardous waste
combustors; final rule. Federal Register 64:52828. September 30.
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U.S. EPA. 1999b. Integrated Risk Information System (IRIS) at http://www.epa.gov/iris.
Updated March 3.
U.S. EPA. 1999c. Health assessment document for diesel emissions. U.S. EPA Science
Advisory Board Review Draft. Office of Research and Development. Washington, DC.
EPA/600/8-90/057D. November.
U.S. EPA. 1999d. Control of emissions of air pollution from 2004 and later model year
heavy-duty highway engines and vehicles; revision of light-duty truck definition;
proposed rule. Federal Register 64:58471. October 29.
U.S. EPA. 1999e. Regulatory impact analysis, control of air pollution from new motor
vehicles, tier 2 motor vehicle emissions standards and gasoline sulfur control
requirements. Office of Air and Radiation . EPA420-R-99-023.
U.S. EPA. 1999f. Analysis of the impacts of control programs on motor vehicle toxics
emissions and exposure in urban areas and nationwide (volumes I and E). Prepared for
U.S. EPA by Sierra Research, Inc. and Radian International Corporation/Eastern
Research Group. EPA 420-R-99-029 and EPA420-R-99-030. November 30.
U.S. EPA. 1999g . Evaluation of air pollutant emissions from subsonic commercial jet aircraft.
Prepared by ICF Consulting Group, Fairfax, VA. Prepared for U.S. EPA, Office of
Mobile Sources, Engine Programs and Compliance Division, Ann Arbor, MI.
EPA/420/R-99/013. April.
U.S. EPA. 2000a. Clean Air Scientific Advisory Council review of the draft diesel health
assessment document. U.S. EPA Science Advisory Board, Washington DC. EPA-SAB-
CASAC-00-004.
U.S. EPA. 2000b. Tier 2 motor vehicle emission standards and gasoline sulfur control
requirements. Federal Register 65:6698. February 10.
U.S. EPA. 2000c. Proposed heavy-duty engine and vehicle standards and highway diesel fuel
sulfur control requirements. Federal Register 65:35430. June 2.
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5. Assessment of Progress Toward Goals
This discussion of our assessment activities first focuses on how we generally intend to
assess progress in meeting the goals of the Strategy. We then discuss in more detail our methods
and tools for estimating health risks and describe more specifically how we intend to apply these
risk assessment methods and tools to assess progress and support implementation of the Strategy.
As we move from a focus on emissions reductions toward a focus on estimated risk
reduction, we note that Agency risk assessment and decisionmaking have historically focused on
the likelihood of health effects associated with exposure to individual environmental
contaminants. In recent years, our risk assessment emphasis has shifted increasingly to a greater
consideration of multiple pollutants, endpoints, pathways and routes of exposure, and integrated
reduction of risks. This more complex assessment is often called "cumulative risk assessment,"
defined according to who or what is at risk of adverse effects, from identifiable sources and
stressors, through several routes of exposure over varied timeframes. While various integrated
approaches are now being used within the Agency, we realize that there are significant gaps in
methods, models, and data that limit our ability to assess cancer and noncancer risks associated
with cumulative exposure to mixtures of pollutants having different endpoints. We've identified
both short-term and long-term research needs to fill these gaps, as highlighted in Chapter 6 of
this Report. Progress toward more refined assessments of cumulative risks will depend upon the
pace and evolution of our policy and guidance on cumulative risks and the underlying research.
5.1 Overview of Health Risks
Assessing progress in reducing cumulative risks from HAP will require us to move away
from a focus on assessing reductions in tons per year emitted, toward a focus on estimating
reductions in cancer and noncancer risks associated with lower emissions.
"Cancer" describes a group of related diseases that affect a variety of organs and tissues.
Cancer results from a combination of genetic damage and non-genetic factors that favor the
growth of damaged cells. Cancer currently causes approximately one fourth of all deaths in the
U.S. (American Cancer Society, http://www.cancer.org/statistics/index.html). Cancer is
associated with a wide range of factors, of which exposure to HAP is only one. Other causes of
cancer, including genetic susceptibility, background radiation, diet, smoking, and other lifestyle
factors, are thought to be the dominant factors determining total cancer incidence. Against the
very high total cancer mortality rate of about one in four from all risk factors, the rate of cancer
incidence associated with HAP alone cannot be observed directly. Attributing cancer to HAP is
also complicated by the fact that many cancers do not appear for years or decades after exposure
and, therefore, may have been caused by exposures long past and in different locations. In order
to distinguish cancer risks associated with HAP from cancer risks due to other factors, we'll need
to rely on modeled estimates of cancer risk rather than on direct measurements for assessing the
Strategy's progress toward the goal of 75 percent reduction in cancer incidence associated with
HAP.
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Adverse health effects other than cancer ("noncancer risks") include a wide range of
health endpoints in all organ systems (e.g., cardiovascular, immune, liver, or kidney)1. As with
cancer, other factors such as genetics, diet, lifestyle, and other exposures (e.g., smoking) may
exert a dominant influence over incidence of adverse noncancer health effects. Therefore, as
with carcinogens, we expect to rely primarily on risk estimates to assess progress, rather than on
direct measurements of changes hi the incidence of adverse noncancer health impacts due to
reductions in emissions.
The CAA sets a clear numerical goal for reductions in cancer incidence, but specifies
only a "substantial" reduction in public health risks for effects other than cancer. We see a need
to define and clarify this goal more fully as we work to implement this Strategy, but we haven't
yet developed a specific numerical goal for risk reductions for various noncancer effects. One
major purpose of our noncancer risk assessments will be to provide a sound technical basis for
developing and defining noncancer goals that are quantifiable, attainable, and consistent with the
CAA.
5.2 The EPA Risk Assessment Paradigm
Because cancer and noncancer health impacts can't be directly isolated and measured, we
and others have spent more than two decades developing an extensive set of risk assessment
methods, tools, and data that serve the'purpose of estimating health risks for many of our
programs. Our risk assessment science has been extensively peer-reviewed, is widely used and
understood by the scientific community, and continues to expand and evolve as scientific
knowledge advances. We intend to use the most current and appropriate risk estimation methods
in tracking progress under the Strategy.
Our framework for assessing and managing risks reflects the risk assessment and risk
management paradigm set forth by the National Academy of Sciences in 1983, shown in diagram
form in Exhibit 5-1. The inner circle of the figure divides the risk assessment and management
process into four general phases. The first three phases (exposure assessment, dose-response
assessment, and risk characterization) comprise risk assessment. The fourth phase (risk
management, shown shaded) involves evaluation of information provided by the risk assessment
by the environmental manager who makes a risk management decision. The outer circle of the
figure depicts a cycle of specific milestones or information produced during each phase of the
process. This figure is intended to present a generalized model of our framework, but readers
should realize that the framework is always applied in a flexible way to fit unique factors of
specific environmental problems.
'Some HAP that cause cancer may also cause adverse noncancer health effects at environmentally relevant
doses. Thus, when we discuss "noncarcinogens," we mean substances that may potentially cause noncancer effects in
humans. Some of the same substances may also be evaluated as carcinogens.
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EXHIBIT 5-1
EPA PARADIGM FOR RISK ASSESSMENT AND RISK MANAGEMENT
Fate
(All Media)
Personal Exposure
(Inhalation,
Non-inhalation)
Estimated Risks
and Uncertainties
5.2.1 Exposure Assessment
Our 1992 guidelines for exposure assessment (U.S. EPA, 1992) establish a broad
framework for exposure assessments by describing the general concepts of exposure assessment,
including definitions and associated measurement units, and by providing broad guidance on the
planning and conduct of an exposure assessment. The guidelines also provide information on
presenting the results of the exposure assessment and characterizing uncertainty. Although the
guidelines focus on exposure of humans to chemical substances, much of the guidance also
pertains to assessing ecological exposure to chemicals, or to human exposures to biological,
radiological, or other agents.
The guidelines define human exposure as contact with a chemical or agent at the visible
external boundary of a person, including skin and openings into the body such as mouth and
nostrils (but not necessarily contact with exchange boundaries where absorption may take place,
such as skin, lung, and gastrointestinal tract). Therefore, an exposure assessment is the
quantitative or qualitative evaluation of contact and includes such characteristics as intensity,
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frequency, and duration of contact. Often, an assessment will also evaluate the rate and route at
which a chemical crosses the external boundary (dose) and the amount absorbed (internal dose).
The numerical output of an exposure assessment may be either exposure or dose, depending on
the purpose of the evaluation and available data.
An exposure assessment has three major components: source characterization,
environmental fate and transport characterization, and characterization of personal exposure.
These components are discussed individually below.
Source Characterization
hi the first step of exposure assessment for air toxics, the specific HAP emitted and the
sources of their airborne emissions are determined. Data are collected on the emission rates of
the pollutants and parameters of the sources. Knowledge of the emission rate and release
characteristics enables the pollutant fate and transport to be estimated.
Ideally, the emission estimates are from direct measurements of source emissions.
Although direct measurement is likely to provide the most accurate data for an emission source,
these data are typically not available, as such sampling is often time- and resource-intensive.
When specific emission measurements are not feasible or available, other emission estimation
methods, including material balances and emission factors, are sometimes used as alternate
methods. Emission factors indicate the quantity of a pollutant typically released to the
atmosphere for a particular source operation and are usually considered to be representative of an
industry or emission type as a whole. Each approach to estimating emissions, including use of
direct measurement data, has an inherent level of uncertainty, which adds to the overall
uncertainty of a risk analysis.
Depending on the analysis, source and emissions data can be derived from broad-scale
emission inventories, specific data collection efforts with particular industries, or information
from Regional, State, or local air toxics agencies. Other information, such as the geographic
location of release points, the temporal pattern of emissions (e.g., periodic "puffs" vs. constant
emission rates), and the release height may be necessary depending on the level of detail needed
or types of exposure examined in the assessment.
Environmental Fate and Transport Characterization
After the pollutants of interest and their sources and emission rates are defined, the
exposure assessment process continues with estimation of pollutant fate and transport. This step
describes how the pollutant is transported, dispersed, and transformed over the area of interest.
Initially, the fate of the emitted pollutants is largely determined by the source release
characteristics. After pollutants are released to the atmosphere, their transport, dispersion, and
transformation are governed by meteorological principles, terrain characteristics, wet and dry
deposition rates, and certain chemical properties of the HAP (e.g., aqueous solubility, vapor
pressure, molecular diffusivity, melting point, and adsorptivity). For a limited subset of HAP, it
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is important to consider deposition from air to soil, vegetation, or waterbodies. For others, such
deposition is not important.
A variety of mathematical models, each with specific data needs, has been developed or
are under development to describe the transport and fate of pollutants released to the atmosphere.
The model chosen must be appropriate for the intended application and may vary among
estimates of short-term peak concentrations immediately adjacent to a facility, long-term
concentrations over a city-wide area, or deposition over hundreds or even thousands of miles.
The HAP's reactivity and persistence will influence its fate as well and can be important factors
in estimating exposure for certain pollutants. Additionally, secondary transformation products of
some HAP may need to be identified for consideration in risk assessment. High quality,
representative meteorological information is crucial to a valid exposure assessment for air toxics,
as well as information on local topography. Any available HAP monitoring data can be used
either to check the validity of modeled concentration estimates or as a primary or supplemental
source of information for the exposure assessment itself.
For a limited subset of HAP, greater human and ecological exposures to the HAP occur
through non-inhalation exposures than through inhalation exposures. These HAP typically are
persistent in the environment, have a strong tendency to bioaccumulate, and exhibit moderate to
high toxicity. Exposure assessments can consider exposures that occur through routes other than
inhalation by using multipathway models. The simplest multipathway exposure assessments
require chemical-specific data (e.g., octanol-water partition coefficient (K^)) to model the
partitioning of the chemical in the environment and uptake rates (e.g., 2 liters water/day) to
predict intakes. Combining this information yields general predictions of non-inhalation
exposure.
Characterization of Personal Exposure
After ambient concentrations have been derived, human exposures to these
concentrations are determined, hi this component, the study population is defined in terms of
geographic distribution and other characteristics relevant to the exposure pathways of concern.
For the more frequently performed human inhalation exposure analyses, the locations of
resources, homes, workplaces, schools, and other receptor points will partially determine the
extent of actual exposure. Factors such as age, sex, and activity patterns affect the amount of
pollutant actually inhaled by an individual, while mobility of the subject affects the concentration
levels to which an individual is exposed over time. Depending on the focus of the analysis, 5 to
10 percent output of the exposure assessment may vary, hi some cases, the most highly exposed
five to ten percent of the population may need to be well-characterized, while for others, the
distribution of exposures across a wider area is needed. Information on specific sensitive
populations, such as children or the elderly, is another layer of detail that may often be needed in
refined analyses.
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As with inhalation, assessing non-inhalation exposure to human populations involves
combining pollutant concentration information with relevant information concerning the study
population. After identification of the relevant exposure pathways, information such as soil,
drinking water, and food ingestion rates (often including specific foods, such as fish, beef, pork,
eggs, root vegetables, grains, and fruit), generally for both adults and children, as well as contact
frequencies with soil and surface water, may be needed. Some activities of particular interest for
non-inhalation modeling are subsistence farming and subsistence fishing because of the unique
dietary habits of these two groups (i.e., eating much more garden vegetables and fish,
respectively). Also, as with inhalation exposure, the extent to which these factors are included in
the risk assessment depends on the purpose of the assessment, available resources, uncertainties
in the assessment, and data quality and quantity. Not only are the data requirements often
extensive, particularly when many different pathways are being assessed, but the computational
demands also can be quite large in a multimedia, multipathway assessment.
5.2.2 Dose-Response Assessment
The dose-response assessment phase of the risk assessment produces two sequential
analyses (Exhibit 5-1, outer circle). The first analysis is the hazard identification, which
identifies contaminants that may pose health hazards at environmentally relevant concentrations
and qualitatively describes the effects that may occur in humans. The second analysis is the
human health dose-response, which generally describes the relationship between exposure
received and likelihood of effects in quantitative terms.
Hazard Identification
The dose-response assessment phase begins with hazard identification, in which we
identify contaminants that are suspected to pose health hazards, describe the specific forms of
toxicity (neurotoxicity, carcinogenicity, etc.) that they may cause, and evaluate the conditions
under which these forms of toxicity might be expressed in exposed humans. The types of effects
that are relevant to a particular chemical (e.g., cancer, noncancer) are determined as part of the
hazard identification. The current approaches for dose-response assessment and risk
characterization can differ for various types of effect. Factors such as the route of exposure, the
type and quality of the effects, the biological plausibility of findings, the consistency of findings
across studies, and the potential for bioaccumulation all contribute to the strength of the hazard
identification statement.
There are many sources of information that can be brought to bear in the hazard
identification. Exhibit 5-2 summarizes important sources of information for hazard
identification.
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EXHIBIT 5-2
SOURCES OF INFORMATION FOR HAZARD IDENTIFICATION
Epidemiologic Data. Epidemiologic studies of human populations exposed to HAP in occupational
settings otin the general environment can provide valuable information on the effects of HAP. These
studies have advantages over other sources of information in that they directly assess the effects of
exposure to humans and, in the case of studies of the general population, address exposures that
actually occur in the environment. In addition, recent work with biomarkers (chemicals in the body
which allow for better quantification of exposure) promises to boost the utility of epidemiology in the
future. Shortcomings include concerns about the relevance of high exposure levels often seen in
occupational studies to lower levels of environmental contamination, concerns over the control of
confounding variables (such as tobacco use) that may obscure true causal relationships (or imply false
ones), difficulties in adequately characterizing exposure, and the difficulty most epidemiologic studies
have in discerning subtle effects.
Human Data from Case Reports or Controlled Exposure Studies. Where available, human health
effects data from case reports or controlled exposure studies can be extremely valuable, although such
data generally have shortcomings. Case reports often involve one or a small number of people,
limiting the ability to generalize from them, and they may involve exposures very different than
typical environmental exposures. For most HAP and effect types of interest, controlled human
exposure studies are unlikely to be available.
Animal Toxicology Data. High quality studies of human populations exposed to HAP are rare, due
to both expense and the inherent limitations of epidemiology. As a result, EPA and others commonly
rely on animal studies to infer potential risk to humans. Animal toxicologic data are typically much
easier to obtain than good epidemiologic data, and effects can be explicitly linked with exposure to
the HAP(s) being tested with little fear of confounding. However, issues of high-to-low dose
relevance are compounded by the need to extrapolate the effects seen in animals to those anticipated
in humans. Although there have been considerable advances in understanding the relevance of
specific results in animal studies to human biology, such extrapolations remain a considerable source
of uncertainty. The EPA has operated under the conservative public health policy that assumes that
adverse effects seen in animal studies indicate potential effects in humans.
Short-term in Vitro Assays. In vitro ("test tube") tests can be carried out quickly and at relatively
low cost, and they can provide valuable information on specific aspects of a pollutant's toxicity, such
as a particular mechanism of mutagenicity that may be an initiating event for cancer. However, such
tests typically provide only supporting information about a pollutant's effects, as few tests have been
developed that are specific to a particular effect or disease.
Structure-activity Relationships (SARs). By comparing the molecular structure of a pollutant with
that of others of known toxicity, toxic effects can sometimes be inferred, particularly if there is
knowledge about the mechanism of action. This approach is often useful when examining the hazards
associated with individual compounds within a class of related compounds (e.g., dioxins) or when
identifying compounds for future study. Although structure-activity analyses are rarely a substitute
for existing experimental or epidemiologic data, and represent a relatively uncertain basis for hazard
identification, they are useful when experimental data are absent.
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Noncancer Effects - Chronic and Acute. Due to the wide variety of endpoints, hazard
identification procedures for noncancer effects are less formally described in EPA guidance than
are procedures for the identification of carcinogens. The EPA has published guidelines for
assessing several specific types of noncancer effects, including mutagenicity (U.S. EPA, 1986a);
developmental toxicity (U.S. EPA, 1991); neurotoxicity (U.S. EPA, 1998a); and reproductive
toxicity (U.S. EPA, 1996a).
For identification of long-term (chronic) hazards other than cancer, we review the health
effects literature and characterize its strengths and weaknesses, using a narrative approach rather
than a formal classification scheme. Available data on different endpoints are arrayed and
discussed, and the effects (and their attendant dose/exposure levels) are described. Particular
attention is given to effects that occur at relatively low doses or that may have particular
relevance to human populations. Information is presented in a narrative description that
discusses factors such as the methodological strengths and weaknesses of individual studies (as
well as the overall database), the length of time over which the studies were conducted, routes of
exposure, and possible biological mechanisms. We consider the severity of effects, which may
range from severe frank effects that can cause incapacitation or death to subtle effects that may
occur at the cellular level but are early indicators of toxic effects. Not all effects observed in
laboratory studies are judged to be adverse. The distinction between adverse and non-adverse
effects is not always clear-cut, and considerable professional judgment is required in applying
criteria to identify adverse effects. All of these observations are integrated into a presentation
that gives a concise profile of the lexicological properties of the pollutant.
hi addition to toxicity related to chronic exposures, many HAP also can cause toxic
effects after acute (short-term) exposures lasting from minutes to several hours. Indeed, for some
pollutants, acute exposures are of greater concern than chronic exposures. The hazard
identification step for acute effects is comparable to that for chronic effects, with the primary
difference being the duration of exposure. As with chronic exposures, the severity of effects
from acute exposures may vary widely. While several EPA offices have addressed acute
exposures across a variety of regulatory programs, we have only recently drafted Agencywide
guidance on how to assess toxic effects from short-term exposures. This guidance for acute
reference exposure (ARE) levels, when completed, will assist Agency acute risk assessment
activities (U.S. EPA, 1998b).
Cancer. The EPA's 1986 Guidelines for Carcinogen Risk Assessment (U.S. EPA,
1986b) provide guidance on hazard identification for carcinogens. The approach recognizes
three broad categories of data: (1) human data (primarily epidemiological); (2) results of long-
term experimental animal bioassays; and (3) supporting data, including a variety of short-term
tests for genotoxicity and other relevant properties, pharmacokinetic and metabolic studies,
physio-chemical properties, and SARs. hi hazard identification of carcinogens under the 1986
guidelines, the human data, animal data, and "other" evidence are combined to characterize the
weight of evidence regarding the agent's potential as a human carcinogen into one of several
hierarchic categories:
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Group A - Carcinogenic to Humans: Applies when there are adequate human data to
demonstrate the causal association of the agent with human cancer (typically
epidemiologic data).
Group B - Probably Carcinogenic to Humans: Agents with sufficient evidence (i.e.,
indicative of a causal relationship) from animal bioassay data, but either limited (i.e.,
indicative of a possible causal relationship, but not exclusive of alternative explanations)
human evidence (Group Bl), or with little or no human data (Group B2).
Group C - Possibly Carcinogenic to Humans: Agents with limited animal evidence
and little or no human data.
Group D - Not Classifiable as to Human Carcinogenicity: Agents without adequate
data either to suggest or refute the suggestion of the human carcinogenicity.
Group E - Evidence of Noncarcinogenicity for Humans: Agents that show no
evidence for carcinogenicity in at least two adequate animal tests in different species or in
both adequate epidemiologic and animal studies (U.S. EPA, 1986b).
In 1996, we proposed major revisions of the carcinogen hazard identification scheme.
The proposed revision to the cancer risk assessment guidelines (U.S. EPA, 1996b), currently
under public review prior to finalization, focuses on narrative statements describing the main
lines of evidence and their interpretation, replacing the current pre-defined hierarchical categories
with alphabetic designations. The proposed guidelines also replace the system of stepwise
consideration of different types of data with a single comprehensive evaluation process that
stresses the coherence of various data elements. The result is a single scientific interpretation
that evaluates, to the extent possible, how well the commonality of mode of carcinogenic action
between human beings and the various test systems has been established. Emphasis is also
placed on defining the qualitative conditions under which carcinogenic hazards might be
expected. If warranted, limitations to the finding of carcinogenic hazard can be drawn based on
route of exposure, existence of other factors needed for tumorigenesis, and doses below which
elevation of cancer risk is not expected.
Human Health Dose-Response
Human health dose-response assessment is the characterization of the relationship
between the concentration, exposure, or dose of a pollutant and the resultant health effects. The
nature of quantitative dose-response assessment varies among pollutants. Sufficient data often
exist for criteria air pollutants, such as ozone or carbon monoxide, so that relatively complete
dose-response relationships can be characterized. In such cases, there is no need for
extrapolation to lower doses because adequate health effects data are available, often in humans,
at environmental levels. However, such is not the case for most air toxics. Most epidemiologic
and toxicologic data on HAP typically result from exposure levels that are high relative to
environmental levels.
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In summary, dose-response assessment methods for HAP generally consist of two parts.
First is the evaluation of data in the observable range, and second is the extrapolation from the
observable range to low doses/risks. Recent terminology refers to the result of analysis in the
observable range as the "point of departure" from which extrapolation begins. The approaches
used for evaluation in the observable range are similar for all types of effects, while the Agency's
current extrapolation methods differ considerably for cancer and noncancer effects. The 1996
draft cancer guidelines bring a greater degree of consistency to the extrapolations.
Noncancer Effects - Chronic. The inhalation RfC and oral RfD are the primary Agency
consensus quantitative toxicity values for use in noncancer risk assessment. The RfC or RfD is
defined as an estimate, with uncertainty spanning perhaps an order of magnitude, of an inhalation
exposure/oral dose to the human population (including sensitive subgroups) that is likely to be
without appreciable risks of deleterious effects during a lifetime. The RfC or RfD is derived
after a thorough review of the health effects database for an individual chemical and
identification of the most sensitive and relevant endpoint and the principal study(ies)
demonstrating that endpoint. Inhalation RfCs are derived according to the Agency's Methods for
Derivation of Inhalation Reference Concentrations and Application of Inhalation Dosimetry
(U.S. EPA, 1994a). The RfC or RfD should represent a synthesis of the entire data array. The
evaluation of and choice of data on which to base the RfC or RfD derivation are critical aspects
of the assessment and require scientific judgment.
Derivation of the RfC or RfD begins with identification of the critical adverse effect from
the available valid human and animal study data, followed by identification of a lowest-observed-
adverse-effect level (LOAEL) or, preferably, a no-observed-adverse-effect level (NOAEL). The
LOAELs or NOAELs from animal studies are converted to human equivalent concentrations
(HECs) using dosimetric methods (described in U.S. EPA, 1994a). The NOAEL[HEC] or
LOAEL[HEC] from one or a few studies that is representative of the threshold region of
observable effects is the key value gleaned from evaluation of the dose-response data. The RfC
or RfD is then derived by consistent application of uncertainty factors (UFs) to account for
recognized uncertainties in the extrapolation from the experimental data and exposure conditions
to an estimate (the RfC or RfD) appropriate to the assumed human lifetime exposure scenario
(U.S. EPA, 1994a).
The standard UFs are applied as appropriate for the following extrapolations or areas of
uncertainty:
Laboratory animal data to humans;
Average healthy humans to sensitive humans;
Subchronic to chronic exposure duration;
LOAEL to NOAEL; and
Incomplete database.
The composite UF will depend on the number of extrapolations required. The RfCs have
been derived using composite UFs that range from 10 to 3,000, with most RfCs using factors of
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100 to 1,000. The use of order-of-magnitude uncertainty factors for RfCs and RfDs and the
definition of the RfC or RfD as having "uncertainty spanning perhaps an order of magnitude" are
indications of the general lack of precision in the estimates.
It should be noted that exposures above an RfD or RfC do not necessarily imply
unacceptable risk or that adverse health effects are expected. Because of the inherent
conservatism of the RfC/RfD methodology, the significance of exceedances must be evaluated
on a case-by-case basis, considering such factors as the confidence level of the assessment, the
size of UFs used, the slope of the dose-response curve, the magnitude of the exceedance, and the
number or types of people exposed at various levels above the RfD or RfC.
Typically, screening assessments will identify HAP for which exposures may exceed the
RfC or RfD, and therefore have some potential to cause adverse effects. Because risk for
noncarcinogens is dependent on total exposure to a particular pollutant (as opposed to
incremental exposures as for carcinogens), it will be important for assessments to consider all
sources of exposure. These screening assessments may identify for further study sources that
exceed a default percentage (e.g., 20%) of a HAP exposure above an RfD or RfC. Sources that
appear to contribute to RfD or RfC exceedances for HAP at the screening level may be
prioritized for further analysis using more refined and localized assessment methods. In contrast
to screening assessments, refined assessments developed in support of regulatory standards may
include consideration of total uncertainty in the RfC or RfD, evidence of nonadditive interactions
with other HAP, and actual percentage of contribution to total exposures.
The EPA is currently developing a risk management framework for the residual risk
program. This framework is being developed to facilitate decisionmaking to protect public
health with an "ample margin of safety." As part of the ample margin of safety framework, one
must first determine the "acceptability" of risks based on health considerations alone. The
framework will also include guidelines for appropriate consideration of factors other than risk in
regulatory decisionmaking, e.g., cost, economic impacts and feasibility. The framework, which
will be completed in time for the first residual risk standard, will address evaluating the
significance of exposures above the RfC or RfD on a case-by-case basis considering the factors
identified above.
Noncancer Effects - Acute. Methods for dose-response assessment of acute exposures
are substantially similar to the approach for chronic exposure. Risk assessment for acute
inhalation exposure is complicated by the steep concentration-response curves that are often
observed, and because small differences in exposure duration (in some cases, a few minutes)
need to be taken into account. Because increased exposure duration increases the incidence and
severity of response, acute toxicity criteria or exposure guideline values are developed for a
specified duration (e.g., one hour). Although many acute toxicity studies only report incidence of
death, it is preferred to base criteria on studies that evaluate additional endpoints, including
clinical signs, clinical chemistry, and histopathology. For an inhalation criterion, the exposure
duration of the study should ideally be the same as the one of interest (e.g., one hour). If
significant interpolation across exposure durations is required, multiple studies are preferred to
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improve the quality of the interpolation. We are currently developing a new Agency method for
acute dose-response assessment, the resultant value of which is an ARE (U.S. EPA, 1998b).
Cancer. Our cancer risk assessment guidelines of 1986 adopted a default assumption
that chemical.carcinogens would exhibit risks at any dose (U.S. EPA, 1986b). Extrapolation of
cancer risk using the linearized multistage model, which results in a linear extrapolation of risk in
the low dose region, was proposed as a reasonable upper-bound on risk, and this approach has
been used for most chemicals with adequate data since then. However, as stressed in the
Proposed Guidelines for Carcinogen Risk Assessment (U.S. EPA, 1996b), when there are
adequate mechanistic data to suggest that other models would be more appropriate to estimate
low exposure risk, they may be used on a case-by-case basis. In the absence of such data, the
assumption of response linearity is maintained although the modeling scheme has been
simplified.
In cancer dose-response assessments relying on ingestion animal studies for which
chemical-specific data are not available to guide the scaling of results to human equivalents, a
default scaling factor based on the body mass raised to the 3/4 power of the test animals relative
to humans is generally used to calculate a human equivalent dose. For inhalation exposure
studies, dosimetric methods such as those used in developing RfCs are generally used to
calculate a HEC from animal data. Dose-response models such as the multistage model have
historically been used to calculate upper-bound unit risk estimates. Typically, EPA has relied on
the unit risk estimate as a quantitative measure of potential cancer hazard. A unit risk estimate
represents an estimate of the increased cancer risk from a lifetime (assumed 70 year) exposure to
a concentration of one unit of exposure. The unit risk estimate for inhalation exposures is
typically expressed as risk per microgram per cubic meter for air contaminants. The unit risk
estimate is a plausible upper-bound estimate of the risk (i.e., the risk is not likely to be higher but
may be lower and may be zero).
Since the publication of the our original cancer guidelines (U.S. EPA, 1986b),
considerable new knowledge has been developed regarding the processes of chemical
carcinogenesis and the evaluation of human cancer risk. Currently, a revision of the cancer
guidelines is in process (U.S. EPA, 1996b) that represents a considerable departure from the
original guidelines (see Exhibit 5-3 for key differences in the dose-response assessment step
between the two sets of guidelines). As mentioned above, a fundamental and important advance
in the proposed revision is the distinction between linear and nonlinear modes of action. The
cancer data in the observable range are analyzed using a dose-response model similar to the
models used for noncancer effects. The method of extrapolation to lower doses from the point of
departure differs depending on whether the assessment of the available data on the mode of
action of the chemical indicates a linear or nonlinear mode of action.
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EXHIBIT 5-3
SUMMARY OF MAJOR DIFFERENCES BETWEEN
EPA'S 1986 GUIDELINES (U.S. EPA, 1986b) AND 1996 PROPOSED GUIDELINES FOR
CARCINOGEN RISK ASSESSMENT (U.S. EPA, 1996b)
1986 Guidelines
Default model used for linear dose-response
relationships is the "linearized multistage"
procedure.
Dose-response evaluation is limited to
carcinogenicity data.
1996 Proposed Guidelines
Biologically based dose-response models are
used whenever data are sufficient.
Recommended default approaches include the
margin of exposure approach (comparison of
exposure level and point of departure) and
linear extrapolation to zero dose, zero response.
If appropriate, data on noncarcinogens effects
may be used to help characterize the
carcinogenicity dose-response relationship.
A linear extrapolation is generally appropriate when the evidence supports a mode of
action of gene mutation due to direct deoxyribonucleic acid (DNA) reactivity or another mode of
action that is thought to be linear in the low dose region. For linear extrapolation, a straight line
is drawn from the point of departure to the origin, and the risk at any concentration is determined
by interpolation along that line. A linear mode of action also will serve as a default when
available evidence is not sufficient to support a nonlinear extrapolation procedure, even if there
is no evidence for DNA reactivity.
Nonlinear methods are used when there is sufficient evidence to support a nonlinear
mode of action. A nonlinear mode of action could involve a dose-response pattern in which the
response falls much more quickly than linearly with dose, but still indicating risk at low doses.
Alternatively, the mode of action may theoretically have a threshold if, for example, the cancer
response is a secondary effect of toxicity or an induced physiological change which is a threshold
phenomenon. In most cases, we will not try to distinguish between modes of action with a "true
threshold" and those that are nonlinear through the origin, because data are rarely sufficient to
make this determination. As a default science policy, nonlinear extrapolation to low doses will
not be performed because there is no current basis to choose a model or determine the shape of
the dose-response function. However, as more specific information on a HAP's mechanism of
action becomes available and where the data are sufficient to support the use of alternative
models, we will use them.
5.2.3 Risk Characterization
The final product in the risk assessment process is the risk characterization, in which the
information from the previous steps is integrated and an overall conclusion about risk is
synthesized that is complete, informative, and useful for decisionmakers. The nature of the risk
characterization will depend on the information available, the regulatory application of the risk
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information, and the resources (including time) available. In all cases, however, major issues
associated with determining the nature and extent of the risk should be identified and discussed.
Further, the EPA Administrator's March 1995 Policy for Risk Characterization (U.S. EPA,
1995a) specifies that a risk characterization "be prepared in a manner that is clear, transparent,
reasonable, and consistent with other risk characterizations of similar scope prepared across
programs in the Agency." The 1995 Guidance for Risk Characterization (U.S. EPA, 1995b) lists
several guiding principles for defining risk characterization in the context of risk assessment.
The three principles with respect to the information content and uncertainty aspects of risk
characterization are as follows:
(1) The risk characterization integrates the information from the exposure and dose-response
assessments, using a combination of qualitative information, quantitative information,
and information regarding uncertainties. A good characterization should include different
kinds of information from all portions of the foregoing assessment, carefully selected for
reliability and relevance.
(2) The risk characterization includes a discussion of uncertainty and variability. The risk
assessor must distinguish between variability (arising from true heterogeneity) and
uncertainty (resulting from a lack of knowledge).
(3) Well-balanced risk characterizations present risk conclusions and information regarding
the strengths and limitations of the assessment for other risk assessors, EPA
decisionmakers, and the public. "Truth in advertising" is an integral part of the
characterization, discussing all noteworthy limitations while taking care not to become
mired in analyzing factors that are not significant.
The 1995 Guidance for Risk Characterization (U.S. EPA, 1995b) identifies several
guiding principles, shown in Exhibit 5-4, with respect to descriptions of risk.
Risk assessments are intended to address or provide descriptions of risk to: (1)
individuals exposed at average levels and those in the high-end portions of the risk distribution;
(2) the exposed population as a whole; and (3) important subgroups of the population such as
highly susceptible groups or individuals (e.g., children), if known. Because cancer and
noncancer dose-response assessment methods are currently quite different, risk characterizations
also differ and are discussed separately.
Noncancer Effects. Unlike cancer risk characterization, noncancer risks typically are not
expressed as a probability of an individual suffering an adverse effect. Instead, "risk" for
noncancer effects typically is quantified by comparing the exposure to the reference level as a
ratio. The resultant HQ can be expressed as an equation, where HQ equals the exposure/
reference level. Exposures or doses below the reference level (HQ<1) are not likely to be
associated with adverse health effects. With exposures increasingly greater than the reference
level (i.e., HQs increasingly greater than 1), the potential for adverse effects increases. The HQ,
however, should not be interpreted as a probability of adverse effects.
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EXHIBIT 5-4
GUIDING PRINCIPLES WITH RESPECT TO RISK DESCRIPTORS
Information about the distribution of individual exposures is important to
communicating the results of a risk assessment. Both high-end and central tendency
descriptors are used to convey the variability in risk levels experienced throughout the
population.
Information about population exposure leads to another important way to describe
risk. Both a probabilistic number of cases (or environmental impacts) and an expected
percentage of the exposed population (or ecological resource) with risk greater than a certain
level are valuable ways to present information.
Information about the distribution of exposure and risk for different subgroups of the
population are important components of a risk assessment. Highly susceptible
individuals or areas should be identified as well as those highly exposed, when possible.
Situation-specific information adds perspective on possible future events or regulatory
options. Consideration of alternative scenarios when conducting risk assessment can aid in
risk management decisions.
An evaluation of the uncertainty in the risk descriptors is an important component of
the uncertainty discussion in the assessment. Both quantitative and qualitative
evaluations of uncertainty can be useful to users of the assessment.
While some potential environmental hazards may involve significant exposure to only a
single compound, exposure to a mixture of compounds that may produce similar or dissimilar
noncancer health effects is more common. In a few cases, reference levels may be available for a
chemical mixture of concern or for a similar mixture. In such cases, risk characterization can be
conducted on the mixture using the same procedures used for a single compound. However,
noncancer health effects data are usually available only for individual compounds within a
mixture. Li screening-level assessments for such cases, a conservative HI approach, in which all
the HQs for individual contaminants are summed, is sometimes used. This approach is based on
the assumption that even when individual pollutant levels are lower than the corresponding
reference levels, some pollutants may work together such that their potential for harm is additive
and the combined exposure to the group of chemicals poses greater likelihood of harm. This
assumption of dose additivity is most appropriate to compounds that induce the same effect by
similar modes of action (U.S. EPA, 1986c). As with the HQ, the HI should not be interpreted as
a probability of adverse effects, nor as strict delineation of "safe" and "unsafe" levels (U.S. EPA,
1986c; U.S. EPA, 1989). Rather the HI is a rough measure of potential for risk and needs to be
interpreted carefully.
Although the HI approach encompassing all chemicals in a mixture may be appropriate
for a screening-level study (U.S. EPA, 1989), it is important to note that application of the HI
equation to compounds that may produce different effects, or that act by different mechanisms,
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could overestimate the potential for effects. Consequently, in a refined assessment, it is more
appropriate to calculate a separate HI for each noncancer endpoint of concern when only
mechanisms of action are known to be similar (U.S. EPA, 1986c).
Cancer. Risks for cancer are generally expressed as either individual risks or population
risks. The distribution of exposures and individual risks within a given population can also be
presented, providing an estimate of the number of people exposed to various predicted levels of
risk. The Agency's risk characterization guidelines recommend that risk assessments describe
individual risk, population risk, and risk to important subgroups of the population such as highly
exposed or highly susceptible groups (U.S. EPA, 1995b). For air toxics emissions, cancer risks
can be estimated by multiplying the corresponding exposure by the unit risk estimate. Our dose-
response assessments for carcinogens are based on mathematical models and assumptions that
support extrapolation from high to low doses and from nonhuman test species to humans. As a
matter of science policy, many of these assumptions are protective to avoid underestimating
cancer risks where data are incomplete. The most important of these assumptions for most
carcinogenic chemicals is that risk is proportional to dose, with no threshold dose below which
there is no risk. Our dose-response assessments for inhalation of carcinogens are expressed as a
"unit risk," that is, risk per microgram per cubic meter of daily exposure during a lifetime. The
unit risk is defined as a conservative estimate of an individual's excess probability of contracting
cancer at the end of 70 years exposure to a continuous level of one microgram per cubic meter.
Risks from exposures to concentrations other than one microgram per cubic meter are modeled
as proportional, with half the concentration producing half the estimated risk, and so on.
Each word in the above definition of unit risk carries significant meaning. First, the unit
risk is a conservative rather than a "best" estimate. This means that the actual unit risk is
unknown and is very likely to be lower than estimated and very unlikely to be higher. Second, as
already described, risks are estimated rather than measured. Third, the unit risk applies to an
individual, although cancer incidence in a population can be estimated across a group by
aggregating the risk of each person. Fourth, unit risk estimates focus only on the route of
exposure being analyzed. Fifth, unit risks are expressed in terms of probability. For example, we
may determine the unit risk of a particular HAP to be one in ten thousand per microgram per
cubic meter. This means that, often thousand people who continuously inhale an average of one
microgram per cubic meter of this particular HAP for 70 years, no more than one would be
expected to contract cancer from the exposure. Sixth, risks are generally expressed in terms of
contracting cancer, not dying from it. Finally, exposures are averaged over a 70-year lifetime to
account for long-term exposures to low levels of carcinogens.
Cancer risk is defined as the upper-bound probability of contracting cancer following
exposure to a pollutant at the estimated concentration over a 70-year period (assumed human
lifespan). This predicted risk focuses on the additional risk of cancer predicted from the
exposure being analyzed, beyond that due to any other factors. Estimates of risk are usually
expressed as a probability represented in scientific notation as a negative exponent of 10. For
example, an additional risk of contracting cancer of 1 chance in 10,000 (or one additional person
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in 10,000) is written as 1x10"4. Because unit risk estimates are typically upper-bound estimates,
actual risks may be lower than predicted.
Population risk is an aggregated estimate of individual risks, integrated across the entire
population within the given area of analysis. The estimated level of individual risk for each
population group (separated geographically, demographically, or both) is multiplied by the
number of people in that group, producing an estimate of the incidence of cancer cases in the
group during a lifetime of exposure. As with individual risk estimates, EPA has typically
calculated these cancer incidence estimates based on upper-bound unit risk values. Therefore,
they provide a high-end estimate of future cancer risk. The population risk estimates for each
population group are then summed to provide a prediction of excess cancer incidence in the
entire exposed population. These lifetime incidence estimates are sometimes divided by 70 to
obtain an upper-bound prediction of the number of cancer cases per year.
People are often exposed to multiple chemicals rather than a single chemical. In those
few cases where weight of evidence classifications and unit risk estimates are available for the
chemical mixture of concern or for a similar mixture, risk characterization can be conducted on
the mixture using the same procedures used for a single compound. However, cancer dose-
response assessments and unit risk estimates are usually available only for individual compounds
within a mixture. Consequently, in screening-level assessments of carcinogens for which there is
an assumption of a linear dose-response, the cancer risks predicted for individual chemicals may
be added to estimate total risk.
For carcinogens being assessed based on the assumption of nonlinear dose-response, the
margin-of-exposure approach (MOE, analogous to the HQ approach for noncarcinogens) may be
considered, consistent with the proposed revision of EPA's cancer guidelines (U.S. EPA, 1996b).
The MOE approach leaves the decision about the appropriate reduction in exposure compared to
the point of departure (i.e., the observable toxicity data) up to the risk manager.
In the risk characterization step of final assessments, estimates of health risk will be
presented in the context of uncertainties and limitations in the data and methodology.
Uncertainties and limitations related to the hazard identification and dose-response assessment
may also be discussed. The degree to which all types of uncertainty need to be quantified and the
amount of uncertainty that is acceptable varies. For a screening-level analysis, a high degree of
uncertainty is often acceptable, provided that conservative assumptions are used to bias potential
error toward protecting human health. Similarly, a regionwide or nationwide study will be more
uncertain than a site-specific one. In general, the more detailed or accurate the risk
characterization, the more carefully uncertainty needs to be considered.
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5.3 Methods, Tools, and Data to Estimate Risk
5.3.1 Assessing Exposures and Characterizing Risks
In general, the choice of appropriate risk characterization approaches will be influenced
by both the availability of data to support exposure assessment, and the level of detail and
resolution needed to support the purpose of the assessment. Possible approaches range from
simple weighting adjustments of emissions data or ambient concentrations to detailed
multipathway risk assessments. We've identified four basic approaches that we plan to use for
various assessments to evaluate the progress of the Strategy in reducing estimated risk. Each of
these approaches uses the same dose-response information described above, but relies on
different types of data to represent exposures. The four basic approaches we intend to use are:
(1) emissions or ambient concentration weighting, (2) comparisons between ambient
concentrations and RBCs2, (3) comparisons between estimated exposures and RBCs that may
yield quantitative estimates of risk, and (4) quantitative estimates of carcinogenic risk for
individuals and populations.
Approaches (1) and (2) are considered hazard-based approaches because they lack the
dispersion and/or human exposure modeling steps of an exposure assessment and, therefore,
cannot provide quantitative estimates of risk. However, they can provide valuable information,
subject to substantial uncertainty, that may be useful in evaluating progress toward risk reduction
goals. In contrast, approaches (3) and (4) are considered risk-based approaches because they do
incorporate exposure assessments and thereby can provide quantitative risk estimates, although
these too are usually subject to substantial uncertainty. Below, we will compare the differences
in these approaches.
(1) Weighted emissions or ambient concentrations. Weighting of emissions or
ambient concentrations is the least resource-intensive approach of the four in terms of data needs
and computational requirements3. This hazard-based approach combines HAP emissions or
monitored HAP concentrations (acting as surrogates for exposure) with weighting factors
(developed from unit risks and reference concentrations) that account for differences in relative
toxicity among HAP. Other weighting factors could also potentially be developed to account for
differences in dispersion characteristics or variations in population density or behavior.
2RBCs for cancer are ambient concentrations associated with specific levels of cancer risk, assuming 70 years
of continuous exposure. RBCs for noncancer effects are ambient concentrations that pose no appreciable risk to
humans, assuming continuous exposure. The use of RBCs does not imply a judgment that the concentrations are either
acceptable or unacceptable, only that they have been derived in the same way for all HAP.
3Peer-reviewed examples of this approach include the EPA/Office of Pollution Prevention and Toxic
Substances' Risk-Based Environmental Indicators (Science Advisory Board, 1998), the EPA/Office of Solid Waste's
WMPT (U.S. EPA, 1998c), and the EPA/Office of Air Quality Planning and Standards' ranking analysis for urban HAP
(Smith etal., 1999).
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The toxicity adjustment is intended to account for differences in toxic potency among
substances, placing all emissions data on the same scale of hazard potential. For example,
acrylamide is approximately 160 times more potent a carcinogen than benzene, such that
weighting by potency would consider one ton of acrylamide emissions equivalent to 160 tons of
benzene. In a cumulative analysis, emissions or concentrations of each HAP would be weighted
by its relative potency to allow for direct comparison and aggregation across HAP (with
carcinogenic and noncarcinogenic estimates aggregated separately). This type of analysis permits
comparisons of relative hazard between pollutants with large mass emissions and low toxicity
(e.g., many non-chlorinated volatile compounds) against pollutants with small mass emissions
but high toxicity (e.g., dioxin).
As discussed above, the weighted emissions- or concentration-based approach lacks the
last two steps of an exposure assessment, and therefore doesn't provide a quantitative estimate of
risks. Also, because of the absence of these important exposure assessment steps, it isn't
possible to say how closely changes in weighted emissions or concentrations will be related to
changes in health risks. Nevertheless, emissions and ambient concentrations clearly have a
strong influence over exposure and risk, and we anticipate that the toxicity-weighting approach
will provide useful information to estimate progress where appropriate data for more refined
assessment approaches aren't available.
(2) Ratios of ambient concentrations to RBCs. A second type of hazard-based
approach is the comparison of ambient HAP concentrations with RBCs4. Ambient
concentrations may be measured or modeled. Appropriate modeling approaches for estimating
ambient concentrations at different spatial scales using emissions data include national-scale and
urban- to neighborhood-scale air quality models, as well as multimedia models for urban- to
neighborhood-scale analyses.
The RBCs used for comparison are derived from unit risks or reference concentrations.
Specifically, cancer RBCs can be defined in terms of a fixed risk level (e.g., HAP concentrations
conservatively estimated to result in a 1 in 10,000 or a 1 in 1,000,000 upper-bound risk of
contracting cancer from a lifetime exposure at the RBC). Noncancer RBCs can be defined in
terms of estimates of continuous exposure levels at which even sensitive subgroups are likely to
be without any appreciable risk of adverse effects during a lifetime.
Because it is more complex than emissions-weighting, this type of analysis brings two
significant advantages. First, it supports a more complete treatment of ambient HAP
concentrations that are already below noncancer RBCs, for which further reductions may not
carry significant health benefits. Second, the use of dispersion models to predict ambient
concentrations can potentially account for variations in factors such as location of exposed
"Peer-reviewed examples of the use of this approach include the concentration-toxicity screen used by EPA's
Superfund program to select contaminants and exposures for detailed risk assessment (U.S. EPA, 1989) and EPA's
CEP, which compared modeled ambient air concentration estimates with RBCs (termed "health benchmarks" by the
authors) for 148 HAP nationwide (Woodruff et al., 1998).
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populations relative to sources of HAP, differences in meteorological conditions, and differences
in fate and transport characteristics among HAP.
Nevertheless, this approach still lacks the third, human behavior-related step in an
exposure assessment. Therefore, it doesn't provide a quantitative estimate of risk, and its use in
estimating progress is subject to greater uncertainty than approaches (3) and (4), below. Changes
in health risks may not precisely track changes in concentration/RBC ratios. However, because
ambient concentrations are important determinants of exposure and risk, we anticipate that the
concentration/RBC approach will provide useful information to estimate progress where
exposure assessment is not possible.
(3) Ratios of exposures to RBCs. A third type of approach begins with measured or
modeled ambient HAP concentrations and adds further refinement by overlaying estimates or
measurements of population exposures. Thus, this risk-based approach is qualitatively different
from the first two hazard-based approaches, because it incorporates all three steps of an exposure
assessment.
While human exposures are directly affected by ambient concentrations, they're also
influenced by behavioral factors such as time spent outdoors, periodic movements (such as
commuting) within an urban area, and activity levels. Exposures may be estimated with
exposure models that simulate the behavioral factors that determine exposure. Human exposure
may also be directly measured by personal monitoring, in which subjects wear small air samplers
and record their daily activities.
These estimated or measured exposures are then compared to RBCs5 (as described above
for approach (2)). Analogous to the comparisons in approach (2), hazard potential would
typically be presented in terms of ratios of the exposure concentrations divided by RBCs. The
additional complexity of estimating exposure provides three significant advantages over
considering ambient concentrations alone. First, it provides a more realistic comparison with
RBCs, which are based on unit risks and reference concentrations usually derived from doses
actually received by test organisms. Second, exposure estimates can take into account behavioral
differences between populations in different cities, or between different demographic groups.
Third, exposure estimates support combining effects of multiple HAP, considering non-additivity
and similarities or differences in toxic mechanisms. Comparison of exposures with reference
concentrations for noncancer effects (surrogates for RBCs) is currently the most advanced
approach used for assessing noncarcinogenic HAP, although this may change in the future for
some substances.
(4) Risk estimation. A fourth type of approach that can be used to estimate cancer
incidence (but typically not for noncancer assessments) is comprehensive risk estimation,
5Peer-reviewed analyses of this type of analysis include many single-substance risk assessments. Several
examples concern the fuel additives MMT (Davis et al., 1998; U.S. EPA, 1994b) and MTBE (U.S. EPA, 1993).
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focusing on the most exposed individual or on entire populations or subgroups6. We'll derive
risk estimates by combining exposure estimates with dose-response assessment results in terms
of unit cancer risk estimates. Risk estimates will also consider nonstandard dose-response
models and complex interactions among different HAP, if information is available. Such risk
estimates represent the most refined analysis of the four approaches considered. Comprehensive
assessments may contain modeling to account for environmental fate and transport of released
pollutants, estimation of exposures to different subpopulations, detailed dose-response
assessments for each HAP, and information on complex, nonadditive interactions among HAP.
Results are expressed in terms of probabilities of developing cancer during a lifetime. Cancer
risks are usually aggregated across HAP by addition, but nonadditive interactions are included if
data permit.
In its most complete form, risk estimation produces results in probabilistic form (that is,
with calculations considering a range of cancer risks and the likelihood of each), expressed in
terms of a frequency distribution rather than as a single deterministic estimate. Of currently
available approaches, risk estimation, presented probabilistically, provides the most complete,
best-supported, and most accurate presentation of both risk and the variability and uncertainty
surrounding it. However, this risk-based approach is much more resource- and calculation-
intensive than are simpler approaches, and is often not possible to conduct due to data
limitations.
5.3.2 Summary
We anticipate tracking progress in reducing estimated cumulative risks from air toxics in
urban areas by relying on estimates of health risk rather than by directly observing reductions in
adverse health impacts in human populations. We consider these health risk estimates to be
reasonable and appropriate indicators of progress toward meeting the goals of the Strategy. Their
use is made necessary by the long latency period for cancer, the high background rate of many
health effects (including cancer), and complexities involved in attributing various noncancer
health effects to specific environmental causes. Our assessments will use a variety of
approaches, including some that do not include all exposure assessment steps. In some cases the
information may be too uncertain to support conclusions. We intend to evaluate these
approaches against each other, in terms of their ability to estimate risk and their resource and data
requirements, when supporting data become available during 2000. These results will assist us in
determining the scope, refinement, and precision of future assessments developed to reflect
different purposes under the Strategy.
6Examplesof suchmultichemical,multipathwayriskassessments include manyperformedby EPA'sSuperfund
program under the Risk Assessment Guidelines for Superfund (U.S. EPA, 1989).
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5.4 The Overall Risk Assessment Approach for the Strategy
In previous sections, we discussed the key role that assessing air quality, exposure, and
estimated risks will play in assessing progress toward meeting the goals of the Strategy. In
addition, these assessment activities will, over time, also serve the following broader purposes:
Improve the definition of the goal for "substantial" reduction in noncancer risk;
Support development of national area and mobile source standards;
Support decisions on how to conduct future risk assessments;
Evaluate the effectiveness of each of the four approaches to characterizing risk
reductions, described above;
Provide guidance for State, local and Tribal agency efforts in conducting local
assessments and developing risk reduction programs at the State, local, and Tribal levels;
and
Guide us in determining significant research needs to better inform future assessments.
Our assessment approach will be generally iterative in nature so as to take advantage of
emerging science, new data, and improved tools that become available as future assessments are
performed. Consistent with this approach, beginning in mid-2000, we'll conduct an initial set of
assessments that will be based on final, updated emissions data. Future assessments will reflect
the best available data, methods, and tools.
Our national database of air toxics emissions from major, area, and mobile sources, the
NTI, will be a fundamental component of our risk assessments. We are now completing a
baseline NTI representing the 1990 to 1993 period, and obtaining State review of a draft 1996
NTI suitable for dispersion and exposure model inputs (scheduled for completion in 1999). We
plan to update the NTI every three years and to conduct future risk assessments to coincide with
these revisions. Monitored air toxics concentrations will also be an important component of our
assessment activities, in part to help us evaluate and refine our air quality models. We are now
working with the States to design and implement a national air toxics monitoring network that
will provide important information for future assessment activities.
5.4.1 Designing the Assessments
We'll tailor each assessment to the purpose(s) it is to serve (e.g., measuring progress
against the 75 percent estimated cancer incidence reduction goal). Accordingly, assessments will
vary in scope, level of refinement, and, thus, data and resource requirements. The scope of each
assessment will generally be defined by the following characteristics:
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The number of HAP to be evaluated (all 188 or some subset);
The types of sources included (area, major, mobile);
-. The spatial resolution (e.g., aggregation of results on the national, State, urban, or
neighborhood scale); and
The pathways/media to be evaluated (inhalation/air only or multipathway/
multimedia).
Further, for each assessment, we need to specify an appropriate approach to use in
estimating progress toward our risk reduction goals, since, as discussed above, it will not be
possible to directly measure reduction in cancer incidence or noncancer risks attributable to
hazardous air pollutant emissions. Alternative approaches range from rough approximations to
more precise risk estimates, with data and resource requirements increasing for more precise
assessments that require greater refinement.
5.4.2 Addressing Disproportionate Risks
Disparities in risks from air toxics in the urban environment may exist between different
cities, between neighborhoods or demographic groups within a city, or within a similarly-
exposed population that includes sensitive groups. In our assessments, we intend to pay
particular attention to areas, populations, and sensitive groups with substantially higher-than-
average risks.
While differences in risk between different urban areas may be discernible from national
screening-level modeling, more refined modeling will generally be needed to evaluate localized
disparities within any one urban area. This is because highly localized disparities may be
obscured by the simplifying assumptions that are necessarily inherent in national screening-level
assessments. For this reason, the ability of EPA or State and local authorities to assess localized
risk disparities will depend on the availability of detailed data on emissions and population
distribution, local-scale models, and sufficient resources.
5.5 Designing Future Assessments
We'll conduct a series of assessments starting in mid-2000 and periodically thereafter at
appropriate times during the implementation of the Strategy. The assessments will include both
national-scale and urban-scale analyses. All assessments will incorporate the most current data,
information, and assessment tools available. As the Strategy progresses, we may eventually use
risk assessment tools that are now only in early development, or perhaps have not yet been
envisioned. For this reason, we can't describe in detail the assessments that will be conducted
several years from now.
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5.5.1 Initial Assessments - National
We'll conduct an initial national assessment in mid-2000 to serve several purposes. First,
we'll develop an estimate of progress that has already been made toward the goals of the strategy.
Consistent wijh section 112(k) of the CAA, which focuses on reducing ambient concentrations of
HAP to levels "below those currently experienced," we've established 1990 as the base year for
assessing progress. To estimate progress since the base year, we'll compare the base year
emissions inventory to the inventory for 1996, due to be completed in 1999, using a weighted
emissions analysis. This assessment will be limited to the weighted-emissions approach because
the 1990 base year inventory, although a comprehensive county-level inventory, will lack the
source-specific information necessary to support air quality modeling. Subsequent assessments,
however, will not be limited in this way because emission inventory data, beginning in 1996, will
include information needed for modeling7.
Second, the initial national assessment will provide basic information to assist us in
prioritizing HAP and source categories for regulatory development, based on their relative
importance as contributors of risk. Third, the assessment will provide the clearest and most
current picture of inter-urban and demographic disparities in risk and will provide insight on
more refined analyses that may be appropriate to identify types of sources associated with
particularly high risk levels. Fourth, we intend to use information from the initial assessment to
develop a more complete and quantitative goal for a "substantial" reduction in noncancer risk.
Finally, we'll use the initial assessment to compare different hazard- and risk-based approaches.
In particular, we intend to correlate results of assessment approaches (1) and (2) (which lack
exposure assessments) with exposure assessment-based approaches to determine their relative
accuracy and to quantify uncertainties. These comparisons, in combination with data and
resource availability, will help us to scope the details of future assessments and finalize our
estimates of progress from 1990 to 1996.
We'll use all four types of approaches (emissions weighting, comparisons between
ambient concentrations and exposure estimates, RBCs, and modeled estimates of risk) in the
initial national assessments, to the extent possible. We plan to use the ASPEN model to estimate
national air quality concentrations in conjunction with the use of the Hazardous Air Pollutant
Exposure Model (HAPEM) to estimate national exposures. We'll conduct screening level
analyses before progressing to more refined analyses to ensure that we're allocating appropriate
amounts of resources to each assessment, given our information needs. The assessment will
'As part of our CEP, the ASPEN model, used to estimate HAP ambient concentrations nationwide, was
developed and tested using a 1990 emissions inventory based on the limited HAP information that was available in the
mid-1990s (prior to the substantial improvements now reflected in the 1993 NTI). While that first national-scale
modeling exercise provided the screening-level information that we've used in conjunction with other information in
creating the urban HAP list, we believe that the uncertainties in the CEP's 1990 emission inventory are too large to
support a meaningful comparison with modeled concentrations for future years that will result from the application of
the ASPEN model using updated emissions inventories. These updated inventories, starting with the 1996 NTI, are
specifically designed to include sufficient source-specific information to support air quality modeling.
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focus on inhalation exposures, with the expectation of including multipathway exposures, as
appropriate, in subsequent assessments. The initial assessment will include all urban areas in the
United States, and we anticipate presenting results with county- and/or urban-scale resolution.
The assessment will address as many HAP as the data support, but will include at least the 33
HAP considered in the initial national scale assessment.
5.5.2 Initial Assessments - Urban
We plan to conduct urban-scale assessments for a few selected cities over the next few
years to serve as case studies that may be particularly useful as guidance for State, local and
Tribal program assessments. We'll also provide technical support and risk assessment tools for
authorities that wish to conduct their own local assessments to analyze area-specific progress and
intra-urban disparities. The experience we gain through these analyses will also help us refine
future assessments.
We'll develop these initial urban assessments using the specific approaches that are
appropriate for the quality of data available. Each assessment will describe a single urban area,
and we anticipate presenting the results with high spatial resolution (e.g., a one kilometer grid).
The scope of each assessment will address a subset of HAP that we identify as being priority
HAP for the particular urban area being assessed. We plan to consider both inhalation and
multipathway exposures as appropriate and as available data permit.
5.5.3 Periodic Assessments
In the years following the initial national assessment, we'll conduct new analyses at
appropriate intervals as new data become available. These periodic assessments will serve two
principal purposes. First, they'll measure progress toward the goals of the Strategy, considering
all actions taken that reduce HAP emissions for any purpose. These include Federal, State, local
and Tribal actions, as well as voluntary initiatives by local communities and industry. Second,
the new analyses will assist us in prioritizing which future regulatory actions would be most
effective in making further progress. We'll develop the periodic assessments using the specific
approaches that have proved most efficient (that is, the least resource-intensive approach that
accomplishes the purpose of the assessment). Assessments will include all urban areas in the
U.S., with results presented on county- and urban-scale level resolution. Assessments will
address the full list of 188 HAP, to the extent to which emissions, monitoring, and health data are
available. If appropriate tools become available, periodic assessments for bioaccumulative HAP
will include multimedia exposures.
By measuring ongoing progress, periodic assessments will also inform us when we have
met our goals, and will help us to measure the degree to which we have reduced disparities in
risk. The approaches used for such goal-specific comparisons will be determined by the results
of earlier assessments and will be developed to fit the Strategy's purposes.
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5.6 References
Davis, J.M., Jarabek, A.M., Mage, D.T., and J.A. Graham. 1998. The EPA health risk
assessment of methylcyclopentadienyl manganese tricarbonyl (MMT). Risk Analysis 18:
57-70,.
Science Advisory Board. 1998. Review of the Toxics Release Inventory (TRI) relative risk-
based environmental indicators methodology. SAB Report No. EPA-SAB-EEC-98-007.
Available on-line at http://www.epa.gov:80/sciencel/eec9807.pdf.
Smith, R.L., French, C.L. and R. Thompson. 1999. Ranking and selection of hazardous air
pollutants for listing under section 112(k) of the Clean Air Act Amendments of 1990.
Technical Support Document. EPA Docket A-97-44.
U.S. EPA. 1986a. Guidelines for mutagenicity risk assessment. Federal Register 51:34006-
34012. September 24.
U.S. EPA. 1986b. Guidelines for carcinogen risk assessment. Federal Register 51:33992-
34003. September 24.
U.S. EPA. 1986c. Guidelines for the-health risk assessment of chemical mixtures. Federal
Register 51:34014-34025. September 24.
U.S. EPA. 1989. Risk assessment guidance for Superfund, volume I: human health evaluation
manual. Office of Emergency and Remedial Response. EPA/540/1-89/002.
U.S. EPA. 1991. Guidelines for developmental toxicity risk assessment. Federal Register
56:63798-63826.
U.S. EPA. 1992. Guidelines for exposure assessment. Federal Register 57:22888-22938. May
29.
U.S. EPA. 1993. Assessment of potential health risks of gasoline oxygenated with methyl
tertiary butyl ether (MTBE). Office of Research and Development. EPA/600/R-93/206.
U.S. EPA. 1994a. Methods for derivation of inhalation reference concentrations and application
of inhalation dosimetry. Washington, DC.
U.S. EPA. 1994b. Reevaluation of inhalation health risks associated with
methylcyclopentadienyl manganese tricarbonyl (MMT) in gasoline. Office of Research
and Development. EPA/600/R-94/062.
U.S. EPA. 1995a. Policy for risk characterization ("Browner Memorandum"). Office of the
Administrator, Washington, DC. March.
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U.S. EPA. 1995b. Guidance for risk characterization. Science Policy Council, Washington,
DC. February.
U.S. EPA. 1996a. Guidelines for reproductive toxicity risk assessment. EPA/630/R-96/009.
September.
U.S. EPA. 1996b. Proposed guidelines for carcinogen risk assessment. Office of Research and
Development, Washington, DC. EPA/600/P-92/003C.
U.S. EPA. 1998a. Guidelines for neurotoxicity risk assessment. Federal Register 63:26926. May
14.
U.S. EPA. 1998b. Methods for exposure-response analysis for acute inhalation exposure to
chemicals: development of the acute reference exposure. Review draft. Office of
Research and Development, Washington, DC. EPA/600/R-98/051.
U.S. EPA. 1998c. Waste Minimization Prioritization Tool spreadsheet document for the RCRA
waste minimization PBT chemical list docket (#F-98-MMLP-FFFFF). Available on-line
at http ://www.epa.gov/epaoswer/hazwaste/minimize/chemlist/intro.pdf.
Woodruff, T.J., Axelrad, D.A., Caldwell, J., Morello-Frosh, R., and A. Rosenbaum. 1998.
Public health implications of 1990 air toxics concentrations across the United States.
Environmental Health Perspectives 106(5): 245-251.
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6. Research Needed to Address Knowledge Gaps
The purpose of this chapter is to summarize the types of scientific information (and
related research) needed to better inform future risk assessment and risk management judgments
that will be made in carrying out the Strategy. To provide some perspective, we are also
providing a summary of planned and/or ongoing EPA research activities'. Also, while we have
not undertaken a complete inventory of State and local research activities, we mention them in
the chapter where we are aware of them. State and local activities are especially important since
the Strategy recognizes that the responsibility for reducing health risks from exposure to urban
HAP is shared by all levels of government.
This chapter details the development of EPA research strategies and research plans which
reflect Agency commitments to specific actions within specified time periods. To aid this
process, research needs presented in this chapter are categorized into both short-term (less than
five years) and long-term needs (greater than five years). We are now developing, with this
chapter as a starting point, an Air Toxics Research Strategy that will identify key questions that
need to be answered and the research that needs to be conducted by EPA and others to answer
them.
The scientific needs presented in this chapter are organized around the risk
assessment/risk management approach described previously, which links the elements of risk
assessment (i.e., the description of a health problem, including whether one exists) with risk
management (i.e., actions to address the risk). Consistent with this approach, research needs are
presented below in four areas:
1. Exposure assessment information needs, which include research into the areas of
emission sources, environmental concentrations, and human exposure factors;
2. Health effects information needs, including hazard determinations and dose-
response assessments, which include toxicity and mode of action research, as well
as development of methods and models for producing probabilistic dose-
responses assessments with reduced uncertainty;
3. Risk assessment/characterization information needs, which include development
of assessment methods for chemical mixtures and techniques for risk
communication; and
'EPA research and assessment activities are performed by various EPA offices and laboratories including
the Office of Research and Development, the Office of Air Quality Planning and Standards, the Office of
Transportation and Air Quality, the Office of Prevention, Pesticides, and Toxic Substances, and Regional Offices.
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4. Risk management information needs, which include emission control assessments
and pollution prevention alternatives with a focus on categories of area sources.
6.1 Exposure Assessment
An exposure assessment provides estimates of exposures that are occurring or are
anticipated to occur under specified conditions. Exposure assessments include:
An emissions source assessment;
An evaluation of transformation and fate;
A determination of environmental concentrations;
A characterization of pathways that may lead to exposure; and
An understanding of population characteristics and activity profiles influencing contact
between a person and a contaminant, and aggregation of exposure across pathways and
chemicals.
hi order to assess human exposures to urban HAP, information is needed on emissions
(from area, major, and mobile sources), on atmospheric transport and fate, on actual exposures to
populations of interest, and on methods to measure the HAP at the places of interest (e.g., at
sources, in different media). Also, because it is impossible to measure all the events of interest,
models of these events are needed. To be fully effective, the models should encompass the
source-to-exposure relationship. Thus, models of contaminant distribution, apportionment, and
population activity profiles are needed to assess and predict microenvironmental exposures,
preferably on a probabilistic basis. These models should be founded on scientific principles and
evaluated using a variety of data. Developing such models is an iterative process, with the
scientific foundation improving at each iteration. It is important that the models explicitly
address uncertainty and that they be sufficiently detailed so that they can identify the most
effective risk reduction approach, should that be necessary. For example, knowledge of which
sources and pathways result in the highest exposures can form the basis for optimal risk
management. Descriptions of the wide range of exposure-related research needs follow.
Need 1: Improved ambient monitoring methods, characterization, and network
design to support a national ambient air toxics monitoring network
Description: The current lack of a national ambient air toxics monitoring network
hampers efforts to characterize ambient levels of HAP. Such a network is needed in the Strategy
to support efforts to provide information that will assist in:
Evaluating models;
Characterizing risk;
Tracking progress with respect to the risk goals over time; and
Targeting areas of concern.
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Monitoring methods should be developed for those urban HAP for which no methods are
currently available. Field (ambient) studies of macro and micro environments require methods
that are sensitive to ambient concentrations of HAP. The spatial extent to which such point
measurements are valid needs to be determined to allow the assignment of an air quality
measurementto a representative area rather than to just a point location in space. These efforts
can build on the previous work performed to support the monitoring for the criteria pollutants.
Research is needed to evaluate the uncertainties and limitations of current ambient monitoring
methods and to improve methods where appropriate. This work should include, for example, an
evaluation of current minimum detection limits with respect to expected ambient levels,
background concentrations, and health reference levels. Evaluation of "natural background
levels" of HAP through ambient monitoring needs to be completed. This should build on
existing work and would help define levels of HAP which cannot be reduced through traditional
control programs. Research is needed to evaluate the amount of monitoring data (and
measurements) needed to develop estimates of annual average concentrations with an appropriate
level of confidence. The usefulness of emerging ambient measurement methods for national
application (e.g., Light Detecting and Ranging (LJDDAR), other optical methods, mobile sampling
methods, etc.) need to be evaluated and refined as appropriate.
EPA Activities: We are developing a plan for a national air toxics monitoring network
that will build directly on existing monitoring efforts managed by individual State and local air
pollution agencies. The network will foster scientific consistency across those existing networks
with respect to pollutants measured, methodologies used, and quality assurance techniques
employed. Also, it will expand the measurement of air toxics to new areas across the country
with the aim of providing a more comprehensive assessment of ambient air toxics levels
nationwide, with a particular emphasis on higher population areas. This monitoring network will
be designed (in collaboration with the States) to site monitors that will assist in the evaluation of
national scale modeling assessments and to facilitate tracking progress with respect to
emissions/risks reductions. Other monitors will be sited to support localized assessment
activities.
Need 2: Improved area source emissions estimation methodologies and spatial
allocation methods
Description: Area source categories present special challenges for estimating emissions.
For example, they include stationary emissions sources that are individually too small, too
numerous, or too dispersed to be inventoried as individual sources (e.g., landfills, and residential
fuel combustion).
We often estimate area source emissions using "top-down" approaches that require a
combination of emission factors and source activity data. The available activity data may exist
only for large areas, such as the Nation as a whole, or at the State level. Once emissions are
estimated at this top level, they must then be spatially allocated down to smaller areas in order to
support control strategy development, dispersion and exposure modeling studies, or simply to
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permit comparisons of emissions in different geographic areas. A "bottom-up" approach, on the
other hand, would involve collection of actual measured emissions from individual sources. This
approach more accurately estimates emissions, but often is not practical because of the cost of
collecting such data for a large number of area sources and source categories. Emission factors
for area sources come from various source tests or other industry specific data (e.g., mass
balance). Sometimes emission factors are supported by data from several facilities, but often
there are only one or two tests to support them. Therefore, area source emission factors should
be improved as new data are collected.
The availability, geographic level of specificity, and overall quality of the activity data for
area sources vary from one category to another. Most often, the activity data are obtained from
published business and manufacturing sources, governmental statistics publications, and
background information from EPA regulatory programs. Examples of sources of activity data
are industrial trade associations, the Department of Commerce's Bureau of the Census, the
Department of Transportation, the Department of Energy's Energy Information Administration,
and various State and local government planning and regulatory agencies. Emissions are
allocated geographically by a number of methods. For major sources, the emissions for each
facility may be assigned to counties or more specific geographic locations based the address of
the facility or its latitude and longitude. Highway passenger vehicle emissions can be assigned to
counties based on total county VMT data, which are normally available from State Departments
of Transportation (DOTs). Sub-county allocation of these emissions may be based on VMT
estimates for specific major roadway links and travel demand model outputs produced by local
Metropolitan Planning Organizations (MPOs). Area source emissions are typically more difficult
to allocate to counties and sub-county areas. Most often, where facility specific data are not
available, emissions are assigned to individual counties or other areas using a surrogate factor for
area source activity. Some examples of surrogate approaches include apportioning national
emissions to counties based on population, and apportioning emissions from specific industrial
sectors to counties based on Standard Industrial Classification (SIC) code-based employment
statistics.
These area source estimation methods have several weak points, particularly when the
estimates are to be used in dispersion models to predict ambient pollutant concentrations for very
small geographic areas, like census tracts. Actual measures of area source activity for small areas
are normally not available. Existing methods are thought to produce results with a high degree of
uncertainty, but the actual activity data needed to establish credible uncertainty measures are not
readily available. New and improved methods for area source emissions estimation and spatial
allocation of area source emissions are needed to avoid inaccuracies resulting from the
"smearing" effect of the methods described above. Development of such methods requires the
completion of rigorous and demanding survey activities to establish credible databases that can
be used to develop improved area source methods. While area source needs have been
determined to have the higher priority, there is still a need to improve emissions data for major
sources over the longer term.
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EPA Activities: We have developed a baseline NTI representative of the 1990 -1993
period, and are now updating these data to a 1996 base year. The objective of the NTI is to
provide a compilation of emissions estimates for all CAA listed HAP for point, area, and mobile
sources. The NTI therefore will serve as the most comprehensive emissions inventory of air
toxics. The NTI incorporates available information from the TRI, State and local inventory data,
data from various regulatory programs, and data from other special studies. Also, we have been
conducting research to develop an improved method for estimating area source emissions.
Need 3: Methodologies that allow for identification and speciation of important HAP
and their combustion and transformation products
Description: Some chemicals are inventoried as compound classes like "mercury
compounds" or "chromium compounds." In addition, VOCs include many individual organic
species, some of which have been listed as HAP. Some chemical species included in these
composite chemical groups are likely to contribute to public health impacts while others may be
relatively harmless. There is currently a shortage of data available to characterize individual
species, particularly at the source category emissions level.
EPA Activities: We have begun studies to characterize the emissions of mercury and
mercury compounds from chlor-alkali manufacturing facilities, believed to be the largest non-
combustion source of mercury and speciated mercury compounds (i.e., elemental mercury,
mercuric chloride, and mercuric oxide). We also maintain facilities for characterizing HAP
emissions from combustion sources, such as boilers, rotarykilns, and municipal waste
combustors (MWC). The MWC program performs basic research on MWC pollutant formation
and on control mechanisms for acid gas, trace organic, and trace metal emissions. We also have
conducted analyses of the products of incomplete combustion of agricultural plastic, and of
emissions from the open burning of household waste in barrels.
For mobile sources, we perform in-house vehicle testing programs for determining the
effects on emissions of a variety of vehicle operating conditions, including various temperatures,
malfunctioning emissions control systems, driving schedules, and fuels. We emphasize such air
toxics as benzene and total aromatics, 1,3-butadiene, formaldehyde, acetaldehyde, other
aldehydes, MTBE, and primary particles.
Need 4: A more accurate nonroad mobile source emissions characterization
Description: Nonroad mobile sources include a wide variety of mostly gasoline and
diesel-powered equipment used for nonroad transportation purposes, industrial and construction
activities, agricultural operations, recreational, and other purposes. Examples include aircraft,
farm tractors, lawn and garden tractors, snowmobiles, and recreational marine vessels. As is the
case for area sources, emissions from nonroad mobile sources are estimated using emission
factors and estimates of source activity. As for highway mobile sources, emissions result from
the incomplete combustion of motor fuels and evaporation of motor fuel components. In general,
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the data needed to estimate emissions include an estimate of the population that exists for a
particular class of equipment, an estimate of the average number of hours of use in a year, the
average load factor and power requirement for the equipment while in use, and information to
spatially and temporally allocate the equipment use. Emission factors for nonroad equipment are
based on emissions tests for specific equipment, and may be adjusted to consider deterioration of
equipment with age and to account for any applicable emissions controls on the equipment.
Emission standards for most nonroad categories have only recently been adopted so that many of
the engines in use today were placed in service before controls were applied.
We are currently developing an emissions model for nonroad equipment. This model,
NONROAD, estimates VOC and other criteria pollutant emissions using methods like those
described above. Draft versions of this model have been released for review. The model does
not include methods for aircraft and rail locomotives, or commercial marine vessels. To extend
the capabilities of NONROAD to cover air toxics, more research is needed to characterize toxic
emission rates (either in absolute terms or as fractions of total VOC emissions). The nonroad
mobile source category includes a wide variety of subcategories, each of which may have
different emission characteristics because engine sizes and designs, duty cycles, fuel
consumption, and approaches to engine cooling and fuel management vary.
Considerable uncertainty is inherent in the methodologies that are used to estimate
nonroad engine activity for the temporal and spatial scales needed to support air quality or
exposure modeling for urban areas. Typically, there are no State or Federal equipment
registration databases that can be used to determine equipment populations. Also, there is no
system to measure equipment utilization at either the national or local levels. The national
estimates of equipment populations, lifetimes, and utilization are based on limited survey data.
To improve the methods for estimating nonroad engine activity in urban areas, more complete
information for both national and local equipment population and utilization is needed. Field
survey data to better establish nonroad equipment activity levels in urban areas are needed to
improve the databases that are needed to develop improved activity level estimation methods, to
correlate nonroad equipment activity with other available surrogate parameters that may be better
indicators of equipment activity, and to better define the uncertainty bounds of existing methods.
EPA Activities: As discussed above, we are developing a comprehensive nonroad
emissions model, called NONROAD, which estimates emissions for criteria pollutants. In
addition, our National Exposure Research Laboratory (NERL) is conducting some limited testing
to better characterize toxics emissions from some categories of nonroad equipment (e.g.,
lawnmowers and other lawn and garden equipment, and marine engines).
Need 5: Improved characterization of air toxics from trucks and improvement of
modal emissions modeling capabilities for all vehicle classes
Description: The highway vehicle category includes emissions from the operation of all
classes of motor vehicles (e.g., light duty gasoline vehicles, light duty gasoline trucks, heavy duty
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diesel trucks) on the Nation's highways and streets. Emissions are usually estimated using an
emission factor model, such as the EPA MOBILE model or the California EMFAC model, in
combination with estimates of VMT, which are developed by State or local transportation
planning departments. The EPA's MOBILES model calculates fleet average emission factors for
specific calendar years, expressed as grams of pollutant emitted per mile of travel. Built into the
model are computational methods that will adjust the calculated emission factors to reflect how
the age distribution of the vehicle fleet, average vehicle travel speeds, ambient temperatures, the
effects of local vehicle Inspection and Maintenance (I/M) programs, and other modal variables,
such as movement up a grade, affect emission rates.
For carbon monoxide, VOCs, and nitrogen oxides, basic vehicle emission rates are
derived from standard EPA laboratory tests, the Federal Test Procedure (FTP) for highway
vehicles. For estimation of air toxic emissions, data to develop emission factors are more
limited. However, it is generally accepted that implemented control standards for reduction of
VOC emissions can achieve proportional reductions. Some additional research to verify that
VOC controls are achieving the expected effects in controlling toxics, especially in unusual
driving and ambient conditions, may be appropriate. Relative to other vehicle classes, however,
the toxic emissions from light duty gasoline fueled cars and trucks are reasonably well
characterized. Not as much information exists to characterize toxic emissions from heavy-duty
trucks, which are primarily diesel-fueled vehicles.
The following three research components describe various aspects of work that would be
useful to improve the characterization of air toxics from medium and heavy duty trucks. First, a
significant research need exists for the development of improved toxics emission factors activity
data. In the past, most of our efforts for improving highway vehicle emission models have been
focused on passenger vehicles. However, medium and heavy duty truck emissions, most notably
PM emissions, may add significantly to the human health risks posed by exposure to motor
vehicle emissions. Diesel exhaust is thought to be a likely human carcinogen at ambient levels of
exposure. The EPA has prepared a draft health assessment document that was reviewed by
CAS AC in December 1999. The document is currently being revised to address the review
panel's comments and will be reviewed again in late 2000. The temporal and spatial operating
patterns for diesel vehicles are significantly different than for personal passenger vehicles.
Highway-vehicle-travel-demand forecasting models concentrate on predicting passenger vehicle
trips, not truck trips. Thus, there is a need for better characterizations of real world truck activity
and emissions rates on current and emerging technologies in urban areas. Second, in addition to
research designed to improve emissions characterization (in terms of g/mile and g/min emission
factors), work is also needed to construct models that will predict population exposure levels
using existing emission factors. This type of work is needed for all air toxics but especially
diesel exhaust where questions have been raised about the usefulness of models (such as the
HAPEM as developed for mobile sources) which use vehicle carbon monoxide emissions to
estimate exposure to diesel exhaust. Third, additional work is needed on size distribution and
chemical composition of diesel particulate emissions from new technology engines. While there
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is extensive work under way on size distribution of diesel particulates from new technology
engines, it is too early to make any conclusions.
The MOBILES and total VMT approach is best suited for estimating emissions for county
or comparable political subdivision-size areas. Due to the complexity of factors that affect
highway vehicle emissions, this approach may yield very uncertain emissions estimates, when
used for smaller areas, such as the grid cells needed for atmospheric modeling, or for individual
road links. A more sophisticated modeling approach is needed to obtain highway vehicle
emission estimates that are accurately resolved in space and time for small areas. Highway
vehicle emissions vary considerably based on the operating mode of the engine. For example,
following a cold start, hydrocarbon emissions are significantly higher than during hot stabilized
operation. This is due primarily to the lower emission control effectiveness of the vehicles's
catalytic converter and the need for increased fuel enrichment to promote proper vehicle
operation while the engine is cold. Variations in highway vehicle emission rates result from fuel
enrichment events caused by "real world" engine loads imposed on vehicles traveling up
roadway grades, carrying heavy loads, or hard accelerations by drivers. An alternate modeling
approach that employs engine operation mode-based emission factors and uses Geographic
Information System (GIS) technology for managing the increased detail of spatial data is capable
of producing more accurate estimates of highway vehicle emissions for the detailed temporal and
spatial scales that are needed to support air quality dispersion modeling and population exposure
studies.
EPA Activities: Pursuant to section 202(1) of the.CAA, in 1993 we released the Motor
Vehicle-Related Air Toxics Study (U.S. EPA, 1993). This study summarized information on
emissions of toxic air pollutants associated with motor vehicles and motor vehicle fuels, as well
as estimated exposures and potential risks. The study also provided cancer risk estimates for
several air toxics for different years under various control scenarios. We've recently updated the
emissions and exposure analyses done for this study to account for new information (U.S. EPA,
1999a).
The MOBILE6 emission factor model, when released, will incorporate additional and
improved algorithms for estimation of criteria pollutants.
Also, we have been working with the Georgia Institute of Technology to develop a GIS-
based modal emissions model for ozone precursor pollutants for highway vehicles (the Mobile
Emissions Assessment System for Urban and Regional Evaluation or MEASURE). By the end
of 1999, MEASURE will also include some simple capabilities for estimation of air toxics and
PM emissions.
In addition, we have conducted a limited number of on-road emissions measurements for
heavy duty diesel trucks, primarily aimed at identifying modal emissions rates and correction
factors for nitrogen oxide and PM. This work is being extended to provide for collection of data
for PAH and other toxic species.
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Additional motor vehicle research focuses on in-house vehicle testing, "real-world"
vehicle testing, and human exposure to vehicle emissions in cabin air.
Need 6: Development of source-based urban-scale air quality models for the urban
HAP
Description: As mentioned previously, it is necessary to understand the relationship
between source emissions and the concentrations of chemicals in the media that may come in
contact with humans. Adequate modeling is very important, since measuring all potential
exposure scenarios is not feasible. While existing models may be applied to urban areas, no air
dispersion model has currently been developed that is tailored specifically to the urban
environment. Ultimately, the most effective model (which will actually be a combination of
models) should estimate the relationships among the source, the ambient air, and the exposure
dose. In this section, we describe the first component of this relationship, from source to the
ambient air. A separate Need 7 describes research that will estimate concentrations in
microenvironments for use in exposure studies, the second component of the relationship. It is
important to recognize that while Need 6 and Need 7 outline needs for exposure assessment in a
modeling framework, measurement methods and data collection studies are equally important for
the development, evaluation, and use of any model.
In order to develop and operate'a numerical simulation model for the fate and transport
of any HAP, a scientific understanding of key chemical and physical properties for that pollutant
under typical atmospheric conditions is needed. Additionally, some HAP will be transported
and dispersed without undergoing any significant chemical transformations (i.e., they are non-
reactive). Other HAP undergo significant chemical transformations or are formed in the air as a
result of atmospheric transformation of their precursors. For example, formaldehyde is directly
emitted from some sources and is created as a result of the atmospheric transformation of other
pollutants present. Particle-gas phase partitioning in the atmosphere may also be important for
certain HAP. Some HAP are semi-volatile and can exist simultaneously in both gaseous and
aerosol forms. The fraction of the total HAP air concentration in each form is a function of the
chemical and physical properties of the HAP, the atmospheric conditions, the concentrations of
precursors, and the availability of condensate nuclei. Thus, a simulation model for semi-volatile
HAP should simulate the behavior of key interacting aerosol materials, not just the gaseous and
aerosol fraction of the HAP in question-likewise for HAP that are totally in particulate form with
no significant gaseous fraction. These HAP, as particles, may coagulate to form larger particles
which deposit through settling out and washout to the earth's surface differently than smaller
particles. Therefore, to provide accurate representations of the atmospheric behavior of these
HAP, a numerical simulation model should include both chemical and physical behavior of the
HAP being considered as well as the surrounding HAP constituents. These processes, together
with terrestrial and aquatic fate and transport processes, can be important for assessing non-
inhalation pathways of exposure (e.g., ingestion or absorption) that are associated with deposition
of these pollutants in soil, water, and various media.
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For urban-scale modeling, a comprehensive atmospheric model should also simulate the
fate and transport of the pollutant on a local scale. To predict maximum impacts and
concentration gradients required to assess human exposure, horizontal simulation may have to
have a resolution on the order of hundreds of meters. The vertical resolution of existing
simulation models for photochemical oxidants and acidic deposition are expected to be sufficient
for urban HAP studies. Further, the model domain size for a typical urban study is on the order
of 100 kilometers (km). No such modeling capability currently exists at these resolutions to
simulate the necessary physical and chemical processes to predict urban HAP fate and transport.
If the HAP in question can be transported long distances (i.e., beyond the 100-km range), then
nesting of a larger-scale grid model (or regional-scale model) within the urban study area will be
required. Regional-scale models for some HAP do exist, but their usefulness on a local scale is
still very much in doubt due to model approximations about small-scale air flows and
atmospheric reactions of the HAP in question. Further, model evaluation is difficult because of
the lack of any monitoring techniques capable of measuring ambient air concentrations of the
HAP in question at temporal and spatial scales of the study.
EPA Activities: We previously developed and applied regional-scale Lagrangian-type
models for certain HAP (i.e., mercury, dioxins and furans) with very simple or chemical specific
treatments for chemical and physical processes. These Lagrangian models are currently used to
model HAP that are transported over long distances, but cannot accurately model many HAP at
the spacial scale that need to be considered. Generally, they provide 40-km or larger horizontal
resolution, which may be inadequate or inappropriate for some urban assessments.
We have also previously developed and applied a more local-scale, emissions-based
Eulerian-type model, the Industrial Source Complex 3 (ISC3) model, for some HAP in candidate
urban areas. As mentioned above, while this may have been appropriate for some HAP, there are
still many questions associated with the spatial and temporal uncertainties of modeling HAP with
this method.
We are now developing a new comprehensive air model of acid deposition, tropospheric
oxidants, and aerosols with available horizontal resolutions down to 4 kilometers. This model,
the Community Multi-scale Air Quality (CMAQ) model (Byun et al., 1998), is designed to
operate within the Models-3 system. Models-3 is a flexible, software system designed to
simplify the development and use of environmental assessment and decision support tools for a
wide range of applications from regulatory and policy analysis to understanding the interactions
of atmospheric chemistry and physics. This effort could serve as a basis for the development of
urban-scale HAP models with nesting capabilities within larger-scale models. Current chemical
mechanisms of tropospheric chemistry within the CMAQ model are available as a starting point
for this work. These mechanisms could probably be expanded to include the many additional
reaction pathways and species necessary to describe the detailed transformations of HAP, as well
as significant pathways for the production of HAP from non-HAP precursors.
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We have developed a set of integrated models, the Integrated Exposure Methodology
(IBM), that permits estimation of concentrations of stack-emitted pollutants in various media and
associated exposures. This methodology was used in the Mercury Study Report to Congress
(U.S. EPA, 1997) and in the Study of Hazardous Air Pollutant Emissions from Electric
Utility/Steam Generating Units (U.S. EPA, 1998), mandated by the 1990 CAA Amendments.
We are developing a modeling system called the Total Risk Integrated Methodology
(TRIM), which is intended to provide a framework that is scientifically defensible, flexible, and
user-friendly, for assessing human health and ecological risks resulting from multimedia (air,
water, soil and food), multipathway (via inhalation, ingestion, and absorption exposure routes)
exposure to air toxics and to criteria pollutants. The modeling system will consist of multiple
modeling tools from which to select, depending on the level of analysis, data availability, and
needed outputs. TRIM will track the movement of pollutant mass through a comprehensive
system of compartments. Over time and with additional research, the compartments will attempt
to represent all possible locations of the pollutant in the physical and biological environments of
a defined study area or species. Also, the modeling system should make use of mass conserving
relationships, fugacity, and biokinetics to determine the movement of HAP, and, thus, will be
able to provide an inventory of a pollutant throughout the entire system. Also, the modeling
system will reflect an integration of uncertainty and variability analysis capabilities.
Need 7: An understanding of the distribution of human exposures (including
susceptible subpopulations) and the pathways by which HAP reach humans
Description: Human exposure to HAP occurs at the point of contact between the
environmental concentration and the personal receptor. If addressed, previous research needs
(see Need 6) would enable improved estimation of air quality. However, further refinement in
scale may be needed to estimate the population distribution of exposures in an urban
environment. For example, a HAP at a 4-km distance may undergo transport and transformation
processes in the ambient air during and after penetration into indoor environments before
contacting a human. Also, many additional sources could be present within this "4-km grid" and
contribute to overall exposure. To account for these possibilities, models developed around
sound scientific principles, evaluated with measurements from targeted studies, and capable of
providing probabilistic estimates of the number of persons exposed to different concentrations of
HAP of interest, should be developed.
Exposure to HAP can more accurately be evaluated in a microenvironmental modeling
framework which considers the human as a receptor passing through a series of
microenvironments in which exposure occurs. Clearly, there are two critical factors in this
approach: (1) characterizing the range and variability of HAP concentrations in each
microenvironment, and (2) characterizing the nature of the human exposure in each
microenvironment (i.e., when, how long, how often, and with what intensity do people come in
contact with the HAP in each microenvironment). Both elements are involved in characterizing
susceptible subpopulations. For example, people with low incomes may live closer to sources;
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children spend different times in different microenvironments compared to adults; and people
with pre-existing diseases (e.g., asthma) also have different activity patterns.
Estimating exposure to HAP is complicated by the range of temporal and spatial scales of
emissions that may significantly contribute to personal exposures. Significant HAP emissions
may come from a few point sources with high emissions or a collection of sources with relatively
low emissions. Exposures of interest may be for an hour or a lifetime. The longer the duration
of exposure, the more complicated the assessment, given the variability in the exposure and in
personal activities. Although daily exposure may best be evaluated by a model that considers the
human receptor as passing through a series of microenvironments of exposure, long-term
exposure estimates require development of reliable simplified modeling methods because it is
not practical to follow every individual through a daily series of activities.
Research to bridge the gap between available regional-scale models of air pollution
transport and stochastic and probabilistic models of personal exposure, include: a) the
development of models and data that consider key human exposure microenvironments, b)
studies of concentration measurements and activity patterns to support modeling evaluation on
selected urban HAP, c) measurements of HAP in various media to which susceptible
populations may be exposed to ensure that models adequately capture those populations likely to
receive high-end exposures or be more biologically sensitive, and d) development of databases
and integration of all data. The data on demography, geography, meteorology, human activity
patterns, source emissions, and regional/urban/microenvironmental scale concentrations would
need to be integrated. These data support the application of a HAP population-based
probabilistic modeling system of personal exposures. It is important that both the inherent
variability and the uncertainty of all significant factors for connecting emission sources,
environmental concentrations and the magnitude, duration, and frequency of human exposures be
understood, and models be developed so that risks may be assessed and managed.
In the context of activity patterns and microenvironments, an existing gap is the need for
personal monitoring (e.g., personal monitoring exposure to VOCs and other air toxics through
use of gasoline fueled lawn and garden equipment, including commercial equipment which is
typically used for many hours per day). The development of biological markers of exposure such
as breath, hair, or tissue samples would also help characterize personal exposure of VOCs and
other air toxics. An adjunct to the need to determine personal exposure is the long-term need to
identify indoor air exposures. In the short-term, this need may be satisfied by knowing the
indoor/outdoor ratios of the urban HAP, but in the long-term, more specific data are needed on
the movement of HAP between indoors and outdoors. Toxics can absorb onto other items in the
indoor environment and then be re-released later as the concentration of the toxic is reduced.
Therefore, information on the potential sinks and reservoirs of HAP would add useful
information to the indoor characterizations of exposures.
EPA Activities: We have completed some studies, the National Human Activity Pattern
Survey (NHAPS) and Total Exposure Assessment Methodology (TEAM), that can contribute
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limited hitman activity and personal exposure data in support of this need. The NHAPS did not
evaluate susceptible subpopulations, and TEAM measured only a small number of HAP. Even
so, these studies provide valuable direction for the design of necessary follow-up studies. We
have developed databases for supporting human exposure modeling [e.g., Consolidated Human
Activity Database (CHAD) and Total Human Exposure database and Advanced Simulation
Environment (THERdbASE)]. We also have a small ongoing project to develop
microenvironmental exposure measurements and models for mobile-source related emissions.
These studies will contribute both measurements and models toward developing air pathway,
human exposure estimates along and near highways (including urban street canyons). We have
sponsored the development of receptor models for source apportionment. Chemical Mass
Balance models, and models like UNMIX, have been developed and tested on particulate and
other pollutants. Their application to microenvironmental and personal exposure measurements
is both feasible and reasonable. These past and present projects are helpful in providing some of
the needed data and models.
We are currently using models to estimate ambient levels of air toxics which will
subsequently be used as inputs to an exposure model, HAPEM. This exposure model will
provide national exposure estimates to air toxics based on the 1996 NTI. This work will be
completed in the spring of 2000. We have a small project that develops breath analysis methods
for VOCs. Though we currently have no projects on source test methods or ambient methods for
the urban HAP, we have recently developed a prototype real-time monitor for formaldehyde.
While HAPEM is currently being applied, there are many areas where additional information
developed through research is needed to improve the model.
Recently, we sponsored the National Human Exposure Assessment Survey (NHEXAS)
which is a multiroute exposure study focusing on metals, pesticides, PAHs, and VOCs. In
addition, we recently funded two research centers (New Jersey Medical School and University of
California at Berkeley) to develop comprehensive exposure models for a large spectrum of air
pollutants, including HAP. Coordination between this particulate matter initiative and the urban
air toxics initiative will be beneficial to the urban air toxics program.
6.2 Health Effects and Dose-Response Assessment
Various types of toxicity, mode of action, and interactive (mixture) information are
needed to reduce uncertainty in our estimates of risks from exposure to urban air toxics. The
needed information includes cancer and noncancer (acute and chronic) toxicity information for
HAP and risk assessment techniques that can combine data, produce statistical likelihood of risk
from HAP exposure, and reduce uncertainty through the application of better extrapolation
models (e.g., animal to human, low dose to high dose).
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Need 8: Use alternative sources of human health effects data (chronic and acute) for
urban HAP to develop and update dose-response assessments
Description: As described in Chapter 3, a variety of sources of dose-response
information was relied upon in identifying the urban HAP.
Additional health effects assessments, including the development of inhalation reference
concentrations and oral reference doses for chronic noncancer effects and acute reference
exposures for acute effects are needed for a number of the urban HAP. Although enough
information exists to raise our concern level and to select urban HAP presenting the greatest
threat to public health, more information is needed to complete the knowledge base necessary for
quantitative risk assessment, especially for the assessments of mixtures. The EPA's Integrated
Risk Information System (IRIS) lacks cancer unit risk estimates for 13, and RfCs and RfDs for
24 and 21, respectively, of the 33 urban HAP identified in the July 19,1999 Federal Register
Notice of the Integrated Urban Air Toxics Strategy (U.S. EPA, 1999b). Consequently, unless
peer-reviewed, dose-response assessments can be obtained from other sources, significant
uncertainty will be present in any risk assessments performed for these pollutants. An important
short-term activity is estimation of cancer unit risk and RfCs/RfDs for the HAP that currently
lack this information. Our preference is to obtain inhalation and oral data for these assessments
through the use of EPA's test rule authority (described below).
When no chronic inhalation dose-response assessments have been available for particular
HAP from any source, we have sometimes adapted oral data to inhalation exposure as a short-
term solution. Such conversions are not optimal for deriving inhalation dose-response and risk
assessments because they involve important uncertainties. For example, confounding features
such as portal-of-entry effects and first-pass metabolic effects may play a significant role in
altering the concentration of the dose delivered to the target organ and, thereby, attenuating
expected responses. Because of the relatively large amount of oral data, the development of
validated route-to-route methods and models to extrapolate from oral exposures would expand
our ability to perform risk assessments for urban HAP in the near future.
There is a need to develop acute reference exposure values for the short term using
methods such as EPA's proposed Acute Reference Exposure (U.S. EPA, 1994a) approach, which
is adaptable to any duration of exposure up to 24 hours. These values should be externally peer
reviewed, Agency consensus reviewed, and then listed on IRIS for use in developing risk
assessments under the Strategy. The methods used to generate the values should be evaluated so
that there will be a clearer understanding of the uncertainties associated with each method.
Models and software to facilitate acute dose-response assessments should also be developed over
the long term whereas developing the methods and data are short-term needs.
Another research need is for information to reduce uncertainty associated with the dose-
response assessments now on IRIS. Four HAP (acetaldehyde, acrolein, acrylonitrile, and
ethylene dibromide) have RfCs with relatively high associated uncertainty, i.e., with uncertainty
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factors greater than or equal to 1000. (The RfC methodology involves the application of
uncertainty factors to information in health studies so as to account for chronic noncancer effects
on humans, including sensitive subpopulations. For example, a 10-fold uncertainty factor may be
needed to account for a lack of understanding of human effects when only subchronic animal
studies are available.) Those urban HAP having dose-response assessments on IRIS but that
have not been externally peer reviewed should be updated based on current literature and
reanalyzed to include external peer review and Agency consensus review. Those pollutants
having high uncertainty should be reassessed when test rule data are made available over the
longer term. While awaiting test rule data, evaluation of dose-response information developed
by States could be useful in deriving interim values for use in the short term.
Where multipathway exposures are deemed relevant to exposures to urban HAP (e.g.,
mercury, dioxins), RfDs should be developed, as should route-to-route extrapolation methods,
that allow their use in assessing inhalation risks. No AREs are available for any of the HAP
because the method to calculate them is still being developed. The ARE method currently under
development has been reviewed by the EPA Science Advisory Board (SAB) which recognized
that large amounts of data are required to support ARE derivation by categorical regression.
Finally, the quantitative structure-toxicity relationship (QSTR) approach is another
method for gathering data on the toxicity of urban HAP. By knowing various structural attributes
and functions and how these attributes relate to toxicity, QSTR models can predict relative
toxicities of urban HAP. Thus far, QSTR model outputs have provided the probability of a
compound being carcinogenic and are most appropriate for use in ranking toxicity but not in
developing quantitative health assessments themselves (i.e., RfCs or cancer unit risks).
Therefore, a short-term research need is to develop the QSTR for the urban HAP and the other
HAP on the list in order to expand our knowledge database. A longer-term research need is to be
able to use the QSTR to actually predict cancer unit risks or noncancer reference values.
EPA Activities: EPA's authority for acquiring lexicological testing data is found in
section 112(b)(4) of the CAA. We have proposed to use the test rule authority under the Toxic
Substance Control Act (TSCA) section 4(a) which will require testing of 21 HAP. We noted
deficiencies in testing guidelines previously used under TSCA section 4(a) and promulgated
eleven harmonized test guidelines. Pharmacokinetic studies and other mechanistic studies were
also requested in the test rule protocols to support route-to-route extrapolation and to inform
EPA of toxicity by routes other than inhalation. The only urban HAP included in that initial test
rule is ethylene dichloride. Additional lexicological testing needs to be conducted, and an
amalgamated test rule considered by EPA and ATSDR for the Children's Risk Initiative, Urban
HAP, ATSDR VOC, and the metals rule. Testing needs for the urban HAP are candidates for the
amalgamated test rule.
Some of the completed assessments and some of the planned assessments have high
uncertainty associated with their conclusions based on the underlying lexicological data. In order
to significantly reduce the uncertainty of dose-response assessments, future lesl rule dala will be
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used for dose-response reanalyses. In addition, only a few of the cancer unit risks on IRIS were
developed using the approach described in the Proposed Guidelines for Carcinogen Risk
Assessment (U.S. EPA, 1996). An updating of present IRIS cancer unit risk values consistent
with the proposed guidelines should be accomplished in the longer term. Exhibit 6-1 presents
the current status of activities to update IRIS.
EXHIBIT 6-1
STATUS OF FYOO IRIS ACTIVITIES FOR URBAN HAP
Completed
Arsenic Compounds
Beryllium Compounds
Chromium Compounds
Methylene Diphenyl
Diisocyanate (MDI)
In Progress
Acetaldehyde
Benzene
1,3 -Butadiene
Cadmium Compounds
Chloroform
1 ,3-Dichloropropene
Dioxin
Ethylene Oxide
Formaldehyde
Nickel Compounds
POM
Quinoline
Styrene
Tetrachloroethylene
Trichloroethylene
Vinvl Chloride
Scheduled New Starts
Acrolein
Arsenic (inorganic)
1 ,2-Dibromoethane
Methylene Chloride
Methyl Mercury
The IRIS program has recently been altered to provide improved Agency consensus
review and external peer review of dose-response assessments. We have ensured that external
peer review has been conducted or is planned for the assessments listed in Exhibit 6-1. Although
all of the assessment activities for the chemicals in Exhibit 6-1 do not include the development of
an RfC, as data are made available (e.g., through test rules), including those relevant to
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noncancer dose-response assessments, more RfCs will be derived. Pollutants with high
uncertainty factors (>1000) will be reassessed as data become available. No ARE values are
available for any HAP, but a framework for their incorporation into IRIS is being considered.
The MRLs, acute exposure guidance levels (AEGLs), and levels of concern (LOCs) maybe
developed as they are necessary to estimate hazard. Work has progressed on using QTSR models
to rank 250 disinfection byproducts for the Water Program. This method holds potential for any
further ranking of HAP by toxicity as well.
Section 202(1) of the Clean Air Act requires EPA to identify the need for and consider
regulation for control of HAP from motor vehicles and motor vehicle fuels. These regulations
are at a minimum to apply to emissions of benzene and formaldehyde. The following three
ongoing mobile source pollutant health assessment efforts will inform us as we continue our
work as part of the Strategy:
Benzene health assessment. Benzene is a carcinogen found in baseline gasoline and
reformulated fuels. Calculating the cancer unit risk for benzene will serve to estimate a
risk associated with use of fuels containing this hazardous air pollutant. The benzene
RfC and RfD are being completed.
1,3-Butadiene health assessment. 1,3-Butadiene is a common emission product and
carcinogen resulting from combustion of gasoline and reformulated fuels. The health
assessment of 1,3-hmtadiene was reviewed by the SAB in 1998, and the final assessment
document is expected in late 2000.
Fuel additive risk assessments. The health risk assessments of fuel additives, such as
methylcyclopentadienyl manganese tricarbonyl MMT (Davis et al., 1998; U.S. EPA,
1994b), are being conducted in support of various EPA mobile source programs. MMT is
an organic manganese compound that can be used as an octane enhancer. Questions have
been raised about whether there may be inhalation risks associated with exposure to
manganese emissions from MMT-fueled vehicles.
Need 9: Development of statistical and mode of action methods for developing acute
and chronic dose-response assessments
Description: The lack of toxicity data or the availability of seemingly disparate data
often forces the application of uncertainty factors and default assumptions when developing
dose-response assessments. Certain cases may arise where multiple toxicity studies are available
for developing dose-response assessments. Methods of combining data for cancer and noncancer
dose-response assessments that include confidence profiles (Bayesian statistics) or meta-analysis,
for example, need to be developed, codified, and incorporated into software packages for easy
use. The development of many of these methods can be completed over the shorter term.
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The current methodology for developing RfCs divides gases into three classes based on
their reactivity and solubility. Developing dose-response assessments on the basis of these
classes offers increased certainty and reduces the number of mode of action parameters necessary
to define gas behavior. The current RfC methodology utilizes a paradigm which describes gas
solubility using mass transfer coefficients. Gas models that can predict the dosimetry of reactive
and nonreactive gases and water soluble and insoluble gases are needed. Thus, over the shorter
term, mass transfer coefficients are needed for the three categories of gases: Category 1, which
are highly water soluble, rapidly reactive, and do not penetrate to blood; Category 2, which are
water soluble and show accumulation in the blood; and Category 3, which are water insoluble
and perfusion limited. This physical process of mass transfer should also be coupled with
chemical reactions in the system.
Estimating risks associated with human exposure to priority urban air toxics under the
Strategy will best be done on the basis of probability. The determination of cancer unit risk
factors for HAP readily permits such determinations of risk or probability for cancer endpoints.
However, for noncancer endpoints, EPA has no definitive methodology for determining risk
above reference levels such as the RfC. The RfC is useful in that it indicates a reference
concentration below which it can be reasonably expected that no adverse effects will occur, even
in the most sensitive subpopulations. The basis of the RfC, which includes the application of
either a single point no-observed-adverse-effect level (NOAEL) or a statistical approach such as
the benchmark dose (BMD) (U.S. EPA, 1995), does not permit it to be used in probabilistic risk
assessments where knowing the probability of the occurrence of a health effect in a population is
desired. Though the BMD method utilizes data over a range of doses, the data are normalized to
a single effect. If higher exposure/doses are encountered, other endpoints would likely be
manifested making the basis of the BMD (dose-response for a single sentinel effect) no longer
relevant. It is important to understand that any dose-response method that utilizes a single dose-
response function, where response is a single endpoint, cannot provide a probabilistic risk
assessment by simply assuming higher doses will produce higher probabilities based on the dose-
response function originally chosen. Thus, both the NOAEL and BMD approaches provide
deterministic dose-response assessments, but not probabilistic ones. Categorical regression and
Bayesian statistics may be useful in developing methods for probabilistic risk assessments, but
these methodologies need to be developed on large adequate databases. Probabilistic approaches
to dose-response assessments are a longer-term need. Developing noncancer risk as a probability
also avoids the problem of having to combine probabilistic exposure assessments with
deterministic dose-response assessments. Guidance on the biological motivation and statistical
limitations of combining data involving different endpoints would be of added value.
The BMD method and related software are being developed as other tools for developing
both acute and chronic noncancer dose-response assessments. This methodology has many
similarities to the cancer dose-response method which utilizes curvilinear data fitting. Currently,
BMD methods are being used for the development of dose-response assessments entered on
IRIS. New software is being readied that will serve to facilitate the selection of models, provide
statistical comparisons, and present results in a graphical manner. A finite set of models for
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dichotomous data (incidence) are now available, but over the longer term additional models for
continuous data (quantitative increases or decreases in a metric) will be needed to develop
additional risk assessments. Guidelines for censoring data to develop more relevant dose-
response curves and adjusting for poor fit of models are also needed.
The ARE method is a process for developing acute dose response assessments that
includes the single point NOAEL approach, the BMD approach, and categorical regression
depending on the data availability. The ARE is defined as the exposure (concentration and
duration) with an uncertainty spanning an order of magnitude that is not likely to cause adverse
effects in a human population, including sensitive subgroups, when exposed on an acute and
intermittent basis. Adverse-effect levels are those at which there are increases in frequency,
magnitude, or severity of effects due to exposure, which are considered to be adverse.
Intermittent implies sufficient time between exposures such that there is no effect of one
exposure on the effect of the next, and acute exposure is defined as one of less than 24 hours.
Standard methods using the NOAEL and the BMD approaches as used in derivation of RfCs, and
RfDs are invoked for ARE derivation with limited amounts of data. When more complete data
sets are available encompassing sufficient concentration and duration information, then a
categorical regression approach is used to combine the data from different studies and derive the
ARE. The ARE methodology uses categorical regression data from many studies. Data are
grouped into categories such as no-observed-adverse effects, adverse effects, or frank effects.
No-observed-adverse effects and adverse effects have been defined previously. Frank effects are
those effects occurring at levels that produce frankly apparent and very severe effects, such as
irreversible functional impairment or mortality. Effects data from different experiments,
different animals, and different endpoints may be plotted and regressed by category across
exposure duration. All the ARE methods sacrifice some certainty. The categorical regression
procedure holds the most promise to determine dose-response across various durations of
exposure. As a longer-term need, an adaptation of this method or other methods should be
developed to reduce uncertainty while still allowing development of dose-response assessments
across a duration of exposure.
The magnitude of response to a toxic chemical exposure is often dependent on both the
concentration and the duration of the exposure. The response has been related to their product
with an assumption that their product is a constant (a linear assumption). A significant number
of RfCs, which are assessments of chronic noncancer effects, are based on subchronic studies in
animals with no knowledge of whether a linear relationship exists between the toxic response at
greater exposure (considering concentration and duration) and that at lower exposure.
Operationally, this lack of understanding is usually accounted for by use of a 10-fold uncertainty
factor. Over the longer term, an understanding is needed of the appropriate response metrics
(e.g., peak height, area under the curve, peak duration, and frequency of response) to help guide
the use of data in developing dose-response assessments of less than chronic exposure durations.
Advances in cancer research leading to proposed changes in EPA's guidelines for cancer
risk assessment (U.S. EPA, 1996) have necessitated an improved knowledge of mode of action.
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To develop cancer unit risk estimates under the new guidelines, we will have to understand the
binding and repair of exogenous agents to DNA on (1) cancer induction, receptor-mediated
mechanisms of action, and (2) mechanisms of toxicant interference with critical cellular
pathways such as signal transduction and receptors involved in cell growth. Gaps in our
knowledge of mode of action as it relates to human susceptibility also present significant
uncertainty in cancer and noncancer dose-response assessments. The National Research Council
has recognized that with respect to cancer, EPA does not account for person-to-person variations
in susceptibility. Factors such as carcinogen metabolism, DNA-adduct formation, DNA-repair
rate, synergistic effects of carcinogens, and age may contribute to different modes of action that
influence susceptibility to cancer. Research is needed over the longer term to understand the
effects of receptor mediation on dose response of toxic chemicals and to model the interaction of
environmental chemicals with receptors. In addition, the susceptibility of humans should be
compared to human epidemiological and animal toxicological data to validate the assumption of
similar susceptibility. Modes of action responsible for increased susceptibility of certain
subpopulations (e.g., children, elderly, asthmatics) should be identified and described over the
longer term in order to reduce uncertainty in dose-response assessments.
EPA Activities: Some work is ongoing to develop methods for combining data. We are
using a meta analysis technique to combine data for health assessments when the available data
are directed toward the same endpoint. We have conducted some preliminary research on the use
of Bayesian statistics as a way of combining studies to develop a confidence profile around
parameters such as a NOAEL. Such a synthesis of data incorporates the uncertainty of parameter
estimates and provides visual display of distribution about a central point. Uncertainties in dose-
response assessments are also being reduced by research which incorporates mechanistic data.
We are also studying a class of chemicals with a common mode of action, endocrine disrupters,
which bind to androgenic receptors for reproductive or developmental endpoints in order to
determine cumulative risk for multiple chemicals within the same mode-of-action class.
We have several activities which are integral to reducing uncertainty in RfCs and cancer
unit risk estimates. Physiologically based pharmacokinetic (PBPK) models for priority HAP
(e.g., trichloroethylene and MTBE as shorter-term examples) which permit improved estimation
of target tissue concentrations of compounds needed for derivation of RfCs are being developed.
A long-term research activity is the development of improved pulmonary dosimetry models for
gases and particles. Uptake efficiency data in the upper and lower respiratory tract of nonhuman
primates and rodents, which will permit calculation of mass transfer coefficients for certain types
of gases, are being gathered. We are compiling a guidance document for use in interspecies
adjustments and incorporation of mode of action data that would facilitate development of oral
and inhalation cancer and noncancer dose-response assessments. Use of this guide is expected to
result in improved risk assessments. We are also developing a more precise model of the
regional deposited dose ratio (RDDR) for particles of large and small mass medium aerodynamic
diameters. The original model is being altered such that deposition estimates from the existing
RDDR model will be based on the ICRP66 model structure with modifications of rate and
parameter values as necessary after evaluation and application of new data. This new lung
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dosimetry model is being developed to improve precision of dose-response assessments of
particles and will soon be available as a software product. We are also upgrading the RDDR
model to contain a module for human ventilation activity patterns. Ventilation rates as a function
of oro-nasal switching patterns and activity patterns in children are being compared to the
patterns in adults to determine susceptibility of children to particle deposition. This work is
being conducted in cooperation with the University of North Carolina. New information on
particle emission, transport, exposure assessment, and biological mechanisms will be of great
value to the urban air toxics research program.
We are conducting some preliminary explorations into statistical methods to develop
probabilistic dose-response assessments. Categorical regression is a mathematical tool that can
be used to estimate health risk from chemical exposures. Ordered categories of toxics severity or
pathological staging can be regressed on exposure-dose to estimate the likelihood of observing
any of the categories of severity at any dose level. These estimates can be in the form of
incidence. Preliminary work on the toxiciry of aldicarb has invoked such a procedure and
determined a 0.1 percent probability (risk level) of adverse effects at a dose 10-fold higher than
the aldicarb RfD. We have also undertaken a small amount of initial work regarding the
application of Bayesian statistics to determining risk above a reference level. Building upon
limited Bayesian approaches for estimating dose-response assessments for a single effect,
Bayesian statistics have been used to estimate the probability of adverse effects for aldicarb and
toluene. The Bayesian approach was used to develop distributions of effects from different
sources and then combine these distributions into a single distribution that could be used to
provide probability of a given severity of effect at various exposure-doses. Probabilistic dose-
response assessments will likely require longer-term research.
Current research in the area of dose-response assessments for acute exposures includes
the determination of the effects of the categorical regression model on derived dose-response
assessment estimation versus the role of the data. It is important that the available data drive the
shape of the regression line and not the mathematical model itself. Idealized data sets are being
used to further understand this uncertain aspect of categorical regression of lexicological data. In
vivo uptake experiments in animals and humans and generic PBPK models for central nervous
system (CNS) effects are being studied to determine the magnitude and appropriateness of
performing an interspecies dosimetric adjustment for high exposure concentrations at short
durations. An additional activity is the development of a framework for utilizing data from a
standard acute database previously developed to derive ARE values, bring them to external peer
review followed by Agency consensus review, and finally incorporate them in IRIS. Categorical
regression software that facilitates ARE value development is also being developed. Usable
forms of the ARE methodology will be realized over the shorter term.
We are also conducting research to determine the most appropriate metric for quantifying
toxicity from acute exposures. Given that concentration multiplied by time is often not linear,
other relationships defining toxicity are being sought. Using endpoints of neurotoxicity and
reproductive/developmental toxicity, we are exploring the relevancy of metrics such as peak
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height, area under the curve, peak duration, and frequency of response as better predictors of
dose-response relationships.
6.3 Risk Assessment/Characterization
After an exposure assessment and a dose-response assessment are completed, it is
necessary to combine them into a clear and useful characterization of risk. This section addresses
the need to improve risk assessments of chemical mixtures and also the need for better risk
communication.
Need 10: Improved risk assessment methods for mixtures
Description: It is possible that the combined exposures to multiple pollutants may
produce synergistic or antagonistic effects; effects either more detrimental or less detrimental
than exposure to each pollutant individually. Recent epidemiological evidence indicates
associations between air pollution and increased illness and death in humans are unlikely to be
the result of exposure to a single compound. Rather, exposure to a mixture of pollutants
including tropospheric ozone, PM, and other constituents such as HAP, seems to be correlated
with adverse effects. There are, however, significant gaps in methods, models, and data that
influence the evaluation of the risk to public health from air pollution mixtures. Research is
needed on methods of extrapolation from toxicity information about one or more complex
mixtures of air pollutants to others. Determination of toxic equivalency factors (TEF) is one
approach to gaining information about the toxicity of several compounds within a mixture. More
TEF information on mixture components such as polyorganic matter is needed for urban
assessments. Short-term toxicity tests of actual mixtures, if performed systematically, would
provide information that could be used for priority-setting and risk management.
Other longer-term work that would aid the risk assessment of mixtures is atmospheric
fate and dose-response information on mixtures. This should include basic work on chemical
characteristics and transformation factors which may affect urban HAP transformation and
dispersion in air and other media (e.g., chemical half-life, transformation rates, chemical partition
information). Longer-term information is needed concerning the antagonistic, synergistic, or
additive nature of risks associated with the components of various mixtures. This kind of
information will be useful to EPA as it moves toward enhancing its ability to evaluate cumulative
risks. The needs of the urban air toxics program should influence the priority selection of
chemicals for which binary and higher order interaction data are developed.
EPA Activities: We are presently developing a strategy to conduct laboratory and
clinical studies to identify and quantify the effects associated with exposures to typical mixtures
of pollutants in urban areas of the U.S. Particulate matter, ozone and HAP are the primary
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pollutants of interest, and the endpoints of interest include both carcinogenicity and noncancer
effects, particularly respiratory and immune system responses.
Though resources committed to mixtures research are comparatively small, EPA
maintains a mixtures database to help in the development of risk assessments involving more
than one chemical. A pilot upgrade of the MDCTOX database is under way. This database is an
interaction-based hazard index which can be used to incorporate chemical interactions into risk
assessments for mixtures. The MDCTOX database on interactions is available as an easily-used
computer program. The current version is years out of date, and the revision project is to
establish a priority list of chemical pairs based on their potential interaction and toxicity.
Detailed interaction profiles on these priority pairs are being developed. After the revision is
complete, a new set of 20 priority chemicals or pairs will be selected and binary mixture
interactions data will be gathered, evaluated for binary weight-of-evidence determinations, and
entered into the database. Finally, we will update the profiles for 50 more chemicals to be
included in the database.
In addition, our original Mixtures Guidelines (U.S. EPA, 1986) are being revised and
provide a good first step toward the evaluation and assessment of mixtures. This mixtures risk
guidance document includes several methods for addressing different types of data, from whole
mixture dose-response data to in vitro toxicity data on individual component chemicals. The risk
methods include mathematical models for well-understood interactions as well as decision
frameworks for handling sparse and qualitative data.
We are studying mode of action for cancer to include receptor-mediated toxicity in
humans and model laboratory animals. Research will include studies of polycyclic aromatic
hydrocarbons present in urban environments to assess application of the structure-activity-based
TEF approach as has been applied to dioxin-like compounds (U.S. EPA, 1989). Future
comparative potency research will examine utility of TEF methods to predict biochemical and
toxicological responses in animal models to assess potential human health risks.
Need 11: Development of better information for more effective techniques for
communicating the results of health risk assessments for urban HAP
Description: The results of health risk assessments for urban HAP should be
communicated effectively to those participating in the policy-making process and to various
members of the public who may not have technical or scientific backgrounds. For example, the
general public needs to be provided with information and the tools to protect their families and
communities from exposure to air toxics. Unless a common understanding on the meaning of the
assessments is reached between scientists preparing the assessments and persons using the
assessments to affect policy, the overall process of risk assessment/risk management may be
defeated, sometimes with costly consequences. There are many ideas that can be explored. For
example, near real-time measurement, reporting, and access to air toxics ambient air
concentrations, together with the actual monitored or modeled data, the estimated risk of health
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effects, and the tools for interpreting this information, could be provided to communities
throughout the Nation by use of the Internet. Communication of the science to these audiences,
however, can pose challenges requiring the development of new scientific information.
Various approaches can be investigated, including: 1) adaption and refinement of state-
of-the-art techniques for visualizing air toxics information and evaluating the utility of these
techniques for communicating the information to various stakeholders, including the scientific
community, regulators, and the public; and 2) development of mechanisms to deliver air toxics
information in a timely and easily accessible format (e.g., through the Internet, over radio and
television, in the newspaper). Local or regional maps could be provided through the Internet
with color-coded air toxics concentrations to match predetermined indices of hazard. In keeping
with the Environmental Monitoring for Public Access and Community Tracking (EMPACT)
initiative, these risk communication activities should begin over the shorter term.
EPA Activities: We have developed a pollutant standard index (PSI) for ozone. Time-
relevant air quality data are provided in an easily accessible and understandable format to the
general public for their use in decisionmaking. The approach uses existing air quality monitoring
and telemetry technology coupled with the latest Internet technology to provide time-relevant
data to the public. This project is intended to expand mapping capabilities for ozone, PM, and
air toxics to cover 85 cities across the U.S. Ongoing and completed work includes development
of a new ozone PSI format, development of more descriptive ozone health effects messages that
can be linked to a map on the Internet, and development of hard copy health effects pamphlets
for environmental protection offices (more technical) and doctors' offices (less technical). We
may also conduct focus groups to determine whether the most effective process is being used on
the Internet and in print to communicate the risks of ozone exposure. Expansion of this approach
to air toxics would provide beneficial risk communications to the public and risk managers.
6.4 Risk Management
Engineering information is needed on emissions and emissions reductions over time to
support the application of regulatory strategies and compliance programs to achieve HAP
emissions reductions. The expanded focus on risk-based activities must be supported by the
development of improved risk management tools and information, hi large measure, the needs
for improved emissions information to support risk management are the same as those discussed
under Needs 1 - 5 to support the risk assessment process.
Need 12: Identification of processes contributing to the HAP emissions from area
source categories, and listing of control options and pollution prevention (P2)
alternatives for these processes
Description: Area source categories considered for regulation under section 112(k) also
require technology-based controls, such as GACT standards. More detailed knowledge of the
area sources and their emission-producing processes is needed to identify appropriate control
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technologies and pollution prevention options. This is a short-term task. To identify applicable
control options, it is necessary to identify the processes that produce the HAP emissions.
EPA Activities: Our ongoing pollution prevention (P2) research activities are centered
on the identification, evaluation, and demonstration of source reduction options for industrial and
commercial surface coating and cleaning operations. Planned activities for FY99 include
establishment of an in-house laboratory for testing of low-VOC, low-HAP coating alternatives,
demonstration of P2 techniques for autobody refmishing operations, and coating/cleaning
research for other metal and plastic substrates. We also maintain software tools showing
information on P2 techniques for use by industry, academia, and the regulatory community.
Pollution prevention research areas have included office equipment, aerosol consumer
products, textile products, engineered wood products, and conversion varnishes used on wood
products. In addition, we have focused on the application of P2 techniques for the improvement
of indoor air quality. For example, we have developed a model for analyzing the impact of
sources, sinks, ventilation, and air cleaners on indoor air quality. We have studied emissions
from various combustion sources, including hazardous waste incineration in boilers, rotary kilns,
and other combustors such as municipal waste combustion. The MWC) program supports the
development of revised rules for air pollutant emissions from the MWC source category and
performs basic research on MWC pollutant formation and control mechanisms for acid gas, trace
organic, and trace metal emissions. It also supports field tests, regulation development, and
laboratory research for medical waste incinerators (MWI). Much of the MWC regulatory support
effort has involved the development of good combustion practices and field evaluations of the
performance of air pollution control systems. Additional research has focused on the collection
of experimental data and a statistical approach to determine the effect of combustion- and
sorbent-injection-related parameters on the mechanism of polychlorinated dibenzo-p-dioxin and
polychlorinated dibenzofuran (PCDD and PCDF) formation and prevention in waste combustors.
We have also conducted analyses of the products of incomplete combustion of agricultural
plastic, as well as the open burning of household waste in barrels.
In a broader perspective, many P2 research opportunities are cross-cutting. Multimedia
issues arise with common problems requiring a systems approach. This is why P2 research in the
development of tools and technologies for Life Cycle Analysis (LCA), process simulation, P2
measurement, P2 technology, systems integration, cost effectiveness, environmental impact,
cleaner production design, and generic decision-making tools for reducing risks fit within and cut
across all categories.
Need 13: Identification of pollution prevention alternatives for HAP emissions from
mobile sources
Description: Because P2 has been very broadly defined by the Federal Government,
many environmental quality and related transportation system management options fit within its
scope. Some areas may require an interdisciplinary approach, including emissions control
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experts, transportation system experts, economists and behavioral science specialists. Some P2
strategies relate to the actual reduction of emissions, including HAP emissions, from motor
vehicles, while others relate to changes in the transportation system infrastructure that will in
turn, effect emissions reductions.
EPA Activities: We are involved in a number of activities addressing cleaner fuels and
vehicles:
Partnership for a New Generation of Vehicles (PNGV) a joint industry-government
research and development agreement to develop a vehicle with three times the fuel
efficiency of today's family sedan without sacrificing size, performance, cost, safety, or
emissions. As an active partner in PNGV, EPA's interest in high-efficiency vehicles
includes efforts to ensure low criteria emissions as well as reduced fuel use and low
carbon dioxide..
Development of technology for clean and efficient engines which operate on renewable
alcohol fuels and promotion of the use of advanced technology and emission control
equipment to improve air quality.
Development and evaluation of after-treatment technology to reduce emissions from
diesel engines (particularly to reduce PM [soot], NOx, and sulfur emissions). EPA also
plans to test different diesel fuel formulations to reduce emissions.
6.5 References
Byun, D.W., Ching, J.K.S., Novak, J., and Young, J. 1998. Development and Implementation of
the EPA's Models-3 Initial Operating Version: Community Multi-scale Air Quality
(CMAQ) Model. In: Air Pollution Modeling and Its Application XII, ed. S.E. Gryning
and N. Chaumerliac, Plenum Publishing Corp.
Davis, J.M., Jarabek, A.M., Mage, D.T., and Graham, J.A. 1998. The EPA Health Risk
Assessment of Methylcyclopentadienyl Manganese Tricarbonyl (MMT), Risk Analysis
18: 57-70.
U.S. EPA. 1986. Guidelines for the Health Risk Assessment of Chemical Mixtures. Federal
Register 51(185): 34014-34025.
U.S. EPA. 1989. Interim Procedures for Estimating Risks Associated with Exposures to
Mixtures of Chlorinated Dibenzo-p-dioxins and Dibenzofurans (CDDs and CDFs) and
1989 Update. Washington, DC: Risk Assessment Forum, Office of Research and
Development; EPA/625/3-89/016.
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U.S. EPA. 1993. Motor Vehicle-Related Air Toxics Study. Office of Mobile Sources. EPA-
420/R-93-005. Ann Arbor, MI. April.
U.S. EPA. 1994a. Methods for Exposure-Response Analysis and Health Assessment for Acute
Inhalation Exposure to Chemicals: Development of the Acute Reference Exposure.
Draft Working Paper. Research Triangle Park, NC: Office of Health and Environmental
Assessment.
U.S. EPA. 1994b. Reevaluation of Inhalation Health Risks Associated with Methylcyclopenta-
dienyl Manganese Tricarbonyl (MMT) in Gasoline. Office of Research and
Development, EPA/600/R-94/062
U.S. EPA. 1995. The Use of the Benchmark Dose Approach in Health Risk Assessment.
Washington, DC: Risk Assessment Forum, Office of Research and Development;
EPA/630/R-94/007.
U.S. EPA. 1996. Proposed Guidelines for Carcinogen Risk Assessment. Federal Register
61(79): 17960-18011.
U.S. EPA. 1997. Mercury Study Report to Congress, Vols. I-VDI, EPA-452/R-97-003 through
EPA-452/r-97-010, Washington, D.C.
U.S. EPA. 1998. Study of Hazardous Air Pollutant Emissions from Electric Utility/Steam
Generating Units-Final Report to Congress, EPA-453/R-98-004a and b, Washington,
D.C.
U.S. EPA. 1999a. Estimation of Motor Vehicle Toxic Emissions and Exposure in Selected
Urban Areas, Office of Mobile Sources, Ann Arbor, MI, Report No. EPA 420-D-99-002,
March 1999.
U.S. EPA. 1999b. National Air Toxics Program: The Integrated Urban Strategy; Notice.
Federal Register 64(137): 38705-38740.
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Appendix
HAP Profiles
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OVERVIEW
This Appendix includes fact sheets (or profiles) for each of the 33 urban hazardous air
pollutants (HAP). As discussed in Chapter 3 of this Report, these were identified in the Strategy
as posing the greatest threat to public health in the largest number of urban areas. The fact sheets
for these HAP are arranged in alphabetical order, and each one provides the following
information:
A brief hazard summary;
Various physical properties (e.g., chemical formula, molecular weight, vapor pressure);
Uses (e.g., in manufacturing processes, products, etc.);
Sources and potential for exposure;
How personal exposure can be assessed;
Information on health hazards, including
acute effects,
chronic effects (noncancer),
reproductive/developmental effects,
cancer risks, and
a summary of human health reference values and regulatory and advisory
numbers; and
References.
The main sources of information for the fact sheets include EPA's Integrated Risk
Information System (IRIS), Toxicological Profiles from the Agency for Toxic Substances and
Disease Registry (ATSDR), EPA's Health Effects Assessment documents and International
Agency for Research on Cancer (IARC) monographs, as available. The actual sources for each
fact sheet are listed on the sheet. The summary of human health reference values and regulatory
and advisory numbers includes values developed by EPA and by ATSDR, the California EPA
(CalEPA), the American Conference of Governmental and Industrial Hygienists (ACGIH), the
American Industrial Hygiene Association (AIHA), the National Institute of Occupational Safety
and Health (NIOSH), and the Occupational Safety and Health Administration (OSHA).
Each fact sheet includes definitions of the acronyms used within the fact sheet, with the
exception of the abbreviations for units of measurement (and Hg) listed below.
°C: degrees Centigrade m3: meters cubed
°F: degrees Farenheit mL: milliliter
d: day mm: millimeter
dL: deciliter mg: milligram
g: gram ng: nanogram
h: hour ppb: parts per billion
Hg: mercury ppm: parts per million
kg: kilogram fj,g: microgram
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ACETALDEHYDE
75-07-0
Hazard Summary
Acetaldehyde is mainly used as an intermediate in the synthesis of other chemicals. It is
ubiquitous in the environment and may be formed in the body from the breakdown of
ethanol. Acute (short-term) exposure to acetaldehyde results in effects including irritation
of the eyes, skin, and respiratory tract. Symptoms of chronic (long-term) intoxication of
acetaldehyde resemble those of alcoholism. The U.S. Environmental Protection Agency
(EPA) considers acetaldehyde a probable human carcinogen (Group B2) based on
inadequate human cancer studies and animal studies that have shown nasal tumors in rats
and laryngeal tumors in hamsters.
Please Note: The main sources of information for this fact sheet are EPA's Health Assessment Document for
Acetaldehyde and the Integrated Risk Information System (IRIS), which contains information on inhalation chronic
toxicity of acetaldehyde and the reference concentration (RfC). Other secondary sources include the International
Agency for Research on Cancer (IARC) Monographs on Chemicals Carcinogenic to Humans.
Physical Properties
The chemical formula for acetaldehyde is CH3CHO, and it has a molecular weight of
44.06 g/mol. (1)
Acetaldehyde is a colorless mobile liquid that is flammable and miscible with water. (1,6)
Acetaldehyde has a pungent suffocating odor, but at dilute concentrations, it has a fruity
and pleasant odor. The odor threshold of acetaldehyde is 0.05 ppm (0.09 mg/m3). (1,7)
The vapor pressure for acetaldehyde is 740 mm Hg at 20 °C, and it has a log
octanol/water partition coefficient (log Kow) of 0.43. (1)
Uses
The predominant use of acetaldehyde is as an intermediate in the synthesis of other
chemicals. (1)
Acetaldehyde is used in the production of perfumes, polyester resins, and basic dyes.
Acetaldehyde is also used as a fruit and fish preservative, as a flavoring agent, and as a
denaturant for alcohol, in fuel compositions, for hardening gelatin, and as a solvent in the
rubber, tanning, and paper industries. (1,2)
Sources and Potential Exposure
Acetaldehyde is ubiquitous in the ambient environment. It is an intermediate product of
higher plant respiration and is formed as a product of incomplete wood combustion in
fireplaces and wood stoves, coffee roasting, burning of tobacco, vehicle exhaust fumes,
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and coal refining and waste processing. Hence, many individuals are exposed to
acetaldehyde by breathing ambient air. It should be noted that residential fireplaces and
wood stoves are the two highest sources of emissions, followed by various industrial
emissions. (1)
In Los Angeles, California, levels of acetaldehyde up to 32 ppb have been measured in
the ambient environment. (1)
Exposure may also occur in individuals occupationally exposed to acetaldehyde during its
manufacture and use. (1,2)
In addition, acetaldehyde is formed in the body from the breakdown of ethanol; this
would be a source of acetaldehyde among those who consume alcoholic beverages. (1)
Assessing Personal Exposure
No information was located regarding the measurement of personal exposure to
acetaldehyde.
Health Hazard Information
Acute Effects:
The primary acute effect of inhalation exposure to acetaldehyde is irritation of the eyes,
skin, and respiratory tract in humans. At higher exposure levels, erythema, coughing,
pulmonary edema, and necrosis may also occur and, at extremely high concentrations,
respiratory paralysis and death may occur. (1)
Acute inhalation of acetaldehyde resulted in a depressed respiratory rate and elevated
blood pressure in experimental animals. (1)
Tests involving acute exposure of animals, such as the LC50 and LD50 tests in rats, rabbits,
and hamsters, have demonstrated acetaldehyde to have low acute toxicity from inhalation
and moderate acute toxicity from oral or dermal exposure. (3)
Chronic Effects (Noncancer):
In hamsters, chronic inhalation exposure to acetaldehyde has produced changes in the
nasal mucosa and trachea, growth retardation, slight anemia, and increased kidney weight.
(1,4)
Symptoms of chronic intoxication of acetaldehyde in humans resemble those of.
alcoholism. (5)
The RfC for acetaldehyde is 0.009 mg/m3 based on degeneration of olfactory epithelium
in rats. The RfC is an estimate (with uncertainty spanning perhaps an order of magnitude)
of a continuous inhalation exposure to the human population (including sensitive
subgroups), that is likely to be without appreciable risk of deleterious noncancer effects
during a lifetime. It is not a direct estimator of risk, but rather a reference point to gauge
the potential effects. At exposures increasingly greater than the RfC, the potential for
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adverse health effects increases. Lifetime exposure above the RfC does not imply that an
adverse health effect would necessarily occur. (4)
EPA has medium confidence in the principal studies because appropriate histopathology
was performed on an adequate number of animals and a no-observed-adverse-effect level
(NOAEL) and a lowest-observed-adverse-effect level (LOAEL) were identified, but the
exposure duration was short and only one species was tested; low confidence in the
database due to the lack of chronic data establishing NOAELs and due to the lack of
reproductive and developmental toxicity data; and, consequently, low confidence in the
RfC. (4)
EPA has not established a reference dose (RfD) for acetaldehyde. (4)
Reproductive/Developmental Effects:
No information is available on the reproductive or developmental effects of acetaldehyde
in humans.
Acetaldehyde has been shown, in animals, to cross the placenta to the fetus. (1,4)
Data from animal studies suggest that acetaldehyde may be a potential developmental
toxin. In one study, a high incidence of embryonic resorptions was observed in mice
injected with acetaldehyde. In rats exposed to acetaldehyde by injection, skeletal
malformations, reduced birth weight, and increased postnatal mortality have been
reported. (1,6)
Cancer Risk:
Human data regarding the carcinogenic effects of acetaldehyde are inadequate. Only one
epidemiology study is available that has several limitations including short duration,
small number of subjects, and concurrent exposure to other chemicals and cigarettes.
(1,4,6)
Increased incidences of nasal tumors in rats and laryngeal tumors in hamsters have been
observed following inhalation exposure to acetaldehyde. (1,4,6)
EPA has classified acetaldehyde as a Group B2, probable human carcinogen. (1,4)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk of 2.2 x 10"6 (^g/m3)'1.
EPA estimates that, if an individual were to continuously breathe air containing
acetaldehyde at an average of 0.5 /ng/m3 (5 x 10"4 mg/m3) over his or her entire lifetime,
that person would theoretically have no more than a one-in-a-million increased chance of
developing cancer as a direct result of breathing air containing this chemical. Similarly,
EPA estimates that breathing air containing 5.0 /ig/rn3 (5 x 10"3 mg/m3) would result in
not greater than a one-in-a-hundred thousand increased chance of developing cancer, and
air containing 50.0 /ig/m3 (5 x 10"2 mg/m3) would result in not greater than a one-in-ten
thousand increased chance of developing cancer. For a detailed discussion of confidence
in the potency estimates, please see IRIS. (4)
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Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For acetaldehyde: 1 ppm = 1.8 mg/m3.
To convert from fig/m3 to mg/m3: mg/m3 = (fig/m3) x (1 mg/1,000 fig).
Health Data from Inhalation Exposure
Aoetddehyde
100000
Reguldory, advisory
numbers"
Hedth numbers
LC50 (rets) 07.000 m^m
LGSOOxmsters) (17,000 mg'm3)
NCSHIDLH(3600nngfiTf)
(resprctcr
NO<\ELc(resprctcry)
G8HAPELC360mgfrnrf)
A33Haaling
R(C
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exposed up to one hour without experiencing or developing irreversible or other serious health
effects that could impair their abilities to take protective action.
ACGIH TLV ceiling - American Conference of Governmental and Industrial Hygienists'
threshold limit value ceiling; the concentration of a substance that should not be exceeded during
any part of the working exposure.
LCgo (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health limit; NIOSH recommended exposure limit to ensure that a worker can escape
from an exposure condition that is likely to cause death or immediate or delayed permanent
adverse health effects or prevent escape from the environment.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health Numbers are lexicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL and NOAEL are from the critical study used as the basis for the EPA RfC.
References
1. U.S. Environmental Protection Agency (EPA). Health Assessment Document for
Acetaldehyde. EPA/600/8-86-015A. Environmental Criteria and Assessment Office,
Office of Health and Environmental Assessment, Office of Research and Development,
Research Triangle Park, NC. 1987.
2. M. Sittig. Handbook of Toxic and Hazardous Chemicals and Carcinogens. 2nd ed. Noyes
Publications, Park Ridge, NJ. 1985.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Acetaldehyde. National Center for Environmental Assessment, Office of Research and
Development, Washington, D.C. 1999.
5. The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S.
Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
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6. International Agency for Research on Cancer (IARC). IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Humans: Ally I Compounds,
Aldehydes, Epoxides and Peroxides. Volume 36. World Health Organization, Lyon. 1985.
7. I.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds
compared with threshold limit values and volatilities for 214 industrial chemicals in air
and water dilution. Journal of Applied Toxicology, 3(6):272-290. 1983.
8. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
9. Occupational Safety and Health Administration (OSHA). Occupational Safety and Health
Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29 CFR
1910.1000. 1998.
10. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
11. American Industrial Hygiene Association (AIHA). The AIHA 1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.
1998.
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ACROLEIN
107-02-8
Hazard Summary
Acrolein is primarily used as an intermediate in the manufacture of acrylic acid. It can be
formed from the breakdown of certain pollutants in outdoor air or from burning tobacco
or gasoline. It is extremely toxic to humans from inhalation and dermal exposure. Acute
(short-term) inhalation exposure may result in upper respiratory tract irritation and
congestion. No information is available on its reproductive, developmental, or
carcinogenic effects in humans. The animal cancer data are limited, with one study
reporting an increased incidence of adrenocortical tumors in rats exposed to acrolein in
the drinking water. The U.S. Environmental Protection Agency (EPA) considers acrolein
a possible human carcinogen (Group C).
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on inhalation chronic toxicity of acrolein and the reference concentration (RfC),
and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for Acrolein.
Physical Properties
Acrolein is a water-white or yellow liquid that burns easily and is easily volatilized. (1)
Acrolein has a disagreeable odor and an odor threshold of 0.2 ppm. (1,8)
The chemical formula for acrolein is C3H4O and the molecular weight is 56.06 g/mol. (1)
The vapor pressure for acrolein is 220 mm Hg at 20 °C, and its log octanol/water
partition coefficient (log Kow) is -0.01. (1)
Uses
The largest use for acrolein is as an intermediate in the manufacture of acrylic acid. (1)
Sources and Potential Exposure
Acrolein can be formed from the breakdown of certain pollutants found in outdoor air,
from burning tobacco, or from burning gasoline. (1)
Airborne exposure to acrolein may occur from breathing contaminated air, from smoking
tobacco or proximity to someone who is smoking, or from being near automobiles or oil
or coal power plants. In several large cities, acrolein has been measured at 9 ppb. (1)
Occupational exposure to acrolein could occur in industries that-use acrolein to make
other chemicals. (1)
Small amounts of acrolein may be found in some foods, such as fried foods, cooking oils,
and roasted coffee. (1)
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Acrolein has not been detected in drinking water and is not commonly found in surface
water. (1)
Assessing Personal Exposure
There are currently no tests available to determine personal exposure to acrolein. (1)
Health Hazard Information
Acute Effects:
Acute inhalation exposure to high levels (10 ppm) of acrolein in humans may result in
death. Effects on the lung, such as upper respiratory tract irritation and congestion, have
been noted at acrolein levels ranging from 0.17 ppm to 0.43 ppm. (1-3)
Acrolein is considered to have high acute toxicity, based on short-term animal tests such
as the LC50 test in rats. (1,4)
Chronic Effects (Noncancer):
The major effects from chronic (long-term) inhalation exposure to acrolein in humans
consist of general respiratory congestion and eye, nose, and throat irritation. (1,2,5)
Acrolein is a strong dermal irritant, causing skin burns in humans. (1,2,5)
Animal studies have reported that the respiratory system is the major target organ for
acrolein toxicity. (1,2,5)
The RfC for acrolein is 0.00002 mg/m3 based on squamous metaplasia and neutrophilic
infiltration of nasal epithelium in rats. The RfC is an estimate (with uncertainty spanning
perhaps an order of magnitude) of a continuous inhalation exposure to the human
population (including sensitive subgroups) that is likely to be without appreciable risk of
deleterious noncancer effects during a lifetime. It is not a direct estimator of risk but
rather a reference point to gauge the potential effects. At exposures increasingly greater
than the RfC, the potential for adverse health effects increases. Lifetime exposure above
the RfC does not imply that an adverse health effect would necessarily occur. (3)
EPA has high confidence in the studies on which the RfC was based because adequate
numbers of animals were used, careful attention was paid to experimental protocol, and
together they demonstrated a consistent profile of histopathological changes in the
respiratory system; low to medium confidence in the database due to the lack of chronic
data and adequately conducted reproductive or developmental studies; and, consequently,
medium confidence in the RfC.
EPA has not established a reference dose (RfD) for acrolein. (3)
EPA has calculated a provisional RfD of 0.02 mg/kg/d for acrolein. The provisional RfD
is a value that has had some form of Agency review, but it does not appear on IRIS. The
EPA announced recently (January 12, 2000,65 FR 1863) its plan to conduct an IRIS
health assessment for acrolein to be completed by FY 2002. (6)
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Reproductive/Developmental Effects:
No information is available on the reproductive or developmental effects of acrolein in
humans. (1)
In the one available reproductive animal study, rats were exposed to acrolein by
inhalation, with no effects observed on the number of pregnancies or the number and
weights of the fetuses. (1)
Acrolein has been reported to cause birth defects in rats when injected directly into the
embryonic tissue. (1)
Cancer Risk:
No information is available on the carcinogenic effects of acrolein in humans. (1,3)
Limited animal cancer data are available; one inhalation study in rats reported no
evidence of tumors in the respiratory tract or in other tissues and organs, while another
study reported an increased incidence of adrenocortical tumors in female rats exposed to
acrolein in drinking water. (1,3)
EPA has classified acrolein as a Group C, possible human carcinogen, based on limited
evidence of carcinogenicity in animals, the structural similarity of acrolein to substances
possibly carcinogenic to humans, the carcinogenic potential of one of its metabolites, and
the lack of human data. (3)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For acrolein: 1 ppm = 2.29 mg/m3.
To convert from {ig/m3 to mg/m3: mg/m3 = (fJLg/m3) x (1 mg/1,000 fig).
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Health Data from Inhalation Exposure
Aaolen
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100
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exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-effect level.
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health limit; NIOSH recommended exposure limit to ensure that a worker can escape
from an exposure condition that is likely to cause death or immediate or delayed permanent
adverse health effects or prevent escape from the environment.
NIOSH REL - NIOSH's recommended exposure limit; NIOSH recommended exposure limit for
an 8- or 10-h time-weighted average exposure and/or ceiling.
NIOSH STEL - NIOSH's short term exposure limit; NIOSH recommended exposure limit for a
15-minute period.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h work week.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c This LOAEL is from the critical study used as the basis for the EPA RfC.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Acrolein. Public Health Service, U.S. Department of Health and Human Services,
Atlanta, GA. 1990.
2. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National
Library of Medicine, Bethesda, MD. 1993.
3. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Acrolein. National Center for Environmental Assessment, Office of Research and
Development, Washington, D.C. 1999.
4. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
5. E.J. Calabrese and E.M. Kenyon. Air Toxics and Risk Assessment. Lewis Publishers,
Chelsea, MI. 1991.
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6. U.S. Environmental Protection Agency (EPA). Health Effects Assessment Summary
Tables. FY1997 Update. Solid Waste and Emergency Response, Office of Emergency
and Remedial Response, Cincinnati, OH. EPA/540/R-97-036. 1997.
7. I.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds
compared with threshold limit values and volatilities for 214 industrial chemicals in air
and water dilution. Journal of Applied Toxicology 3(6):272-290. 1983.
8. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
9. Occupational Safety and Health Administration (OSHA). Occupational Safety and Health
Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29 CFR
1910.1000. 1998.
10. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
11. American Industrial Hygiene Association (AIHA). The AIHA 1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook
1998.
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ACRYLONITRILE
107-13-1
Hazard Summary
Exposure to acrylonitrile is primarily occupational: it is used in the manufacture of acrylic
acid and modacrylic fibers. Acute (short-term) exposure of workers to acrylonitrile has
been observed to cause mucous membrane irritation, headaches, dizziness, and nausea.
No information is available on the reproductive or developmental effects of acrylonitrile
in humans. Based on limited evidence in humans and evidence in rats, the U.S.
Environmental Protection Agency (EPA) has classified acrylonitrile as a probable human
carcinogen (Group Bl).
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on inhalation chronic toxicity of acrylonitrile and the reference concentration
(RfC) and the carcinogenic effects of acrylonitrile including the unit cancer risk for inhalation exposure, EPA's
Health Effects Assessment for Acrylonitrile, and the Agency for Toxic Substances and Disease Registry's
(ATSDR's) Toxicological Profile for Acrylonitrile.
Physical Properties
The chemical formula for acrylonitrile is C3H3N, and its molecular weight is 53.06 g/mol.
(1,8)
Acrylonitrile occurs as a colorless liquid that is soluble in water. (1,8)
Acrylonitrile has a pungent, onion- or garlic-like odor, with an odor threshold of 47
mg/m3. (1)
The vapor pressure for acrylonitrile is 100 mm Hg at 22.8 °C, and its log octanol/water
partition coefficient (log Kow) is -0.92. (1)
Uses
Acrylonitrile is primarily used in the manufacture of acrylic and modacrylic fibers. It is
also used as a raw material in the manufacture of plastics (acrylonitrile-butadiene-styrene
and styrene-acrylonitrile resins), adiponitrile, acrylamide, and nitrile rubbers and barrier
resins. (1,6)
Sources and Potential Exposure
Human exposure to acrylonitrile appears to be primarily occupational via inhalation. (1)
Acrylonitrile may be released to the ambient air during its manufacture and use. (1)
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Assessing Personal Exposure
Acrylonitrile can be detected in the blood to determine whether or not exposure has
occurred. Metabolites may be detected in the urine, but some breakdown products are not
specific to acrylonitrile. (1)
Health Hazard Information
Acute Effects:
Workers exposed via inhalation to high levels of acrylonitrile for less than an hour
experienced mucous membrane irritation, headaches, nausea, feelings of apprehension
and nervous irritability; low grade anemia, leukocytosis, kidney irritation, and mild
jaundice were also observed in the workers, with these effects subsiding with the ending
of exposure. Symptoms associated with acrylonitrile poisoning include limb weakness,
labored and irregular breathing, dizziness and impaired judgment, cyanosis, nausea,
collapse, and convulsions. (1-4)
A child died after being exposed to acrylonitrile by inhalation, suffering from respiratory
malfunction, lip cyanosis, and tachycardia before death. Several adults exposed to the
same concentration of acrylonitrile exhibited eye irritation, but no toxic effects. (1,4)
Acute dermal exposure may cause severe bums to the skin. (3)
Acute animal tests, such as the LC50 and LD50 tests in rats, mice, rabbits, and guinea pigs,
have demonstrated acrylonitrile to have high acute toxicity from inhalation and high to
extreme acute toxicity from oral or dermal exposure. (5)
Chronic Effects (Noncancer):
In one study, headaches, fatigue, nausea, and weakness were frequently reported in
chronically (long-term) exposed workers. (6)
In rats chronically exposed by inhalation, degenerative and inflammatory changes in the
respiratory epithelium of the nasal turbinates and effects on brain cells have been
observed. (1,4,6)
The RfC for acrylonitrile is 0.002 mg/m3 based on degeneration and inflammation of
nasal respiratory epithelium in rats. The RfC is an estimate (with uncertainty spanning
perhaps an order of magnitude) of a continuous inhalation exposure to the human
population (including sensitive subgroups) that is likely to be without appreciable risk of
deleterious noncancer effects during a lifetime. It is not a direct estimator of risk but
rather a reference point to gauge the potential effects. At exposures increasingly greater
than the RfC, the potential for adverse health effects increases. Lifetime exposure above
the RfC does not imply that an adverse health effect would necessarily occur. (4)
EPA has medium confidence in the study on which the RfC was based because, although
it was a well-conducted chronic study in an appropriate number of animals, it was
performed on only one species, did not identify a no-observed-adverse-effect level
(NOAEL), was confounded by the early sacrifice of rats with large mammary gland
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tumors and the target organ (nasal turbinates) was examined only at the end of the study
in relatively few animals; medium to low confidence in the database because of the lack
of chronic or subchronic inhalation data in a second species, the lack of reproductive data
by the inhalation route and the existence of an oral study showing reproductive effects;
and, consequently, medium to low confidence in the RfC. (4)
EPA has calculated a provisional reference dose (RfD) of 0.001 mg/kg/d for acrylonitrile
based on decreased sperm counts in mice. The provisional RfD is a value that has had
some form of Agency review, but it does not appear on IRIS. (7)
Reproductive/Developmental Effects:
No information is available on the reproductive or developmental effects of acrylonitrile
in humans.
Fetal malformations (including short tail, missing vertebrae, short trunk, omphalocele,
and hemivertebra) have been reported in rats exposed to acrylonitrile by inhalation. (1,4)
In mice orally exposed to acrylonitrile, degenerative changes in testicular tubules and
decreased sperm count were observed. (1)
Cancer Risk:
A statistically significant increase in the incidence of lung cancer has been reported in
several studies of chronically exposed workers. However, some of these studies contain
deficiencies such as lack of exposure information, short follow-up, and confounding
factors. (1,4,6,8)
In several studies, an increased incidence of tumors has been observed in rats exposed by
inhalation, drinking water, and gavage. Astrocytomas in the brain and spinal cord and
tumors of the Zymbal gland (in the ear canal) have been most frequently reported, as well
as tumors of the stomach, tongue, small intestine, and mammary gland (in females).
(1-4,6,8)
EPA has classified acrylonitrile as a Group Bl, probable human carcinogen. (4)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 6.8 x 10"5
(/ig/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
acrylonitrile at an average of 0.01 /xg/m3 (1 x 10"5 mg/m3), over his or her entire lifetime,
that person would theoretically have no more than a one-in-a-million increased chance of
developing cancer as a direct result of breathing air containing this chemical. Similarly,
EPA estimates that breathing air containing 0.1 pig/m3 (1 x 10"4 mg/m3) would result in
not greater than a one-in-a-hundred thousand increased chance of developing cancer, and
air containing 1.0 /xg/m3 (1 x 10"3 mg/m3) would result in not greater than a one-in-ten
thousand increased chance of developing cancer. For a detailed discussion of confidence
in the potency estimates, please see IRIS. (4)
EPA has calculated an oral cancer slope factor of 0.54 (mg/kg/d)"1. (4)
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Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For acrylonitrile: 1 ppm = 2.17 mg/m3.
Health Data from Inhalation Exposure
Acrylonitrile
10000
1000
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ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effect.
AIHA ERPG - American Industrial Hygiene Association's emergency response planning
guidelines. ERPG 1 is the maximum airborne concentration below which it is believed nearly all
individuals could be exposed up to one hour without experiencing other than mild transient
adverse health effects or perceiving a clearly defined objectionable odor; ERPG 2 is the
maximum airborne concentration below which it is believed nearly all individuals could be
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exposed up to one hour without experiencing or developing irreversible or other serious health
effects that could impair their abilities to take protective action.
LC50 (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-effect level.
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health limit; NIOSH recommended exposure limit to ensure that a worker can escape
from an exposure condition that is likely to cause death or immediate or delayed permanent
adverse health effects or prevent escape from the environment.
NIOSH REL - NIOSH's recommended exposure limit; NIOSH-recommended exposure limit for
an 8- or 10-h time-weighted-average exposure and/or ceiling.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
0 The LOAEL is from the critical study used as the basis for the EPA RfC.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Acrylonitrile. Public Health Service, U.S. Department of Health and Human Services,
Atlanta, GA. 1990.
2. International Agency for Research on Cancer (IARC). IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Humans: Some Monomers, Plastics
and Synthetic Elastomers, and Acrolein. Volume 19. World Health Organization, Lyon.
1979.
3. U.S. Environmental Protection Agency (EPA). Health Assessment Document for
Acrylonitrile (Revised Draft). EPA/600/8-82-007. Environmental Criteria and
Assessment Office, Office of Health and Environmental Assessment, Office of Research
and Development, Research Triangle Park, NC. 1982.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Acrylonitrile, National Center for Environmental Assessment, Office of Research and
Development, Washington, D.C. 1999.
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5. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
6. U.S. Environmental Protection Agency (EPA). Health Effects Assessment for
Acrylonitrile. EPA/600/8-88/014. Environmental Criteria and Assessment Office, Office
of Health and Environmental Assessment, Office of Research and Development,
Cincinnati, OH. 1988.
7. U.S. Environmental Protection Agency (EPA). Health Effects Assessment Summary
Tables. FY1997 Update. Solid Waste and Emergency Response, Office of Emergency
and Remedial Response, Cincinnati, OH. EPA/540/R-97-036. 1997.
8. U.S. Environmental Protection Agency (EPA). Health and Environmental Effects Profile
for Acrylonitrile. EPA/600/X-85/372. Environmental Criteria and Assessment Office,
Office of Health and Environmental Assessment, Office of Research and Development,
Cincinnati, OH. 1985.
9. Occupational Safety and Health Administration (OSHA). Occupational Safety and Health
Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29 CFR
1910.1045. 1998.
10. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEls. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
11. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
12. American Industrial Hygiene Association (AfflLA). The AIHA1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.
1998.
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ARSENIC COMPOUNDS1
107-02-8
Hazard Summary
Arsenic, a naturally occurring element, is found throughout the environment; for most
people, food is the major source of exposure. Acute (short-term) high-level inhalation
exposure to arsenic dust or fumes has resulted in gastrointestinal effects (nausea, diarrhea,
abdominal pain); central and peripheral nervous system disorders have occurred in
workers acutely exposed to inorganic arsenic. Chronic (long-term) inhalation exposure to
inorganic arsenic in humans is associated with irritation of the skin and mucous
membranes. Human data suggest a relationship between inhalation exposure of women
working at or living near metal smelters and an increased risk of reproductive effects,
such as spontaneous abortions. However, as these studies evaluated smelter pollutants in
general, arsenic's role is not clear. Chronic oral exposure has resulted in gastrointestinal
effects, anemia, peripheral neuropathy, skin lesions, hyperpigmentation, and liver or
kidney damage. Inorganic arsenic exposure in humans, by the inhalation route, has been
shown to be strongly associated with lung cancer, while ingestion of inorganic arsenic in
humans has been linked to a form of skin cancer and also to bladder, liver, and lung
cancer. The U.S. Environmental Protection Agency (EPA) has classified inorganic
arsenic as a Group A, human carcinogen.
Arsine is a gas consisting of arsenic and hydrogen. It is extremely toxic to humans, with
headaches, vomiting, and abdominal pains occurring within a few hours of exposure.
Death may occur from kidney failure and pulmonary edema. EPA has not classified arsine
for carcinogenicity.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on inhalation chronic toxicity and the reference concentration (RfC) for arsine,
oral chronic toxicity and the reference dose (RfD) for inorganic arsenic, and the carcinogenic effects of inorganic
arsenic including the unit cancer risk for inhalation exposure, and the Agency for Toxic Substances and Disease
Registry's (ATSDR's) Toxicological Profile for Arsenic.
Physical Properties
Inorganic arsenic is a naturally occurring element in the earth's crust. (1)
Pure inorganic arsenic is a gray-colored metal, but inorganic arsenic is usually found
combined with other elements such as oxygen, chlorine, and sulfur. (1)
The chemical symbol for inorganic arsenic is As, and it has an atomic weight of 74.92
g/mol. (3)
1 This fact sheet addresses the toxicity of the inorganic arsenic compounds as well as the
toxicity of the gaseous arsenic trihydride: arsine.
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The chemical formula for arsine is AsH3, and it has a molecular weight of 77.95 g/mol.
(8)
Arsine is a colorless gas with a disagreeable garlic odor. (8)
Arsenic combined with elements such as oxygen, chlorine, and sulfur forms inorganic
arsenic; inorganic arsenic compounds include arsenic pentoxide, arsenic trioxide, and
arsenic acid. Arsenic combined with carbon and hydrogen forms organic arsenic; organic
arsenic compounds include arsanilic acid, arsenobetaine, and dimethylarsinic acid. (1)
Uses
The major use for inorganic arsenic is in wood preservation; arsine is used in the
microelectronics industry and in semiconductor manufacture. (2)
Until the 1940s, inorganic arsenic solutions were widely used in the treatment of various
diseases, such as syphillis and psoriasis. Inorganic arsenic is still used as an antiparasitic
agent in veterinary medicine and in homeopathic and folk remedies in the U.S. and other
countries. (2)
Sources and Potential Exposure
Inorganic arsenic is found throughout the environment; it is released into the air by
volcanoes, the weathering of arsenic-containing minerals and ores, and by commercial or
industrial processes. (1,2)
For most people, food is the largest source of arsenic exposure (about 25 to 50 /ig/d),
with lower amounts coming from drinking water and air. Among foods, some of the
highest levels are in fish and shellfish; however, this arsenic exists, primarily as organic
compounds, which are essentially nontoxic. (1)
Elevated levels of inorganic arsenic may be present in soil, either from natural mineral
deposits or contamination from human activities, which may lead to dermal or ingestion
exposure. (1)
Workers in metal smelters and nearby residents may be exposed to above-average
inorganic arsenic levels from arsenic released into the air. (1)
Other sources of inorganic arsenic exposure include burning plywood treated with an
arsenic wood preservative or dermal contact with wood treated with arsenic. (2)
Most arsenic poisoning incidents in industry have involved the production of arsine, a
short-lived, extremely toxic gas. (3)
Assessing Personal Exposure
Measurement of inorganic arsenic in the urine is the best way to determine recent
exposure (within the last 1 to 2 days), while measuring inorganic arsenic in hair or
fingernails may be used to detect high-level exposures that occurred over the past 6-12
months. (1)
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Health Hazard Information
Acute Effects:
Inorganic Arsenic
Acute inhalation exposure of workers to high levels of arsenic dusts or fumes has resulted
in gastrointestinal effects (nausea, diarrhea, abdominal pain), while acute exposure of
workers to inorganic arsenic has also resulted in central and peripheral nervous system
disorders. (1)
Acute oral exposure to inorganic arsenic, at doses of approximately 600 pig/kg/d or higher
in humans, has resulted in death. Oral exposure to lower levels of inorganic arsenic has
resulted in effects on the gastrointestinal tract (nausea, vomiting), central nervous system
(CNS) (headaches, weakness, delirium), cardiovascular system (hypotension, shock),
liver, kidney, and blood (anemia, leukopenia). (1,2)
Acute animal tests, such as the LD50 test in rats and mice, have shown inorganic arsenic
to have moderate to high acute toxicity. (5)
Arsine
Acute inhalation exposure to arsine by humans has resulted in death; it has been reported
that a half-hour exposure to 25 to 50 ppm can be lethal. (4)
The major effects from acute arsine exposure in humans include headaches, vomiting,
abdominal pains, hemolytic anemia, hemoglobinuria, and jaundice; these effects can lead
to kidney failure. (4,8)
Arsine has been shown to have extreme acute toxicity from acute animal tests. (5)
Chronic Effects (Noncancer):
Inorganic arsenic
Chronic inhalation exposure to inorganic arsenic in humans is associated with irritation of
the skin and mucous membranes (dermatitis, conjunctivitis, pharyngitis, and rhinitis).
(1,2)
Chronic oral exposure to inorganic arsenic in humans has resulted in gastrointestinal
effects, anemia, peripheral neuropathy, skin lesions, hyperpigmentation, gangrene of the
extremities, vascular lesions, and liver or kidney damage. (1,2)
No chronic inhalation exposure studies have been performed in animals for any inorganic
arsenic compound. (1)
Some studies have suggested that inorganic arsenic is an essential dietary nutrient in
goats, chicks, and rats. However, no comparable data are available for humans. EPA has
concluded that essentiality, although not rigorously established, is plausible. (1,6)
EPA has not established an RfC for inorganic arsenic. (6)
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The California Environmental Protection Agency (CalEPA) has established a chronic
inhalation reference level of 0.00003 mg/m3 based on developmental effects in mice. The
CalEPA reference exposure level is a concentration at or below which adverse health
effects are not likely to occur. It is not a direct estimator of risk, but rather a reference
point to gauge the potential effects. At lifetime exposures increasingly greater than the
reference exposure level, the potential for adverse health effects increases. (7)
The RfD for inorganic arsenic is 0.0003 mg/kg/d based on hyperpigmentation, keratosis,
and possible vascular complications in humans. The RfD is an estimate (with uncertainty
spanning perhaps an order of magnitude) of a daily oral exposure to the human
population (including sensitive subgroups) that is likely to be without appreciable risk of
deleterious noncancer effects during a lifetime. (6)
EPA has medium confidence in the study on which the RfD for inorganic arsenic was
based because, although an extremely large number of people were included in the
assessment (>40,000), the doses were not well characterized and other contaminants were
present. The supporting human toxicity database, while extensive, is somewhat flawed
and, consequently, EPA has assigned medium confidence to the RfD. (6)
Arsine
The RfC for arsine is 0.00005 mg/m3 based on increased hemolysis, abnormal red blood
cell morphology, and increased spleen weight in rats, mice, and hamsters. (4)
EPA has medium confidence in the RfC based on: high confidence in the studies on
which the RfC for arsine was based because the sample sizes were adequate, statistical
significance was reported, concentration dose-response relationships were documented,
three species were investigated, and both a no-observed-adverse-effect level (NOAEL)
and a lowest-observed-adverse-effect level (LOAEL) were identified; and medium
confidence in the database because there were three inhalation animal studies and a
developmental/reproductive study, but no data on human exposure. (4)
Reproductive/Developmental Effects:
Inorganic arsenic
Several studies have suggested that women who work in, or live near, metal smelters may
have higher than normal spontaneous abortion rates, and their children may exhibit lower
than normal birth weights. However, these studies are limited because they were designed
to evaluate the effects of smelter pollutants in general and are not specific for inorganic
arsenic. (1)
Ingested inorganic arsenic can cross the placenta in humans, exposing the fetus to the
chemical. (2)
Oral animal studies have reported inorganic arsenic at very high doses to be fetotoxic and
to cause birth defects. (1)
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Arsine
Human studies have indicated higher than expected spontaneous abortion rates in women
in the microelectronics industry who were exposed to arsine. However, these studies have
several limitations, including small sample size and exposure to other chemicals in
addition to arsine. (4)
Cancer Risk:
Inorganic arsenic
Human inhalation studies have reported inorganic arsenic exposure to be strongly
associated with lung cancer. (1,2,6)
Ingestion of inorganic arsenic in humans has been associated with an increased risk of
nonmelanoma skin cancer and also to an increased risk of bladder, liver, and lung cancer.
(1,6)
Animal studies have not associated inorganic arsenic exposure via the oral route with
cancer, and no cancer inhalation studies have been performed in animals for inorganic
arsenic. (1)
EPA has classified inorganic arsenic as a Group A, human carcinogen. (6)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 4.3 x 10"3
(jtig/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
inorganic arsenic at an average of 0.0002 /xg/m3 (2 x 10"7 mg/m3) over his or her entire
lifetime, that person would theoretically have no more than a one-in-a-million increased
chance of developing cancer as a direct result of breathing air containing this chemical.
Similarly, EPA estimates that continuously breathing air containing 0.002 /ig/m3 (2 x 10"6
mg/m3) would result in not greater than a one-in-a-hundred thousand increased chance of
developing cancer, and air containing 0.02 jig/m3 (2 x 10"5 mg/m3) would result in not
greater than a one-in-ten thousand increased chance of developing cancer. For a detailed
discussion of confidence in the potency estimates, please see IRIS. (6)
EPA has calculated an oral cancer slope factor of 1.5 (mg/kg/d)"1 for inorganic arsenic.
(6).
Arsine
No cancer inhalation studies are available for arsine. (1)
EPA has not classified arsine for carcinogenicity. (4)
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Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For inorganic arsenic: 1 ppm = 3.06 mg/m3. For arsine: 1 ppm = 3.19 mg/m3.
To convert from fJig/m3 to mg/m3: mg/m3 = ([Jig/m3) x (1 mg/1,000 [Jig).
Health Data from Inhalation Exposure (Inorganic Arsenic)
Arsenic
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ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LOAEL - Lowest-observed-adverse-effect level.
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
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to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can
escape from an exposure condition that is likely to cause death or immediate or delayed
permanent adverse health effects or prevent escape from the environment.
NIOSH REL ceiling - NIOSH's recommended exposure limit ceiling; the concentration that
should not be.exceeded at any time.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the CalEPA chronic reference
exposure level.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Arsenic (Draft). U.S. Public Health Service, U.S. Department of Health and Human
Services, Atlanta, GA. 1998.
2. Agency for Toxic Substances and Disease Registry (ATSDR). Case Studies in
Environmental Medicine. Arsenic Toxicity. U.S. Public Health Service, U.S. Department
of Health and Human Services, Atlanta, GA. 1990.
3. U.S. Environmental Protection Agency (EPA). Health Assessment Document for
Inorganic Arsenic. EPA/540/1-86/020. Environmental Criteria and Assessment Office,
Office of Health and Environmental Assessment, Office of Research and Development,
Washington, DC. 1984.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Arsine. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
5. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
6. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Arsenic. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999
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7. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
8. M. Windolz. The Merck Index, An Encyclopedia of Chemicals, Drugs, and Biologicals.
10th ed. Merck and Co., Rahway, NJ. 1983.
9. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents. Biological
Exposure Indices. Cincinnati, OH. 1999.
10. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
11. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
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BENZENE
71-43-2
Hazard Summary
Benzene is found in the air from emissions from burning coal and oil, gasoline service
stations, and motor vehicle exhaust. Acute (short-term) inhalation exposure of humans to
benzene may cause drowsiness, dizziness, headaches, as well as eye, skin, and respiratory
tract irritation, and, at high levels, unconsciousness. Chronic (long-term) inhalation
exposure has caused various disorders in the blood, including reduced numbers of red
blood cells and aplastic anemia, in occupational settings. Reproductive effects have been
reported for women exposed by inhalation to high levels, and adverse effects on the
developing fetus have been observed in animal tests. Increased incidence of leukemia
have been observed in humans occupationally exposed to benzene. The U.S.
Environmental Protection Agency (EPA) has classified benzene as a Group A, human
carcinogen.
Please Note: The main sources of information for this fact sheet are the Agency for Toxic Substances and Disease
Registry's (ATSDR's) lexicological Profile for Benzene and EPA's Integrated Risk Information System (IRIS),
which contains information on the carcinogenic effects of benzene including the unit cancer risk for inhalation
exposure.
Physical Properties
The chemical formula for benzene is CgHg, and it has a molecular weight of 78.11 g/mol.
(4)
Benzene occurs as a volatile, colorless, highly flammable liquid that dissolves easily in
water. (1,7)
Benzene has a sweet odor with an odor threshold of 1.5 ppm (5 mg/m3). (1)
The vapor pressure for benzene is 95.2 mm Hg at 25 °C, and it has a log octanol/water
partition coefficient (log Kow) of 2.13. (1)
Uses
Benzene is used as a constituent in motor fuels; as a solvent for fats, waxes, resins, oils,
inks, paints, plastics, and rubber; in the extraction of oils from seeds and nuts; and in
photogravure printing. It is also used as a chemical intermediate. Benzene is also used in
the manufacture of detergents, explosives, pharmaceuticals, and dyestuffs. (2,6)
Sources and Potential Exposure
Individuals employed in industries that manufacture or use benzene may be exposed to
the highest levels of benzene. (1)
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Benzene is found in emissions from burning coal and oil, motor vehicle exhaust, and
evaporation from gasoline service stations and in industrial solvents. These sources
contribute to elevated levels of benzene in the ambient air, which may subsequently be
breathed by the public. (1)
Tobacco smoke contains benzene and accounts for nearly half the national exposure to
benzene.(1)
Individuals may also be exposed to benzene by consuming contaminated water. (1)
Assessing Personal Exposure
Measurement of benzene in an individual's breath or blood or the measurement of
breakdown products in the urine (phenol) can provide information on recent personal
exposure. (1)
Health Hazard Information
Acute Effects:
Coexposure to benzene with ethanol (e.g., alcoholic beverages) can increase benzene
toxicity. (1)
Neurological symptoms of inhalation exposure to benzene include drowsiness, dizziness,
headaches, and unconsciousness in humans. Death may result from exposure to very high
levels of benzene. Ingestion of large amounts of benzene may result in vomiting,
dizziness, convulsions, and death in humans. (1)
Exposure to liquid and vapor may irritate the skin, eyes, and upper respiratory tract.
Redness and blisters may result from dermal exposure to benzene. (1,2)
Animal studies show neurologic, immunologic, and hematologic effects from inhalation
and oral exposure to benzene. (1)
Tests involving acute exposure of animals, such as the LC50 and LD50 tests in rats, mice,
rabbits, and guinea pigs, have demonstrated benzene to have low acute toxicity from
inhalation, moderate acute toxicity from ingestion, and low or moderate acute toxicity
from dermal exposure. (3)
Chronic Effects (Noncancer):
Chronic inhalation of certain levels of benzene causes disorders in the blood in humans.
Benzene specifically affects bone marrow (the tissues that produce blood cells). Aplastic
anemia1, excessive bleeding, and damage to the immune system (by changes in blood
levels of antibodies and loss of white blood cells) may develop. (1)
In animals, chronic inhalation and oral exposure to benzene produces the same effects as
seen in humans. (1)
Benzene causes both structural and numerical chromosomal aberrations in humans. (1)
1 Aplastic anemia is a risk factor for developing acute nonlymphocytic leukemia.
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EPA has not established a reference concentration (RfC) or a reference dose (RfD) for
benzene. (4)
The California Environmental Protection Agency (CalEPA) has established a chronic
reference exposure level of 0.06 mg/m3 for benzene based on hematological effects in
humans. The CalEPA reference exposure level is a concentration at or below which
adverse health effects are not likely to occur. It is not a direct estimator of risk, but rather
a reference point to gauge the potential effects. At lifetime exposures increasingly greater
than the reference exposure level, the potential for adverse health effects increases. (5)
ATSDR has established an acute inhalation minimal risk level (MRL) of 0.2 mg/m3 (0.05
ppm) based on immunological effects in mice and an intermediate MRL of 0.01 mg/m3
(0.004 ppm) based on neurological effects in mice. The MRL is an estimate of the daily
human exposure to a hazardous substance that is likely to be without appreciable risk of
adverse noncancer health effects over a specified duration of exposure. (1)
Reproductive/Developmental Effects:
Several occupational studies suggest that benzene may impair fertility in women exposed
to high levels. However, these studies are limited due to lack of exposure history,
simultaneous exposure to other substances, and lack of follow-up. (1)
Available human data on the developmental effects of benzene are inconclusive due to
concomitant exposure to other chemicals, inadequate sample size, and lack of quantitative
exposure data. (1)
Adverse effects on the fetus, including low birth weight, delayed bone formation, and
bone marrow damage, have been observed where pregnant animals were exposed to
benzene by inhalation. (1)
Cancer Risk:
Increased incidence of leukemia has been observed in humans occupationally exposed to
benzene. (1,4)
EPA has classified benzene as a Group A, known human carcinogen. (4)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated a range of 2.2 x 10"6 to 7.8 x 10"6 as the
increase in the lifetime risk of an individual who is continuously exposed to 1 /ig/m3 of
benzene in the air over their lifetime. EPA estimates that, if an individual were to
continuously breathe air containing benzene at an average of 0.13 to 0.45 /*g/m3 (1.3 x
10"4 to 4.5 x 10"4 mg/m3) over his or her entire lifetime, that person would theoretically
have no more than a one-in-a-million increased chance of developing cancer as a direct
result of continuously breathing air containing this chemical. Similarly, EPA estimates
that continuously breathing air containing 1.3 to 4.5 ptg/m3 (1.3 x 10'3 to 4.5 x 10"3 mg/m3)
would result in not greater than a one-in-a-hundred thousand increased chance of
developing cancer, and air containing 13 to 45 /zg/m3 (1.3 x 10"2 to 4.5 x 10"2 mg/m3)
would result in not greater than a one-in-ten thousand increased chance of developing
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cancer. For a detailed discussion of confidence in the potency estimates, please see IRIS.
(4)
EPA has calculated an oral cancer slope factor of 2.9 x 10"2 (mg/kg/d)'1. (4)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For benzene: 1 ppm = 3.26 mg/m3.
To convert from fig/m3 to mg/m3: mg/m3 = (jjig/m3) x (1 mg/1,000
Health Data from Inhalation Exposure
Benzene
100000
10000
1000 i
_ 100
01
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0.01
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numbers'3
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LC50 (rets) C31,951 rngfrrf)
LCSOflTiCB) 01.887 nngfinrf)
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NC8HREL
CaEPAreferencB
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workers can be exposed without adverse effects.
AIHA ERPG - American Industrial Hygiene Association's emergency response planning
guidelines. ERPG 1 is the maximum airborne concentration below which it is believed nearly all
individuals could be exposed up to one hour without experiencing other than mild transient
adverse health effects or perceiving a clearly defined objectionable odor; ERPG 2 is the
maximum airborne concentration below which it is believed nearly all individuals could be
exposed up to one hour without experiencing or developing irreversible or other serious health
effects that could impair their abilities to take protective action.
LC50 (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
NIOSH REL - National Institute of Occupational Safety and Health's recommended exposure
limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure
and/or ceiling.
NIOSH STEL - NIOSH's short-term exposure limit; NIOSH recommended exposure limit for a
15-minute period.
NOAEL - No-observed-adverse-effect level.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
OSHA STEL - Occupational Safety and Health Administration's short-term exposure limit.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The NOAEL is from the critical study used as the basis for the CalEPA chronic reference
exposure level.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Benzene (Update). Public Health Service, U.S. Department of Health and Human
Services, Atlanta, GA. 1997.
2. M. Sittig. Handbook of Toxic and Hazardous Chemicals and Carcinogens. 2nd ed. Noyes
Publications, Park Ridge, NJ. 1985.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
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4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Benzene. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
5. California Environmental Protection Agency (CalEPA). Air Toxics Hot Spots Program
Risk Assessment Guidelines: Pan III. Technical Support Document for the Determination
ofNoncancer Chronic Reference Exposure Levels. SRP Draft. Office of Environmental
Health Hazard Assessment, Berkeley, CA. 1999.
6. The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S.
Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
7. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents. Biological
Exposure Indices. Cincinnati, OH. 1999.
8. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
9. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
10. American Industrial Hygiene Association (AJHA). The AIHA1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.
1998.
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BERYLLIUM COMPOUNDS1
107-02-8
Hazard Summary
Inhalation exposure to beryllium primarily occurs in the workplaces where it is mined,
processed, or converted into alloys and chemicals, or from the burning of coal or fuel oil
and in tobacco smoke. Acute (short-term) inhalation exposure to high levels of beryllium
has been observed to cause inflammation of the lungs or acute pneumonitis (reddening
and swelling of the lungs) in humans; after exposure ends, these symptoms may be
reversible. Chronic (long-term) inhalation exposure of humans to beryllium has been
reported to cause chronic beryllium disease (berylliosis), in which granulomatous lesions
(noncancerous) develop in the lung. Inadequate information is available on the
reproductive or developmental effects of beryllium in humans or animals following
inhalation exposure. Inhalation exposure to beryllium has been demonstrated to cause
lung cancer in rats and monkeys. Human epidemiology studies are limited, but suggest a
causal relationship between beryllium exposure and an increased risk of lung cancer. The
U.S. Environmental Protection Agency (EPA) has classified beryllium as a Group Bl,
probable human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on oral chronic toxicity and the reference dose (RfD) and inhalation chronic
toxicity and the reference concentration (RfC), and the carcinogenic effects of beryllium including the unit cancer
risk for inhalation exposure, EPA's Toxicological Review of Beryllium and Compounds, and the Agency for Toxic
Substances and Disease Registry's (ATSDR's) Toxicological Profile for Beryllium.
Physical Properties
The chemical symbol for pure beryllium is Be, and its atomic weight is 9.012 g/mol. (1)
Pure beryllium is a hard gray metal that does not occur naturally but does occur as a
chemical component of certain kinds of rocks, coal and oil, soil, and volcanic dust. (1)
Beryllium is also present in a variety of compounds such as beryllium fluoride, beryllium
chloride, beryllium sulfate, beryllium oxide, and beryllium phosphate. (1)
Pure beryllium is insoluble in water; however, some of its compounds are soluble in
water. (1)
1 This fact sheet discusses beryllium and beryllium compounds. Most of the information
is on beryllium, except in those cases where there are differences in toxicity between beryllium
and beryllium compounds. In these cases, information on the beryllium compound is presented.
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Uses
Pure beryllium and its metal alloys have applications in electrical components, tools,
structural components for aircraft, missiles, and satellites, and other metal-fabricating
uses. (1)
Beryllium is also used in consumer products, such as televisions, calculators, and
personal computers. (1)
Sources and Potential Exposure
The greatest exposures to beryllium occur in the workplace (i.e., where it is mined,
processed, or converted into alloys and chemicals). (1)
Individuals may also be exposed by inhalation of beryllium dust or fumes from the
burning of coal or fuel oil and in tobacco smoke, by the ingestion of many fruits and
vegetables and water, or through natural occurrence in soils. (1)
The average concentration of beryllium measured in the air in the U.S. during the 1980s
was 0.03 ng/m3. Ambient concentrations measured in 50 cities between 1977 and 1981
were 0.1-0.4 ng/m3. (1)
Assessing Personal Exposure
Beryllium levels can be measured in urine and blood, but the levels in urine are quite
variable, making it difficult to use these levels to assess total exposure. (1)
Beryllium levels in tissues can be measured through biopsy procedures, however the
relationship to exposure is not well documented. (1)
A medical test, termed the antigen-specific lymphocyte transformation test, can be used to
measure hypersensitivity in individuals previously exposed to beryllium and can also be
used to diagnose chronic beryllium disease. (1)
Health Hazard Information
Acute Effects:
Acute inhalation exposure to high levels of beryllium has been observed to cause
inflammation of the lungs and acute pneumonitis (reddening and swelling of the lungs) in
humans; after exposure ends, these symptoms may be reversible. Acute pneumonitis may
cause death. (1-4)
Acute animal tests, such as the LD50 test in rats and mice, have demonstrated beryllium
compounds to vary in acute toxicity, ranging from high to extreme acute toxicity from
oral exposure. (5)
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Chronic Effects (Noncancer):
Chronic occupational exposure of humans to beryllium by inhalation has been reported to
cause chronic beryllium disease (berylliosis), in which granulomatous lesions
(noncancerous) develop in the lung. The onset of these effects may be delayed by 3
months to more than 20 years. Symptoms of chronic beryllium disease include irritation
of the mucous membranes, reduced lung capacity, shortness of breath, fatigue, anorexia,
dyspnea, malaise, and weight loss. In some cases, chronic beryllium disease may cause
death. (1-4)
Animal studies have also reported effects on the lung, such as chronic pneumonitis, from
chronic inhalation exposure. (1-3)
Chronic inhalation exposure has also been observed to cause immunological effects in
humans and animals. (1-3)
A skin allergy may result from dermal exposure to beryllium. Eye contact with beryllium
dust has been observed to cause acute conjunctivitis in humans. (1)
The RfC for beryllium is 0.00002 mg/m3 based on respiratory effects in humans. The RfC
is an estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous
inhalation exposure to the human population (including sensitive subgroups) that is likely
to be without appreciable risk of deleterious noncancer effects during a lifetime. It is not a
direct estimator of risk but rather a reference point to gauge the potential effects. At
exposures increasingly greater than the RfC, the potential for adverse health effects
increases. Lifetime exposure above the RfC does not imply that an adverse health effect
would necessarily occur. (3)
EPA has medium confidence in the RfC due to: medium confidence in the study on
which the RfC is based because a no-observed-adverse-affect level (NOAEL) was not
identified in the study, but a NOAEL slightly below the lowest-observed-adverse-effect
level (LOAEL) was suggested in another study; and medium confidence in the database
due to lack of adequate exposure monitoring in the epidemiology studies and some
uncertainty regarding the mechanism associated with progression to chronic beryllium
disease in beryllium-sensitized individuals. (3)
The RfD for beryllium is 0.002 mg/kg/d based on small intestinal lesions in dogs. (3)
EPA has low to medium confidence in the RfD due to: medium confidence in the study
on which the RfD was based because it was administered by the oral route with multiple
doses for chronic duration, but there were small groups of animals, early mortality at the
high dose level, and no control for potential litter effects; and low to medium confidence
in the database because there is only one chronic study in dogs showing adverse effect
levels. (3)
Reproductive/Developmental Effects:
The potential for beryllium to induce developmental or reproductive effects has not been
adequately assessed.
Limited information is available on the reproductive or developmental effects of
beryllium in humans following inhalation exposure. A case control study found no
association between paternal occupational exposure and the risk of stillbirth, pre-term
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delivery, or small-for-gestational-age infants, although this study has limited sensitivity.
(2,3)
No data are available on reproductive or developmental effects in animals following
inhalation. (2,3)
Cancer Risk:
Several human epidemiological studies have investigated the relationship between
beryllium exposure in workers and lung cancer deaths. Although there are shortcomings
in all the studies, the results are suggestive of a causal relationship between beryllium
exposure and an increased risk of lung cancer. (2,3)
Beryllium compounds have been shown to cause lung cancer from inhalation exposure in
rats and monkeys. (1-3)
EPA has classified beryllium as a Group Bl, probable human carcinogen. (3)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 2.4 x 10"3
(jiig/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
beryllium at an average of 0.0004 ptg/m3 (4 x 10"7 mg/m3) over his or her entire lifetime,
that person would theoretically have no more than a one-in-a-million increased chance of
developing cancer as a direct result of breathing air containing this chemical. Similarly,
EPA estimates that continuously breathing air containing 0.004 /ig/m3 (4 x 10"6 mg/m3)
would result in not greater than a one-in-a-hundred thousand increased chance of
developing cancer, and air containing 0.04 jig/m3 (4 x 10"5 mg/m3) would result in not
greater than a one-in-ten thousand increased chance of developing cancer. For a detailed
discussion of confidence in the potency estimates, please see IRIS. (3)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
Beryllium and its compounds do not exist in the atmosphere in the vapor phase; therefore, an air
conversion factor is not applicable. (1)
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Health Data from Inhalation Exposure
Beryllium
10
Regulcf ory, advisory
numbers1*
NSCBHIDLH(4nr^rrf)
01
c
o
"5
(B
i r-
0.1 r
0.01 r-
0.001 r-
0.0001
0.00001
0.000001
0.0000001
AIHA ERPG2 (P.025 rr^nrf)
C8HAPELA03HTLV
(P.002 m^nrf)
NCAELc(resprctay)(p.CXXDl nr^rrf)
anaer Risk La/a
1 inamllicnrisk
N1C8HREL
(p.OOOSrrg'rT?)
ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
AIHA ERPG - American Industrial Hygiene Association's emergency response planning
guidelines. ERPG 1 is the maximum airborne concentration below which it is believed nearly all
individuals could be exposed up to one hour without experiencing other than mild transient
adverse health effects or perceiving a clearly defined objectionable odor; ERPG 2 is the
maximum airborne concentration below which it is believed nearly all individuals could be
exposed up to one hour without experiencing or developing irreversible or other serious health
effects that could impair their abilities to take protective action.
NIOSH IDLH - National Institute of Occupational Safety and Health's immediately dangerous
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to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can
escape from an exposure condition that is likely to cause death or immediate or delayed
permanent adverse health effects or prevent escape from the environment.
NIOSH REL - NIOSH's recommended exposure limit; NIOSH-recommended exposure limit for
an 8- or 10-h time-weighted-average exposure and/or ceiling.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c This NOAEL is from the critical study used as the basis of the EPA RfC.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Beryllium (Draft). Public Health Service, U.S. Department of Health and Human
Services, Altanta, GA. 1992.
2. U.S. Environmental Protection Agency (EPA). Toxicological Review of Beryllium and
Compounds. In support of summary information on IRIS. National Center for
Environmental Assessment, Washington, DC. 1998.
3. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Beryllium. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
4. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
5. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
6. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
7. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
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8. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents. Biological
Exposure Indices. Cincinnati, OH. 1999.
9. American Industrial Hygiene Association (AIHA). The AIHA 1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.
1998.
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1,3-BUTADIENE
106-99-0
Hazard Summary
1,3-Butadiene is found in ambient air primarily as a compound of motor vehicle exhaust.
Acute (short-term) exposure to 1,3-butadiene by inhalation in humans results in irritation
of the eyes, nasal passages, throat, and lungs, and causes neurological effects such as
blurred vision, fatigue, headache, and vertigo. Epidemiological studies have reported a
possible association between 1,3-butadiene exposure and cardiovascular diseases. No
information is available on the reproductive or developmental effects of 1,3-butadiene in
humans, while animal studies have reported these type of effects. Epidemiological studies
of workers in rubber plants have shown an association between 1,3-butadiene exposure
and increased incidence of leukemia. Animal studies have reported tumors at various sites
from 1,3-butadiene exposure. The U.S. Environmental Protection Agency (EPA) has
classified 1,3-butadiene as a Group B2, probable human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on the carcinogenic effects of 1,3-butadiene including the unit cancer risk for
inhalation exposure, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) lexicological Profile
for 1,3-Butadiene.
Physical Properties
1,3-Butadiene is a colorless gas with a mild gasoline-like odor. (1)
The odor threshold for 1,3-butadiene is 1.6 ppm. (7)
The chemical formula for 1,3-butadiene is 41^, and the molecular weight is 54.09
g/mol. (1)
The vapor pressure for 1,3-butadiene is 2100 mm Hg at 25 °C, and it has an
octanol/water partition coefficient (log Kow) of 1.99. (1)
Uses
1,3-Butadiene is used in the production of rubber and plastics. It is also used in
copolymers including acrylics. (1)
Sources and Potential Exposure
Sources of 1,3-butadiene released into the air include manufacturing and processing
facilities, motor vehicle exhaust, forest fires or other combustion, and cigarette smoke. (1)
1,3-Butadiene was detected in ambient air of cities and suburban areas from 1970 to 1982
at an average level of 0.3 ppb. (1)
Higher levels of 1,3-butadiene may be found in highly industrialized cities or near oil
refineries, chemical manufacturing plants, and plastic and rubber factories. (1)
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1,3-Butadiene has been found in drinking water and in plastic or rubber food containers,
but not in food samples. (1)
Occupational exposure to 1,3-butadiene may occur in the rubber, plastics, and resins
industries. (1)
Assessing Personal Exposure
There is no reliable medical test available at this time to assess personal exposure to
1,3-butadiene. (1)
Health Hazard Information
Acute Effects:
Acute exposure to 1,3-butadiene by inhalation in humans results in irritation of the eyes,
nasal passages, throat, and lungs. Neurological effects, such as blurred vision, fatigue,
headache, and vertigo, have also been reported at very high exposure levels. (1,3)
Dermal exposure to 1,3-butadiene causes a sensation of cold, followed by a burning
sensation, which may lead to frostbite. (1)
Tests involving acute exposure of animals, such as the LC50 test in rats and mice, have
shown 1,3-butadiene to have lew acute toxicity. (1,4)
Chronic Effects (Noncancer):
One epidemiological study reported that chronic (long-term) exposure to 1,3-butadiene
via inhalation resulted in an increase in cardiovascular diseases, such as rheumatic and
arteriosclerotic heart diseases, while other human studies have reported effects on the
blood. (1)
Animal studies have reported effects on the respiratory and cardiovascular systems,
blood, and liver from chronic, inhalation exposure to 1,3-butadiene. (1)
EPA has not established a reference concentration (RfC) or a reference dose (RfD) for
1,3-butadiene. (5)
The California Environmental Protection Agency (CalEPA) has established a chronic
reference level of 0.008 mg/m3 for 1,3-butadiene based on reproductive effects in mice.
The CalEPA reference exposure level is a concentration at or below which adverse health
effects are not likely to occur. It is not a direct estimator of risk, but rather a reference
point to gauge the potential effects. At lifetime exposures increasingly greater than the
reference exposure level, the potential for adverse health effects increases. (6)
Reproductive/Developmental Effects:
No information is available on reproductive or developmental effects of 1,3-butadiene in
humans. (1)
Animal studies using mice have reported developmental effects, such as skeletal
abnormalities and decreased fetal weights, and reproductive effects, including an
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increased incidence of ovarian atrophy, testicular atrophy, and sperm abnormalities from
inhalation exposure to 1,3-butadiene. (1)
Cancer Risk:
A large epidemiological study of synthetic rubber industry workers demonstrated a
consistent association between 1,3-butadiene exposure and occurrence of leukemia (10,
11).
Several epidemiological studies of workers in styrene-butadiene rubber factories have
shown an increased incidence of respiratory, bladder, stomach, and
lymphato-hematopoietic cancers. However, these studies are not sufficient to determine a
causal association between 1,3-butadiene exposure and cancer due to possible exposure to
other chemicals and other confounding factors. (1,5,6)
Animal studies have reported tumors at a variety of sites from inhalation exposure to
1,3-butadiene. (1,5,6)
EPA has classified 1,3-butadiene as a Group B2, probable human carcinogen. However,
based on recently available human data, EPA is evaluating a classification of known
human carcinogen. (5)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from continuously breathing air containing a
specified concentration of a chemical. EPA is currently reevaluating their inhalation unit
risk estimate of 2.8 x 10"4 (/ig/m3)"1 that was derived in 1991. A revised unit risk estimate
of 2.1 x 10"6 (jug/m3)"1 was presented to EPA's Science Advisory Board (SAB) for review
in 1998. As a result of SAB comments, the estimate will be revised and is likely to be
lower than the 1991 value. (12)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For 1,3-butadiene: 1 ppm = 2.21 mg/m3.
To convert from (Jig/m3 to mg/m3: mg/m3 = (/jig/m3) x (1 mg/1,000 (Jt,g).
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Health Data from Inhalation Exposure
1,3-Butod ene
Regulciory, advisory
numbers'3
Hedth numbers
LC50 (rets) (269.8% nrg'rTt)
LC50 (mtE) (285.382 mg'rrf)
- NCSHIDLH (4420n^nt)
AIHAERPS2(442rrgi'nrt)
AIHAERPS-1 (22.1 mgfrrf)
CSHASTEL01
G3EPA reference
etpcsure
Oncer Risk
Level 1 in a
m'llicnrisk
(4x10*
0.000001
ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
AIHA ERPG - American Industrial Hygiene Association's emergency response planning
guidelines. ERPG 1 is the maximum airborne concentration below which it is believed nearly all
individuals could be exposed up to one hour without experiencing other than mild transient
adverse health effects or perceiving a clearly defined objectionable odor;.ERPG 2 is the
maximum airborne concentration below which it is believed nearly all individuals could be
exposed up to one hour without experiencing or developing irreversible or other serious health
effects that could impair their abilities to take protective action.
LCg, (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-affect level.
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NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can
escape from an exposure condition that is likely to cause death or immediate or delayed
permanent adverse health effects or prevent escape from the environment.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
OSHA STEL - OSHA's short-term exposure limit.
a Health numbers are lexicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the CalEPA chronic reference
exposure level.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
1,3-Butadiene. Public Health Service, U.S. Department of Health and Human Services,
Atlanta, GA. 1992.
2. EJ. Calabrese and E.M. Kenyon. Air Toxics and Risk Assessment. Lewis Publishers.
1991.
3. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
4. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
5. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on 1,3-Butadiene. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1999.
6. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
7. J.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds
compared with threshold limit values and volatilities for 214 industrial chemicals in air
and water dilution. Journal of Applied Toxicology, 3(6):272-290. 1983.
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8. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
9. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents. Biological
Exposure Indices. Cincinnati, OH. 1999.
10. Delzell E, Sathiakumar N, Hovinga M, et al. A follow-up study of synthetic rubber
workers. Toxicology 113:182-9. 1996.
11. Macaluso M, Larson R, Delzell E, et al. Leukemia and cumulative exposure to butadiene,
styrene and benzene among workers in the synthetic rubber industry. Toxicology
113:190-202. 1996.
12. U.S. Environmental Protection Agency (EPA). An SAB Report: Review of the Health Risk
Assessment of 1,3-Butadiene. Science Advisory Board, Washington, DC.
EPA-SAB-EHC-99-003. 1998.
13. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
14. American Industrial Hygiene Association (AIHA). The AIHA 1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.
1998.
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CADMIUM COMPOUNDS1
Hazard Summary
The main sources of cadmium in the air are the burning of fossil fuels such as coal
or oil and the incineration of municipal waste. The acute (short-term) effects of
cadmium in humans through inhalation exposure consist mainly of effects on the
lung, such as pulmonary irritation. Chronic (long-term) inhalation or oral
exposure to cadmium leads to a build-up of cadmium in the kidneys that can cause
kidney disease. Cadmium has been shown to be a developmental toxicant in
animals, resulting in fetal malformations and other effects, but no conclusive
evidence exists in humans. An association between cadmium exposure and an
increased risk of lung cancer has been reported from human studies, but these
studies are inconclusive due to confounding factors. Animal studies have
demonstrated an increase in lung cancer from long-term inhalation exposure to
cadmium. The U.S. Environmental Protection Agency (EPA) has classified
cadmium as a Group Bl, probable human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on oral chronic toxicity and the reference dose (RfD), and the carcinogenic
effects of cadmium including the unit cancer risk for inhalation exposure, and the Agency for Toxic Substances and
Disease Registry's (ATSDR's) Toxicological Profile for Cadmium.
Physical Properties
Cadmium is a soft silver-white metal that is usually found in combination with other
elements. (1)
Cadmium compounds range in solubility in water from quite soluble to practically
insoluble. (1)
The chemical symbol for cadmium is Cd and the atomic weight is 112.41 g/mol. (1)
Uses
Most cadmium used in the U.S. today is obtained as a byproduct from the smelting of
zinc, lead, or copper ores. (1)
Cadmium is used to manufacture pigments and batteries and in the metal-plating and
plastics industries. (1)
1 This fact sheet discusses cadmium and cadmium compounds. Most of the information is
on cadmium, except in those cases where there are differences in toxicity between cadmium and
cadmium compounds. In these cases, information on the cadmium compound is presented.
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Sources and Potential Exposure
The largest sources of airborne cadmium in the environment are the burning of fossil
fuels such as coal or oil, and incineration of municipal waste materials. Cadmium may
also be emitted into the air from zinc, lead, or copper smelters. (1)
For nonsmokers, food is generally the largest source of cadmium exposure. Cadmium
levels in some foods can be increased by the application of phosphate fertilizers or
sewage sludge to farm fields. (1)
Smoking is another important source of cadmium exposure. Smokers have about twice as
much cadmium in their bodies as do nonsmokers. (1)
Assessing Personal Exposure
The amount of cadmium present in blood or urine can be measured by atomic absorption
spectrophotometry and used as an indication of cadmium exposure. (1)
A more precise method, called neutron activation analysis, can be used to measure
cadmium concentrations in the liver or kidney. (1)
Health Hazard Information
Acute Effects:
Acute inhalation exposure to high levels of cadmium in humans may result in effects on
the lung, such as bronchial and pulmonary irritation. A single acute exposure to high
levels of cadmium can result in long-lasting impairment of lung function. (1,3,4)
Cadmium is considered to have high acute toxicity, based on short-term animal tests such
as the LC50 test in rats. (5)
Chronic Effects (Noncancer):
Chronic inhalation and oral exposure of humans to cadmium results in a build-up of
cadmium in the kidneys that can cause kidney disease, including proteinuria, a decrease in
glomerular filtration rate, and an increased frequency of kidney stone formation. (1,3,4)
Other effects noted in humans from chronic exposure to cadmium in air are effects on the
lung, including bronchiolitis and emphysema. (1,3,4)
Chronic inhalation or oral exposure of animals to cadmium results in effects on the
kidney, liver, lung, bone, immune system, blood, and nervous system. (1,3)
The RfD for cadmium in drinking water is 0.0005 mg/kg/d, and the RfD for dietary
exposure to cadmium is 0.001 mg/kg/d; both are based on significant proteinuria in
humans. The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of a daily oral exposure to the human population (including sensitive
subgroups) that is likely to be without appreciable risk of deleterious noncancer effects
during a lifetime. It is not a direct estimator of risk, but rather a reference point to gauge
the potential effects. At exposures increasingly greater than the RfD, the potential for
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adverse health effects increases. Lifetime exposure above the RfD does not imply that an
adverse health effect would necessarily occur. (6)
EPA has high confidence in both RfD values based primarily on a strong database for
cadmium toxicity in humans and animals that also permits calculation of pharmacokinetic
parameters of cadmium absorption, distribution, metabolism, and elimination. (6)
EPA has not established a reference concentration (RfC) for cadmium. (6)
The California Environmental Protection Agency (CalEPA) has established a chronic
reference exposure level of 0.00001 mg/m3 for cadmium based on kidney and respiratory
effects in humans. The CalEPA reference exposure level is a concentration at or below
which adverse health effects are not likely to occur. (7)
Reproductive/Developmental Effects:
Limited evidence exists for an association between inhalation exposure and a reduction in
sperm number and viability in humans. (1)
Human developmental studies on cadmium are limited, although there is some evidence
to suggest that maternal cadmium exposure may result in decreased birth weights. (1)
Animal studies provide evidence that cadmium has developmental effects, such as low
fetal weight, skeletal malformations, interference with fetal metabolism, and impaired
neurological development, via inhalation and oral exposure. (1,3,4)
Limited animal data are available, although some reproductive effects, such as decreased
reproduction and testicular damage, have been noted following oral exposures. (1)
Cancer Risk:
Several occupational studies have reported an excess risk of lung cancer in humans from
exposure to inhaled cadmium. However, the evidence is limited rather than conclusive
due to confounding factors. (1,3,6)
Animal studies have reported cancer resulting from inhalation exposure to several forms
of cadmium, while animal ingestion studies have not demonstrated cancer resulting from
exposure to cadmium compounds. (1,3,6)
EPA considers cadmium to be a probable human carcinogen and has classified it as a
Group Bl carcinogen. (6)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 1.8 x 10"3
Oig/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
cadmium at an average of 0.0006 /ig/m3 (6 x 10"7 mg/m3) over his or her entire lifetime,
that person would theoretically have no more than a one-in-a-million increased chance of
developing cancer as a direct result of breathing air containing this chemical. Similarly,
EPA estimates that continuously breathing air containing 0.006 /ig/m3 (6 x 10~6mg/m3)
would result in not greater than a one-in-a-hundred thousand increased chance of
developing cancer, and air containing 0.06 pig/m3 (6 x 10"5 mg/m3) would result in not
greater than a one-in-ten thousand increased chance of developing cancer. For a detailed
discussion of confidence in the potency estimates, please see IRIS. (6)
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Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For cadmium: 1 ppm = 4.6 mg/m3.
To convert from fJ-g/m3 to mg/m3: mg/m3 = ((JLg/m3) x (1 mg/1000 fig).
Health Data from Inhalation Exposure
CdcMum
10000
1000
100
10
1
0.1
0.01
0.001
0.0001
0.00001
0.000001
0.0000001
Hedth numbers0
LC50 (rets) (500 mgfrrf)
Regulctory, advisory
numbers"
MCSHiaH(cLEtalnres)(?nrgftTf)
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exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-affect level.
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life and health; NIOSH concentration representing the maximum level of a pollutant from
which an individual could escape within 30 minutes without escape-impairing symptoms or
irreversible health effects.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the CalEPA chronic reference
exposure level.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Cadmium. Draft for Public Comment. Public Health Service, U.S. Department of Health
and Human Services, Atlanta, GA. 1997.
2. U.S. Environmental Protection Agency (EPA). Deposition of Air Pollutants to the Great
Waters. First Report to Congress. EPA-453/R-93-055. Office of Air Quality Planning
and Standards, Research Triangle Park, NC. 1994.
3. EJ. Calabrese and E.M. Kenyon. Air Toxics and Risk Assessment. Lewis Publishers,
Chelsea, MI. 1991.
4. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
5. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
6. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Cadmium. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
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7. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
8. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
9. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents. Biological
Exposure Indices. Cincinnati, OH. 1999.
10. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
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CARBON TETRACHLORIDE
56-23-5
Hazard Summary
Carbon tetrachloride may be found in both ambient outdoor and indoor air. Human
symptoms of acute (short-term) inhalation and oral exposures to carbon tetrachloride
include headache, weakness, lethargy, nausea, and vomiting. Depression of the central
nervous system (CNS) has also been reported. More severe acute exposures result in
kidney and liver damage and extreme exposures have resulted in delayed pulmonary
edema (resulting from kidney damage). Chronic (long-term) inhalation or oral exposure
to carbon tetrachloride also produces liver and kidney damage in humans. Little
information is available on the reproductive or developmental effects of carbon
tetrachloride in humans. Reproductive effects have been observed in animals exposed to
carbon tetrachloride orally and by inhalation. Human data on the carcinogenic effects of
carbon tetrachloride are limited. Studies in animals have shown that ingestion of carbon
tetrachloride increases the risk of liver cancer. The U.S. Environmental Protection
Agency (EPA) has classified carbon tetrachloride as a Group B2, probable human
carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on oral chronic toxicity of carbon tetrachloride and the reference dose (RfD),
and the carcinogenic effects of carbon tetrachloride including the unit cancer risk for inhalation exposure, and the
Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for Carbon Tetrachloride.
Physical Properties
The chemical formula for carbon tetrachloride is CC14, and its molecular weight is 153.8
g/mol. (1,2)
Carbon tetrachloride is a clear, nonflammable liquid which is almost insoluble in water.
(1)
Carbon tetrachloride has a sweet characteristic odor, with an odor threshold above 10
ppm. (1)
The vapor pressure for carbon tetrachloride is 91.3 mm Hg at 20 °C, and its log
octanol/water partition coefficient (log K^) is 2.64. (1)
Uses
Carbon tetrachloride was produced in large quantities to make refrigerants and
propellants for aerosol cans, as a solvent for oils, fats, lacquers, varnishes, rubber waxes,
and resins, and as a grain fumigant and a dry cleaning agent. Consumer and fumigant uses
have been discontinued and only industrial uses remain. (1)
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Sources and Potential Exposure
Individuals may be exposed to carbon tetrachloride in the air from accidental releases
from production and uses, and from its disposal in landfills. (1)
Carbon tetrachloride is also a common contaminant of indoor air; the sources of exposure
appear to be building materials or products, such as cleaning agents, used in the home. (1)
Workers involved in the manufacture or use of carbon tetrachloride are most likely to
have significant exposures to carbon tetrachloride. (1)
Individuals may also be exposed to carbon tetrachloride by drinking contaminated water.
(1,2)
In the past, ingestion of bread or other products made with carbon tetrachloride-fumigated
grain may have contributed to dietary exposure, but this route of exposure is no longer of
significance. (1)
Assessing Personal Exposure
Measurement of carbon tetrachloride in exhaled breath has been the most convenient
method for determining exposure; measurements in blood, fat, or other tissues have also
been used as indicators of exposure. However, these tests are not routinely available and
cannot be used to predict whether any health effects will result. (1)
Health Hazard Information
Acute Effects:
Acute inhalation and oral exposures to high levels of carbon tetrachloride have been
observed primarily to damage the liver and kidneys of humans. Depression of the CNS
has also been reported. Symptoms of acute exposure in humans include headache,
weakness, lethargy, nausea, and vomiting. (1-6)
Delayed pulmonary edema has been observed in humans exposed to high levels of carbon
tetrachloride by inhalation and ingestion, but this is believed to be due to injury to the
kidney rather than direct action of carbon tetrachloride on the lung. (1)
Acute animal exposure tests, such as the LC50 and LD50 tests in rats, mice, rabbits, and
guinea pigs, have demonstrated carbon tetrachloride to have low toxicity from inhalation
exposure, low-to-moderate toxicity from ingestion, and moderate toxicity from dermal
exposure. (7)
Chronic Effects (Noncancer):
Chronic inhalation or oral exposure to carbon tetrachloride produces liver and kidney
damage in humans and animals. (1,3,6,8)
EPA has not established a reference concentration (RfC) for carbon tetrachloride. (9)
The California Environmental Protection Agency (CalEPA) has established a chronic
reference exposure level of 0.04 mg/m3 for carbon tetrachloride based on liver effects in
guinea pigs. The CalEPA reference exposure level is a concentration at or below which
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adverse health effects are not likely to occur. It is not a direct estimator of risk, but rather
a reference point to gauge the potential effects. At lifetime exposures increasingly greater
than the reference exposure level, the potential for adverse health effects increases. (10)
ATSDR has established an acute inhalation minimal risk level (MRL) of 1.3 mg/m3 (0.2
ppm) based on liver effects in rats, and an intermediate MRL of 0.3 mg/m3 (0.05 ppm)
also based on liver effects in rats. The MRL is an estimate of the daily human exposure to
a hazardous substance that is likely to be without appreciable risk of adverse noncancer
health effects over a specified duration of exposure. (1)
The RfD for carbon tetrachloride is 0.0007 mg/kg/d based on the occurrence of liver
lesions in rats. The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of a daily oral exposure to the human population (including sensitive
subgroups) that is likely to be without appreciable risk of deleterious noncancer effects
during a lifetime. (9)
EPA has medium confidence in the RfD based on: high confidence in the principal study
on which the RfD was based because the study was well conducted and good
dose-response was observed in the liver, which is the target organ for carbon tetrachloride
toxicity; and medium confidence in the database because four additional subchronic
studies support the RfD, but reproductive and teratology endpoints are not well
investigated; and, consequently, medium confidence in the RfD. (9)
Reproductive/Developmental Effects:
No information is available on the reproductive effects of carbon tetrachloride in humans.
Limited epidemiological data have indicated a possible association between certain birth
outcomes (e.g., birth weight, cleft palate) and drinking water exposure. However, as the
water contained multiple chemicals, the role of carbon tetrachloride is unclear. (1)
Decreased fertility and degenerative changes in the testes have been observed in animals
exposed to carbon tetrachloride by inhalation. (1,6)
Birth defects have not been observed in animals exposed to carbon tetrachloride by
inhalation or ingestion. (1,2,8)
Cancer Risk:
Occasional reports have noted the occurrence of liver cancer in workers who had been
exposed to carbon tetrachloride by inhalation exposure; however, the data are not
sufficient to establish a cause-and-effect relationship. (1,6,8,9,11,12)
Liver tumors have developed in rats and mice exposed to carbon tetrachloride by gavage.
(1-4,6,8,9,11,12)
EPA has classified carbon tetrachloride as a Group B2, probable human carcinogen. (8,9)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from continuously breathing air containing a
specified concentration of a chemical. EPA calculated an inhalation unit risk of 1.5 x 10"5
Oig/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
carbon tetrachloride at an average of 0.07 /xg/m3 (7 x 10"5 mg/m3) over his or her entire
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lifetime, that person would theoretically have no more than a one-in-a-million increased
chance of developing cancer as a direct result of breathing air containing this chemical.
Similarly, EPA estimates that continuously breathing air containing 0.7 jug/m3 (7 x 10"4
mg/m3) would result in not greater than a one-in-a-hundred thousand increased chance of
developing cancer, and air containing 7.0 /*g/m3 (7 x 10"3 mg/m3) would result in not
greater than a one-in-a-ten thousand increased chance of developing cancer. (9)
EPA has calculated an oral cancer slope factor of 1.3 x 10"1 (mg/kg/d)"1. For a detailed
discussion of confidence in the potency estimates, please see IRIS. (9)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For carbon tetrachloride: 1 ppm = 6.3 mg/m3.
Health Data from Inhalation Exposure
Gtrbon Terrochloride
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AIHA ERPG - American Industrial Hygiene Association's emergency response planning
guidelines. ERPG 1 is the maximum airborne concentration below which it is believed nearly all
individuals could be exposed up to one hour without experiencing other than mild transient
adverse health effects or perceiving a clearly defined objectionable odor; ERPG 2 is the
maximum airborne concentration below which it is believed nearly all individuals could be
exposed up to one hour without experiencing or developing irreversible or other serious health
effects that could impair their abilities to take protective action.
ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LC50 (Lethal Concentrationso) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-affect level.
NIOSH IDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can
escape from an exposure condition that is likely to cause death or immediate or delayed
permanent adverse health effects or prevent escape from the environment.
NIOSH REL - NIOSH's recommended exposure limit; NIOSH-recommended exposure limit for
an 8- or 10-h time-weighted-average exposure and/or ceiling.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c These cancer risk estimates were derived from oral data and converted to provide the estimated
inhalation risk.
d The LOAEL is from the critical study used as the basis for the CalEPA chronic reference
exposure level.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Carbon Tetrachloride (Update). Public Health Service, U.S. Department of Health and
Human Services, Atlanta, GA. 1994.
2. U.S. Environmental Protection Agency (EPA). Carbon Tetrachloride Health Advisory.
Office of Drinking Water, Washington, DC. 1987.
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3. U.S. Department of Health and Human Services. Hazardous Substances Databank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
4. International Agency for Research on Cancer (IARC). IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Humans: Some Halogenated
Hydrocarbons. Volume 20. World Health Organization, Lyon. 1979.
5. M. Sittig. Handbook of Toxic and Hazardous Chemicals and Carcinogens. 2nd ed. Noyes
Publications, Park Ridge, NJ. 1985.
6. U.S. Environmental Protection Agency (EPA). Health Affects Document for Carbon
Tetrachloride. EPA/600/8-82-00 IF. Environmental Criteria and Assessment Office,
Office of Health and Environmental Assessment, Office of Research and Development,
Cincinnati, OH. 1984.
7. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
8. U.S. Environmental Protection Agency (EPA). Updated Health Effects Assessment for
Carbon Tetrachloride. EPA/600/8-89/088. Environmental Criteria and Assessment
Office, Office of Health and Environmental Assessment, Office of Research and
Development, Cincinnati, OH. 1989.
9. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Carbon Tetrachloride. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
10. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
11. International Agency for Research on Cancer (LARC). IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Humans: Chemicals, Industrial
Processes and Industries Associated with Cancer in Humans. Supplement 4. World
Health Organization, Lyon. 1982.
12. International Agency for Research on Cancer (IARC). IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Man. Volume 1. World Health
Organization, Lyon. 1972.
13. The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S.
Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
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14. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
15. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents. Biological
Exposure Indices. Cincinnati, OH. 1999.
16. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
17. American Industrial Hygiene Association (AIHA). The AIHA 1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.
1998.
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CHLOROFORM
67-66-3
Hazard Summary
Chloroform may be released to the air as a result of its formation in the chlorination of
drinking water, wastewater and swimming pools. Other sources include pulp and paper
mills, hazardous waste sites, and sanitary landfills. The major effect from acute
(short-term) inhalation exposure to chloroform is central nervous system (CNS)
depression. Chronic (long-term) exposure to chloroform by inhalation in humans has
resulted in effects on the liver, including hepatitis and jaundice, and CNS effects, such as
depression and irritability. Little information is available on the reproductive or
developmental effects of chloroform in humans, while animal studies have reported
developmental effects, such as decreased fetal body weight and fetal resorptions, and
reproductive effects, such as decreased conception rates, in animals exposed to
chloroform by inhalation. No studies are available on the carcinogenic effects of
chloroform in humans or animals after inhalation exposure. Chloroform has been shown
to be carcinogenic in animals after oral exposure, resulting in an increase in kidney and
liver tumors. The U.S. Environmental Protection Agency (EPA) has classified chloroform
as a Group B2, probable human carcinogen.
Please Note; The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on oral chronic toxicity and the reference dose (RfD), and the carcinogenic
effects of chloroform including the unit cancer risk for inhalation exposure, and the Agency for Toxic Substances
and Disease Registry's (ATSDR's) Toxicological Profile for Chloroform.
Physical Properties
Chloroform is a colorless liquid that is not very soluble in water and is very volatile. (1,6)
Chloroform has a pleasant, nomrritating odor; the odor threshold is 85 ppm. (1)
The chemical formula for chloroform is CHC13, and it has a molecular weight of 119.38
g/mol. (1)
The vapor pressure for chloroform is 159 mm Hg at 20 °C, and it has a log octanol/water
partition coefficient (log Kow) of 1.97. (1)
Uses
The vast majority of the chloroform produced in the U.S. is used to make HCFC-22. The
rest is produced for export and for miscellaneous uses. (1)
Chloroform was used in the past as an extraction solvent for fats, oils, greases, and other
products; as a dry cleaning spot remover; in fire extinguishers; as a fumigant; and as an
anesthetic. However, chloroform is no longer used in these products. (1)
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Sources and Potential Exposure
Chloroform may be released to the air from a large number of sources related to its
manufacture and use, as well as its formation in the chlorination of drinking water,
wastewater, and swimming pools. Pulp and paper mills, hazardous waste sites, and
sanitary landfills are also sources of air emissions. The background level of chloroform in
ambient air in the early 1990's was estimated at 0.00004 ppm. (1)
Human exposure to chloroform may occur through drinking water, where chloroform is
formed as a result of the chlorination of naturally occurring organic materials found in
raw water supplies. Measurements of chloroform in drinking water during the 1970's and
1980's ranged from 0.022 to 0.068 ppm. (1)
Chloroform may also be found in some foods and beverages, largely from the use of tap
water during production processes. (1)
Assessing Personal Exposure
Chloroform can be detected in blood, urine, and body tissues. However, these methods
are not very reliable because chloroform is rapidly eliminated from the body, and the tests
are not specific for chloroform. (1)
Health Hazard Information
Acute Effects:
The major effect from acute inhalation exposure to chloroform in humans is CNS
depression. At very high levels (40,000 ppm), chloroform exposure may result in death,
with concentrations in the range of 1,500 to 30,000 ppm producing anesthesia, and lower
concentrations (<1,500 ppm) resulting in dizziness, headache, tiredness, and other effects.
(1,2)
Effects noted in humans exposed to chloroform via anesthesia include changes in
respiratory rate, cardiac effects, gastrointestinal effects, such as nausea and vomiting, and
effects on the liver and kidney. Chloroform is not currently used as a surgical anesthetic.
(1,2)
In humans, a fatal oral dose of chloroform may be as low as 10 mL (14.8 g), with death
due to respiratory or cardiac arrest. (1,2)
Tests involving acute exposure of animals, such as the LC50 and LD50 tests in rats, have
shown chloroform to have low acute toxicity from inhalation exposure and moderate
acute toxicity from oral exposure. (3)
Chronic Effects (Noncancer):
Chronic exposure to chloroform by inhalation in humans is associated with effects on the
liver, including hepatitis and jaundice, and CNS effects, such as depression and
irritability. Inhalation exposures of animals have also resulted in effects on the kidney.
(1,2)
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Chronic oral exposure to chloroform in humans has resulted in effects on the blood, liver,
and kidney. (1,2)
EPA has not established a reference concentration (RfC) for chloroform. (4)
The California Environmental Protection Agency (CalEPA) has established a chronic
reference exposure level of 0.3 mg/m3 for chloroform based on exposures resulting in
kidney and liver effects in rats. The CalEPA reference exposure level is a concentration at
or below which adverse health effects are not likely to occur. It is not a direct estimator
of risk, but rather a reference point to gauge the potential effects. At lifetime exposures
increasingly greater than the reference exposure level, the potential for adverse health
effects increases. (5)
ATSDR has established an acute inhalation minimal risk level (MRL) of 0.5 mg/m3 (0.1
ppm) based on exposures resulting in liver effects in mice, an intermediate inhalation
MRL of 0.2 mg/m3 (0.05 ppm) based on worker exposures resulting in liver effects in
humans, and a chronic inhalation MRL of 0.1 mg/m3 (0.02 ppm) also based on liver
effects in humans. The MRL is an estimate of the daily human exposure to a hazardous
substance that is likely to be without appreciable risk of adverse noncancer health effects
over a specified duration of exposure. (1)
The RfD for chloroform is 0.01 mg/kg/d based on exposures resulting in fatty cyst
formation in the livers of dogs. The RfD is an estimate (with uncertainty spanning
perhaps an order of magnitude) of a daily oral exposure to the human population
(including sensitive subgroups-) that is likely to be without appreciable risk of deleterious
noncancer effects during a lifetime. (4)
EPA has medium to low confidence in the RfD due to: medium confidence in the critical
study on which the RfD was based because it was of chronic duration, used a fairly large
number of dogs, measured multiple endpoints using only two treatment doses, and a
no-observed-effect level (NOEL) was not determined; and medium to low confidence in
the database because several studies support the choice of a lowest-observed-adverse-
effect level (LOAEL), but a NOEL was not found. (4)
Reproductive/Developmental Effects:
Little information is available on the reproductive or developmental effects of chloroform
in humans, via any route of exposure. A possible association between certain birth
outcomes (e.g., low birth weight, cleft palate) and consumption of contaminated drinking
water was reported. However, because multiple contaminants were present, the role of
chloroform is unclear. (1)
Animal studies have demonstrated developmental effects, such as decreased fetal body
weight, fetal resorptions, and malformations in the offspring of animals exposed to
chloroform via inhalation. (1)
Reproductive effects, such as decreased conception rates, decreased ability to maintain
pregnancy, and an increase in the percentage of abnormal sperm were observed in
animals exposed to chloroform through inhalation. (1)
Animal studies have noted decreased fetal weight, increased fetal resorptions, but no
evidence of birth defects, in animals orally exposed to chloroform. (1)
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Cancer Risk:
No information is available regarding cancer in humans or animals after inhalation
exposure to chloroform. (1)
Epidemiologic studies suggest an association between cancer of the large intestine,
rectum, and/or bladder and the constituents of chlorinated drinking water, including
chloroform. However, there are no epidemiologic studies of water containing only
chloroform. (1)
Chloroform has been shown to be carcinogenic in animals after oral exposure, resulting in
an increase in kidney and liver tumors. (1)
EPA has classified chloroform as a Group B2, probable human carcinogen. (4)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 2.3 x 10"5
(/ig/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
chloroform at an average of 0.04 //.g/m3 (4 x 10'5 mg/m3) over his or her entire lifetime,
that person would theoretically have no more than a one-in-a-million increased chance of
developing cancer as a direct result of breathing air containing this chemical. Similarly,
EPA estimates that continuously breathing air containing 0.4 jig/m3 (4 x 10"4 mg/m3)
would result in not greater than a one-in-a-hundred thousand increased chance of
developing cancer, and air containing 4.0 /ig/m3 (4 x 10"3 mg/m3) would result in not
greater than a one-in-ten thousand increased chance of developing cancer. For a detailed
discussion of confidence in the potency estimates, please see IRIS. (4)
EPA has calculated an oral cancer slope factor of 6.1 x 10"3 (mg/kg/d)"1. (4)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For chloroform: 1 ppm = 4.88 mg/m3.
To convert from fJLg/m3 to mg/m3: mg/m3 = (fig/m3) x (1 mg/1,000
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Health Data from Inhalation Exposure
Chloroform
1000000 r
Regulatory, advisory
numbers'3
Odche/ cndliva')C22nng'rrf)
A03HTLV(49nr9'rrO
NCSHSTEL
ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LCgo (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-effect level.
NIOSH REL - National Institute of Occupational Safety and Health's recommended exposure
limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure
and/or ceiling.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
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a Health numbers are lexicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c These cancer risk estimates were derived from oral data and converted to provide the estimated
inhalation risk.
d The LOAEL is from the critical study used as the basis for the CalEPA chronic reference
exposure level.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Chloroform. Public Health Service, U.S. Department of Health and Human Services,
Atlanta, GA. 1997.
2. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Chloroform. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
5. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
6. The Merck Index. An Encyclopedia of Chemicals, Drugs, andBiologicals. 11th ed. Ed. S.
Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
7. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
8. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents. Biological
Exposure Indices. Cincinnati, OH. 1999.
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9. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
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CHROMIUM COMPOUNDS
Hazard Summary
Chromium occurs in the environment primarily in two valence states, trivalent chromium
(Cr HI) and hexavalent chromium (Cr VI). Exposure may occur from natural or industrial
sources of chromium.
The respiratory tract is the major target organ for chromium (VI) toxicity, for acute
(short-term) and chronic (long-term) inhalation exposures. Shortness of breath, coughing,
and wheezing were reported from a case of acute exposure to chromium (VI), while
perforations and ulcerations of the septum, bronchitis, decreased pulmonary function,
pneumonia, and other respiratory effects have been noted from chronic exposure. Limited
human studies suggest that chromium (VI) inhalation exposure may be associated with
complications during pregnancy and childbirth, while animal studies have not reported
reproductive effects from inhalation exposure to chromium (VT). The U.S.
Environmental Protection Agency (EPA) has classified chromium (VI) as a Group A,
known human carcinogen. Human studies have clearly established that inhaled
chromium (VI) is a human carcinogen, resulting in an increased risk of lung cancer.
Animal studies have shown chromium (VI) to cause lung tumors via inhalation exposure.
Chromium in is much less toxic than chromium (VI). The respiratory tract is also the
major target organ for chromium (HI) toxicity, similar to chromium (VI). Chromium (HI)
is an essential element in humans, with a daily intake of 50 to 200 jUg/d recommended for
an adult. The body can detoxify some amount of chromium (VI) to chromium (HI).
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on inhalation chronic toxicity and the reference concentration (RfC) and oral
chronic toxicity and the reference dose (RfD), and the carcinogenic effects of chromium including the unit cancer
risk for inhalation exposure, EPA's Toxicological Review of Trivalent Chromium and Toxicological Review of
Hexavalent Chromium, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological
Profile for Chromium.
Physical Properties
The metal, chromium (Cr), is a steel-gray solid with a high melting point and an atomic
weight of 51.996 g/mol. Chromium has oxidation states ranging from chromium (-D) to
chromium (+VI). (1)
Chromium forms a large number of compounds, in both the chromium (HI) and the
chromium (VI) forms. Chromium compounds are stable in the trivalent state, with the
hexavalent form being the second most stable state. (1)
The chromium (DTI compounds are sparingly soluble in water and may be found in water
bodies as soluble chromium (Iff) complexes, while the chromium (VI) compounds are
readily soluble in water. (1)
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Uses
The metal chromium is used mainly for making steel and other alloys. (1)
Chromium compounds, in either the chromium (HI) or chromium (VI) forms, are used for
chrome plating, the manufacture of dyes and pigments, leather and wood preservation,
and treatment of cooling tower water. Smaller amounts are used in drilling muds, textiles,
and toner for copying machines. (1)
Sources and Potential Exposure
Chromium is a naturally occurring element in rocks, animals, plants, soil, and volcanic
dust and gases. (1)
Chromium occurs in the environment predominantly in one of two valence states:
trivalent chromium (Cr IE), which occurs naturally and is an essential nutrient, and
hexavalent chromium (Cr VI), which, along with the less common metallic chromium (Cr
0), is most commonly produced by industrial processes. (1)
Chromium (HI) is essential to normal glucose, protein, and fat metabolism and is thus an
essential dietary element. The body has several systems for reducing chromium (VI) to
chromium (HI). This chromium (VI) detoxification leads to increased levels of chromium
(HI). (1)
Air emissions of chromium are predominantly of trivalent chromium, and in the form of
small particles or aerosols. (1,2)
The most important industrial sources of chromium in the atmosphere are those related to
ferrochrome production. Ore refining, chemical and refractory processing,
cement-producing plants, automobile brake lining and catalytic converters for
automobiles, leather tanneries, and chrome pigments also contribute to the atmospheric
burden of chromium. (3)
The general population is exposed to chromium (generally chromium [IE]) by eating
food, drinking water, and inhaling air that contains the chemical. The average daily intake
from air, water, and food is estimated to be approximately less than 0.2 to 0.4 jttg, 2.0 jtig,
and 60 fig, respectively. (1)
Dermal exposure to chromium may occur during the use of consumer products that
contain chromium, such as wood treated with copper dichromate or leather tanned with
chromic sulfate. (1)
Occupational exposure to chromium occurs from chromate production, stainless-steel
production, chrome plating, and working in tanning industries; occupational exposure can
be two orders of magnitude higher than exposure to the general population. (1)
People who live in the vicinity of chromium waste disposal sites or chromium
manufacturing and processing plants have a greater probability of elevated chromium
exposure than the general population. These exposures are generally to mixed chromium
(VI) and chromium (HI). (1)
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Assessing Personal Exposure
Laboratory tests can detect chromium in the blood, urine, and hair of exposed individuals.
(1,5)
Laboratory tests find it difficult to separate chromium VI from chromium HI; in many
cases analysis is done for total chromium. (1)
Health Hazard Information
Acute Effects:
Chromium VI
Chromium (VI) is much more toxic than chromium (HI), for both acute and chronic
exposures. (1,3,4)
The respiratory tract is the major target organ for chromium (VI) following inhalation
exposure in humans. Shortness of breath, coughing, and wheezing were reported in cases
where an individual inhaled very high concentrations of chromium trioxide. (1,4)
Other effects noted from acute inhalation exposure to very high concentrations of
chromium (VI) include gastrointestinal and neurological effects, while dermal exposure
causes skin bums. (1,4,5)
Ingestion of high amounts of chromium (VI) causes gastrointestinal effects in humans and
animals, including abdominal pain, vomiting, and hemorrhage. (1)
Acute animal tests, such as the LC50 and LD50 tests in rats, have shown chromium (VI) to
have extreme toxicity from inhalation (LC50 = 30-140 mg/m3) and oral (LD50 <100
mg/kg) exposure. (1,6)
Chromium III
Chromium (HI) is an essential element in humans, with a daily intake of 50 to 200 Mg/d
recommended for adults. (1)
Acute animal tests have shown chromium (ffl) to have moderate toxicity from oral
exposure, with LD50 values of 200-2000 mg/kg and much lower toxicity from acute
dietary exposures. (1,6)
Chronic Effects (Noncancer):
Chromium VI
Chronic inhalation exposure to chromium (VI) in humans results in effects on the
respiratory tract, with perforations and ulcerations of the septum, bronchitis, decreased
pulmonary function, pneumonia, asthma, and nasal itching and soreness reported. (1,4,5)
Chronic human exposure to high levels of chromium (VI) by inhalation or oral exposure
may produce effects on the liver, kidney, gastrointestinal and immune systems, and
possibly the blood. (1,4,5)
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Rat studies have shown that, following inhalation exposure, the lung and kidney have the
highest tissue levels of chromium. (1,4,5)
Dermal exposure to chromium (VI) may cause contact dermatitis, sensitivity, and
ulceration of the skin. (1,4,5)
The RfC for chromium (VI) (particulates) is 0.0001 mg/m3 based on respiratory effects in
rats. The RfC is an estimate (with uncertainty spanning perhaps an order of magnitude) of
a continuous inhalation exposure to the human population (including sensitive subgroups)
that is likely to be without appreciable risk of deleterious noncancer effects during a
lifetime. It is not a direct estimator of risk but rather a reference point to gauge the
potential effects. At exposures increasingly greater than the RfC, the potential for adverse
health effects increases. Lifetime exposure above the RfC does not imply that an adverse
health effect would necessarily occur. (7)
EPA has medium confidence in the RfC for chromium VI (particulates) based on medium
confidence in the study on which it was based because of uncertainties regarding upper
respiratory tract, reproductive, and renal effects resulting from the exposures. (7)
The RfC for chromium (VI) (chromic acid mists and dissolved Cr (VI) aerosols) is
0.000008 mg/m3 based on respiratory effects in humans. (7)
EPA has low confidence in the RfC based on low confidence in the study on which the
RfC for chromium (VI) (chromic acid mists and dissolved Cr (VI) aerosols) is based
because of uncertainties regarding the exposure characterization and the role of direct
contact for the critical effect; and low confidence in the database because the supporting
studies are equally uncertain regarding the exposure characterization. (7)
The RfD for chromium (VI) is 0.003 mg/kg/d based on the exposure at which no effects
were noted in rats exposed to chromium in the drinking water. (7)
EPA has low confidence in the RfD based on: low confidence in the study on which the
RfD for chromium (VI) was based because a small number of animals were tested, a
small number of parameters were measured, and no toxic effects were noted at the highest
dose tested; and low confidence in the database because the supporting studies are of
equally low quality and developmental endpoints are not well studied. (7)
Chromium III
Although data from animal studies have identified the respiratory tract as the major target
organ for chronic chromium exposure, these data do not demonstrate that the effects
observed following inhalation of chromium (VI) particulates are relevant to inhalation of
chromium (HI). (8)
EPA has not established an RfC for chromium (HI). (8)
The RfD for chromium (HI) is 1.5 mg/kg/d based on the exposure level at which no
effects were observed in rats exposed to chromium (HI) in the diet. (8)
EPA has low confidence in the RfD based on: low confidence in the study on which the
RfD for chromium (HI) was based due to the lack of explicit detail on study protocol and
results; and low confidence in the database due to the lack of high-dose supporting data.
(8)
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Reproductive/Developmental Effects:
Chromium VI
Limited information on the reproductive effects of chromium (VI) in humans exposed by
inhalation suggest that exposure to chromium (VI) may result in complications during
pregnancy and childbirth. (1)
Animal studies have not reported reproductive or developmental effects from inhalation
exposure to chromium (VI). Oral studies have reported severe developmental effects in
mice such as gross abnormalities and reproductive effects including decreased litter size,
reduced sperm count, and degeneration of the outer cellular layer of the seminiferous
tubules. (1,4)
Chromium III
No information is available on the reproductive or developmental effects of chromium
(HI) in humans. (3)
A study of mice fed high levels of chromium (ffl) in their drinking water has suggested a
potential for reproductive effects, although various study characteristics preclude a
definitive finding. (3)
No developmental effects were reported in the offspring of rats fed chromium (IH) during
their developmental period. (1,3)
Cancer Risk:
Chromium VI
Epidemiological studies of workers have clearly established that inhaled chromium is a
human carcinogen, resulting in an increased risk of lung cancer. Although chromium-
exposed workers were exposed to both chromium (ID) and chromium (VI) compounds,
only chromium (VT) has been found to be carcinogenic in animal studies, so EPA has
concluded that only chromium (VI) should be classified as a human carcinogen. (1,7)
Animal studies have shown chromium (VI) to cause lung tumors via inhalation exposure.
(1,5)
EPA has classified chromium (VI) as a Group A, known human carcinogen by the
inhalation route of exposure. Carcinogenicity by the oral route of exposure cannot be
determined and has been classified by EPA as a Group D. (7)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 1.2 x 10~2
(jug/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
chromium at an average of 0.00008 jug/m3 (8 x 10"8 mg/m3) over his or her entire lifetime,
that person would theoretically have no more than a one-in-a-million increased chance of
developing cancer as a direct result of breathing air containing this chemical. Similarly,
EPA estimates that continuously breathing air containing 0.0008 ptg/m3 (8 x 10"7 mg/m3)
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would result in not greater than a one-in-a-hundred thousand increased chance of
developing cancer during their lifetime, and air containing 0.008 /xg/m3 (8 x 10"6 mg/m3)
would result in not greater than a one-in-ten-thousand increased chance of developing
cancer during their lifetime. For a detailed discussion of confidence in the potency
estimates, please see IRIS. (7)
Chromium III
No data are available on the carcinogenic potential of chromium (HI) compounds alone.
(1,8)
EPA has classified chromium (HI) as a Group D carcinogen, not classifiable as to
carcinogenicity in humans. (8)
EPA has stated that "the classification of chromium (VI) as a known human carcinogen
raises a concern for the carcinogenic potential of chromium (HI)." (8)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For chromium: 1 ppm = 2.12 mg/m3.
To convert from fJig/m3 to mg/m3: mg/m3 = (fig/m3) x (1 mg/1,000
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Health Data from Inhalation Exposure
Chromium
Regufcf ory, advisory
numbers"
Heath numbers
MCSHIDLH (25 rng/nr$(G III)
LC50 (ret s) (45 rra/rrf) (C VI)
CSHAPELOmsf'rr?)
03 met-d cndinsdutle)
C8HAPELA03HTLV
(Serretd) MCSH REL
(O III arpcfe)(p.5 rrg/trf)
A33HTLV MCSH REL
(drcrricaidarpd;)
(0.05rrn/nr>!)
AQ3HTLV(P.01
mg/r
O VI)
Berxtrrak ctse^Cresprctcry)
LCWELa(resdrcfaY)
(D.OCCrrn'rr?)
raqp-oooi
(C VI patiaJcfes)
(drcrricaidmsts)
Oncer Risk
1 in a
rrillicnrisk
0.00000001
ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LC50 (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-affect level.
NIOSH IDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can
escape from an exposure condition that is likely to cause death or immediate or delayed
permanent adverse health effects or prevent escape from the environment.
NIOSH REL - NIOSH's recommended exposure limit; NIOSH-recommended exposure limit for
an 8- or 10-h time-weighted-average exposure and/or ceiling.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
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expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The benchmark dose is from the critical study used as the basis for the EPA's RfC for Cr(VI)
particulates.
d The LOAEL is from the critical study used as the basis for the EPA's RfC for chromic acid
mists and dissolved Cr (VI) aerosols.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Chromium. Public Health Service, U.S. Department of Health and Human Services, Atlanta, GA.
1998.
2. SAIC. PM/Toxics Integration: Addressing Co-Control Benefits. Submitted to U.S.
Environmental Protection Agency, Office of Air Quality Planning and Standards, Research
Triangle Park, NC. 1998.
3. U.S. Environmental Protection Agency (EPA). Toxicological Review ofTrivalent
Chromium. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1998.
4. U.S. Environmental Protection Agency (EPA). Toxicological Review ofHexavalent
Chromium. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1998.
5. World Health Organization (WHO). Chromium. Environmental Health Criteria 61. Geneva,
Switzerland. 1988.
6. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program, National
Library of Medicine, Bethesda, MD. 1993.
7. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Chromium VI. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1993.
8. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Chromium III. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1993.
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9. Occupational Safety and Health Administration (OSHA). Occupational Safety and Health
Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29 CFR 1910.1000.
1998.
10. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
11. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to Chemical
Hazards. U.S. Department of Health and Human Services, Public Health Service, Centers for
Disease Control and Prevention. Cincinnati, OH. 1997.
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COKE OVEN EMISSIONS1
Hazard Summary
Exposure to coke oven emissions may occur for workers in the aluminum, steel, graphite,
electrical, and construction industries. No information is available on the effects of coke
oven emissions in humans from acute (short-term) exposure. Animal studies have
reported weakness, depression, shortness of breath, general edema, and effects on the
liver from acute oral exposure to coke oven emissions. Chronic (long-term) exposure to
coke oven emissions in humans results in conjunctivitis, severe dermatitis, and lesions of
the respiratory system and digestive system. No information is available on the
reproductive or developmental effects of coke oven emissions in humans or animals.
Cancer is the major concern from exposure to coke oven emissions. Epidemiologic
studies of coke oven workers have reported an increase in cancer of the lung, trachea,
bronchus, kidney, prostate, and other sites. Animal studies have reported tumors of the
lung and skin from inhalation exposure to coal tar. The U.S. Environmental Protection
Agency (EPA) has classified coke oven emissions as a Group A, known human
carcinogen.
Please Note: The main source of information for this fact sheet is EPA's Integrated Risk Information System (IRIS),
which contains information on the carcinogenic effects of coke oven emissions including the unit cancer risk for
inhalation exposure. Other secondary sources include the Hazardous Substances Data Bank (HSDB), a database of
summaries of peer-reviewed literature, and The Handbook of Toxic and Hazardous Chemicals and Carcinogens, a
reference book that summarizes the key effects from exposure to hazardous chemicals.
Physical Properties
Coke oven emissions are a mixture of coal tar, coal tar pitch, and creosote and contain
chemicals such as benzo(a)pyrene, benzanthracene, chrysene, and phenanthrene. (1)
Condensed coke oven emissions are a brownish, thick liquid or semisolid with a
naphthalene-like odor, while uncondensed coke oven emissions are vapors that escape
when the ovens are changed and emptied. (2)
The odor threshold for coke oven emissions is not available. The actual chemical content
of the emissions depends on the process variables.
Uses
Chemicals recovered from coke oven emissions are used as a raw material for plastics,
solvents, dyes, drugs, waterproofing, paints, pipecoating, roads, roofing, insulation, and
as pesticides and sealants. (2)
1 Coke oven emissions include coal tar, creosote, and coal tar pitch.
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Sources and Potential Exposure
Occupational exposure to coke oven emissions may occur for those workers in the
aluminum, steel, graphite, electrical, and construction industries. (1)
Assessing Personal Exposure
No information is available on the assessment of personal exposure to coke oven
emissions.
Health Hazard Information
Acute Effects:
No information is available on the effects of coke oven emissions from acute exposure in
humans.
Animal studies have reported weakness, depression, shortness of breath, general edema,
and effects on the liver from acute oral exposure to coke oven emissions. (2)
Chronic Effects (Noncancer):
Chronic exposure to coke oven emissions in humans results in conjunctivitis, severe
dermatitis, and lesions of the respiratory and digestive systems. (2)
Animal studies have reported effects on the liver from chronic oral exposure to coke oven
emissions. (2)
EPA has not established a reference concentration (RfC) or a reference dose (RfD) for
coke oven emissions. (3)
Reproductive/Developmental Effects:
No information is available on the reproductive or developmental effects of coke oven
emissions in humans or animals.
Cancer Risk:
Epidemiologic studies of coke oven workers have reported an increase in cancer of the
lung, trachea, bronchus, kidney, prostate, and other sites. (3)
Animal studies have reported tumors of the lung and skin from inhalation exposure to
coal tar. (3)
EPA has classified coke oven emissions as a Group A, known human carcinogen. (3)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 6.2 x 10"4
(jig/m3)'1. EPA estimates that, if an individual were to continuously breathe air containing
coke oven emissions at an average of 0.002 j^g/m3 (2 x 10"6 mg/m3) over his or her entire
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lifetime, that person would theoretically have no more than a one-in-a-million increased
chance of developing cancer as a direct result of continuously breathing air containing
this chemical. Similarly, EPA estimates that breathing air containing 0.02 /ng/m3 (2 x 10"5
mg/m3) would result in not greater than a one-in-a-hundred-thousand increased chance of
developing cancer during a lifetime, and air containing 0.2 /ig/m3 (2 x 104 mg/m3) would
result in not greater than a one-in-ten-thousand increased chance of developing cancer
during a lifetime. For a detailed discussion of confidence in the potency estimates, please
see IRIS. (3)
Health Data from Inhalation Exposure
GbkeOven Emissions
s
"Si
£
c
o
0)
u
0.1
0.01
0.001
0.0001
0.00001
0.000001
Regulatory, advisory
number sb
Hedth numbers
MCSH REL (cckecvenemssicns)(p.5-0.7 nng/nr?)
CSHAFEL, A33HTLV(ccd ta at*vdctiles)
(P.2mcyrrf) cSHAPELfcckecvenenrissicns)
(axi tcr ptch
vdctiles)
(0.1 rra'nrp)
ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
NIOSH REL - National Institute of Occupational Safety and Health's recommended exposure
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limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure
and/or ceiling.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effects averaged over a normal 8-h workday or a 40-h
workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
References
1. M. Sittig. Handbook of Toxic and Hazardous Chemicals and Carcinogens. 2nd ed. Noyes
Publications, Park Ridge, NT. 1985.
2. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
3. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Coke Oven Emissions. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
4. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
5. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
6. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
7. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
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1,2-DICHLOROETHANE (ETHYLENE BICHLORIDE)
107-06-2
Hazard Summary
Exposure to low levels of 1,2-dichloroethane can occur from breathing ambient or
workplace air. Inhalation of concentrated 1,2-dichloroethane vapor can induce effects on
the human nervous system, liver, and kidneys, as well as respiratory distress, cardiac
arrhythmia, nausea, and vomiting. Similar effects have been reported in animals exposed
by inhalation. Clouding of the cornea and eye irritation have been observed in animals.
Chronic (long-term) inhalation exposure to 1,2-dichloroethane produced effects on the
liver and kidneys in animals. No information is available on the reproductive or
developmental effects of 1,2-dichloroethane in humans. Decreased fertility and increased
embryo mortality have been observed in inhalation studies of rats. The U.S.
Environmental Protection Agency (EPA) has classified 1,2-dichloroethane as a Group B2,
probable human carcinogen. Epidemiological studies are not conclusive regarding the
carcinogenic effects of 1,2-dichloroethane, due to concomitant exposure to other
chemicals. Following treatment by gavage, several tumor types were induced in rats and
mice.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on the carcinogenic effects of 1,2-dichloroethane including the unit cancer risk
for inhalation exposure, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological
Profile for 1,2-Dichloroethane.
Physical Properties
The chemical formula for 1,2-dichloroethane is C2H4C12, and its molecular weight is
98.96 g/mol. (1)
1,2-Dichloroethane occurs as a colorless, oily, heavy liquid that is slightly soluble in
water. (1)
1,2-Dichloroethane has a pleasant chloroform-like odor, with an odor threshold of 6-10
ppm. (1)
The vapor pressure for 1,2-dichloroethane is 64 mm Hg at 20 °C, and its log
octanol/water partition coefficient (log K^) is 1.48. (1)
Uses
1,2-Dichloroethane is primarily used in the production of vinyl chloride as well as other
chemicals. It is used in solvents in closed systems for various extraction and cleaning
purposes in organic synthesis. It is also added to leaded gasoline as a lead scavenger. (1)
It is also used as a dispersant in rubber and plastics, as a wetting and penetrating agent.
(1)
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It was formerly used in ore flotation, as a grain fumigant, as a metal degreaser, and in
textile and PVC cleaning. (1)
Sources and Potential Exposure
Inhalation of 1,2-dichloroethane in the ambient or workplace air is generally the main
route of human exposure. The compound may be released during its production, storage,
use, transport, and disposal. (1)
Exposure may also occur through the consumption of contaminated water. But usually
1,2-dichloroethane will evaporate quickly into the air from the water or soil. (1)
The average levels of 1,2-dichloroethane in the air of seven urban locations in 1980-1981
ranged from 0.1 to 1.5 ppb. (1)
Assessing Personal Exposure
Breath samples may be used to determine whether or not someone has been recently
exposed to 1,2-dichloroethane. (1)
Health Hazard Information
Acute Effects:
Inhaling concentrated 1,2-dichloroethane can be lethal to humans. An occupationally
exposed man died from cardiac arrhythmia after acute (short-term) inhalation exposure to
concentrated vapors of 1,2-dichloroethane; congestion of the lungs, degenerative changes
in the myocardium, and damage to the liver, kidneys, and nerve cells in the brain were
also observed. (1)
Acute inhalation exposure to 1,2-dichloroethane can affect the nervous system, with
effects including narcosis, nausea, and vomiting. (1)
Effects reported in animals exposed by inhalation are similar to those for humans. (1)
Clouding of the cornea and eye irritation have been observed in animals and are thought
to be the result of vapor contact with the eyes. (1)
Cardiac arrhythmia, pulmonary edema, bronchitis, hemorrhagic gastritis and colitis,
depression, and changes in the brain tissue have been reported in humans that ingested
large amounts of 1,2-dichloroethane. (1)
Acute animal tests, such as the LC50 and LD50 tests in rats, mice, and rabbits, have
demonstrated 1,2-dichloroethane to have moderate acute toxicity from inhalation or
dermal exposure and moderate to high acute toxicity from oral exposure. (2)
Chronic Effects (Noncancer):
Chronic inhalation exposure to 1,2-dichloroethane produced effects on the liver and
kidneys in animals. (1)
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Some studies have reported changes in the liver and kidneys and effects on the immune
system and central nervous system (CNS) in animals chronically exposed by ingestion.
(1)
EPA has not established a reference dose (RfD) or a reference concentration (RfC) for
1,2-dichloroethane. (3)
ATSDR has established an intermediate oral minimal risk level (MRL) of 0.2 mg/kg/d
based on kidney effects in animals. The MRL is an estimate of the daily human exposure
to a hazardous substance that is likely to be without appreciable risk of adverse noncancer
health effects over a specified duration of exposure. Exposure to a level above the MRL
does not mean that adverse health effects will occur. The MRL is intended to serve as a
screening tool. (1)
ATSDR has established a chronic inhalation MRL of 0.8 mg/m3 (0.2 ppm) based on liver
effects in animals and an acute inhalation MRL of 0.8 mg/m3 (0.2 ppm) based on
immunological effects in animals. (1)
The California Environmental Protection Agency (CalEPA) has established a chronic
reference exposure level of 0.4 mg/m3 for 1,2-dichloroethane based on liver effects in
rats. The CalEPA reference exposure level is a concentration at or below which adverse
health effects are not likely to occur. (5)
Reproductive/Developmental Effects:
No information is available on the reproductive or developmental effects of
1,2-dichloroethane in humans.
Decreased fertility and increased embryo mortality have been observed in inhalation
studies of rats. (1)
Cancer Risk:
Epidemiological occupational studies could not link exposure to 1,2-dichloroethane
specifically with excess cancer incidence. (1)
An increased incidence of colon and rectal cancer in men over 55 years of age exposed to
1,2-dichloroethane in the drinking water has been reported. However, the study
population was concomitantly exposed to other chemicals. (1)
Following treatment by gavage, several tumor types (including increased incidences of
forestomach squamous-cell carcinomas, circulatory system hemangiosarcomas, mammary
adenocarcinoma, alveolar/bronchiolar adenomas, endometrial stromal polyps and
sarcomas, and hepatocellular carcinomas) were induced in rats and mice. (1,3,4)
An increased incidence of lung papillomas has been reported in mice after topical
application. (1,3)
EPA has classified 1,2-dichloroethane as a Group B2, probable human carcinogen. (3)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit cancer risk estimate of 2.6
x 10"5 (^g/m3)'1. EPA estimates that, if an individual were to continuously breathe air
containing 1,2-dichloroethane at an average of 0.04 /ig/m3 (4 x 10"5 mg/m3) over his or
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her entire lifetime, that person would theoretically have no more than a one-in-a-million
increased chance of developing cancer as a direct result of breathing air containing this
chemical. Similarly, EPA estimates that breathing air containing 0.4 jug/m3 (4 x 10"4
mg/m3) would result in not greater than a one-in-a-hundred thousand increased chance of
developing cancer, and air containing 4.0 /Ag/m3 (4 x 10"3 mg/m3) would result in not
greater than a one-in-ten thousand increased chance of developing cancer. For a detailed
discussion of confidence in the potency estimates, please see IRIS. (3)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For 1,2-dichloroethane: 1 ppm = 4.05 mg/m3. To convert from fig/m3 to mg/m3: mg/m3 = (fjig/m3)
x (1 mg/1,000 fig).
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Health Data from Inhalation Exposure
1,2-Dichloroethcne
100000
10000
1000
100
m"
I 10
£
.2 1
+*
G
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expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
OSHA PEL ceiling - OSHA's permissible exposure limit ceiling value; the concentration of a
substance that should not be exceeded at any time.
a Health numbers are lexicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the CalEPA chronic reference
exposure level.
d These cancer risk estimates were derived from oral data and converted to provide the estimated
inhalation risk.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
1,2-Dichloroethane. Public Health Service, U.S. Department of Health and Human
Services, Atlanta, GA. 1992.
2. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
3. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on 1,2-Dichloroethane. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
4. U.S. Environmental Protection Agency (EPA). Health Effects Assessment for
1,2-Dichloroethane. EPA/540/1-86/002. Environmental Criteria and Assessment Office,
Office of Health and Environmental Assessment, Office of Research and Development,
Cincinnati, OH. 1986.
5. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
6. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
7. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents. Biological
Exposure Indices. Cincinnati, OH. 1999.
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8. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
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1,2-DICHLOROPROPANE (PROPYLENE BICHLORIDE)
78-87-5
Hazard Summary
1,2-Dichloropropane is used as a chemical intermediate in several industries. Acute
(short-term) inhalation exposure to high levels of 1,2-dichloropropane by humans results
in effects on the lungs, gastrointestinal system, blood, liver, kidneys, central nervous
system (CNS), and eyes. No information is available on the chronic (long-term) effects of
1,2-dichloropropane in humans, and animal studies have reported effects on the
respiratory system and blood from chronic inhalation exposure. Limited information is
available on the reproductive or developmental effects of 1,2-dichloropropane in humans.
Animal studies have reported reproductive and developmental effects from
1,2-dichloropropane exposure by gavage. No information is available regarding the
carcinogenic effects of 1,2-dichloropropane in humans from inhalation or oral exposure.
Animal studies have reported an increased incidence of mammary gland tumors in female
rats and liver tumors in male and female mice given 1,2-dichloropropane by gavage. The
U.S. Environmental Protection Agency (EPA) has provisionally classified
1,2-dichloropropane as a Group B2, probable human carcinogen.
Please Note: The main sources of information for this fact sheet are the Agency for Toxic Substances and Disease
Registry's (ATSDR's) Toxicological Profile for 1,2-Dichloropropane and EPA's Integrated Risk Information
System (IRIS), which contains information on inhalation chronic toxicity of 1,2-dichloropropane and the reference
concentration (RfC).
Physical Properties
The chemical formula for 1,2-dichloropropane is CjP^C^, and the molecular weight is
112.99 g/mol. (1)
1,2-Dichloropropane is a colorless liquid which evaporates quickly at room temperature.
(1)
1,2-Dichloropropane has a chloroform-like odor and an odor threshold of 0.25 ppm. (1)
The vapor pressure for 1,2-dichloropropane is 49.67 mm Hg at 25 °C, and it has a log
octanol/water partition coefficient (log Kow) of 1.99. (1)
1,2-Dichloropropane has a half-life in air ranging from 16 to greater than 23 days. (1)
Uses
1,2-Dichloropropane is used as a chemical intermediate in the production of chlorinated
organic chemicals, as an industrial solvent, in ion exchange manufacture, in toluene
diisocyanate production, in photographic film manufacture, for paper coating, and for
petroleum catalyst regeneration. (1)
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1,2-Dichloropropane was used in the past as a soil fumigant for a variety of crops. This
use has been discontinued, and pesticide formulations containing 1,2-dichloropropane are
no longer available in the U.S.. (1)
Sources and Potential Exposure
1,2-Dichloropropane has been detected at low levels in ambient air, with an average level
in air of about 0.022 ppb. (1)
An early 1980s nationwide survey of water supplies derived from groundwater found that
13 of 945 water supplies contained 1,2-dichloropropane at levels around 1 ppb. (1)
Occupational exposure to 1,2-dichloropropane may occur during its production, during its
use in chemical reactions or as an industrial solvent, or from evaporation from wastewater
that contains the chemical. (1)
Assessing Personal Exposure
Medical tests can detect 1,2-dichloropropane in urine and blood. 1,2-Dichloropropane
leaves the body quickly, and thus the tests should be done soon after the exposure. (1)
Health Hazard Information
Acute Effects:
Acute exposure of humans to very high levels of 1,2-dichloropropane from inhalation and
oral exposure results in effects on the gastrointestinal system, blood, liver, kidneys, and
CNS. Additional effects noted in humans, from inhalation exposure only, are effects on
the lung (chest discomfort, shortness of breath, and cough) and the eyes (conjunctival
hemorrhages). (1)
Animal studies have reported effects on the respiratory system, liver, kidneys, eyes, and
CNS from acute inhalation exposure to 1,2-dichloropropane. (1)
Tests involving acute exposure of animals, such as the LC50 and LD50 tests in rats, have
shown 1,2-dichloropropane to have moderate acute toxicity from inhalation and oral
exposure. (1,2)
Chronic Effects (Noncancer):
No information is available on the effects from chronic exposure to 1,2-dichloropropane
in humans from inhalation or oral exposure. (1)
Chronic animal studies, via inhalation exposure, have reported effects on the respiratory
system and blood, while oral animal studies have noted effects on the blood, liver, and
CNS. (1,3)
The RfC for 1,2-dichloropropane is 0.004 mg/m3 based on hyperplasia of the nasal
mucosa in rats. The RfC is an estimate (with uncertainty spanning perhaps an order of
magnitude) of a continuous inhalation exposure to the human population (including
sensitive subgroups) that is likely to be without appreciable risk of deleterious noncancer
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effects during a lifetime. It is not a direct estimator of risk but rather a reference point to
gauge the potential effects. At exposures increasingly greater than the RfC, the potential
for adverse health effects increases. Lifetime exposure above the RfC does not imply that
an adverse health effect would necessarily occur. (4)
EPA has high confidence in the RfC based on: high confidence in the study on which the
RfC was based because it used an adequate number of animals, exposure concentrations,
and controls, examined three species, focused on known target organs, and the incidence
and severity of the nasal lesions were exposure-related, and medium confidence in the
database because there are no chronic inhalation studies. (4)
EPA has not established a reference dose (RfD) for 1,2-dichloropropane. (4)
ATSDR has established an acute oral minimal risk level (MRL) of 0.1 mg/kg/d based on
neurological effects in rats; an intermediate oral MRL of 0.07 mg/kg/d based on
hematological effects in rats; and a chronic oral MRL of 0.09 mg/kg/d based on liver
effects in mice. The MRL is an estimate of the daily human exposure to a hazardous
substance that is likely to be without appreciable risk of adverse noncancer health effects
over a specified duration of exposure. (1)
Reproductive/Developmental Effects:
A case was reported of a woman who was hospitalized with metrorrhagia (bleeding from
the uterus between menstrual periods) after acute inhalation exposure to
1,2-dichloropropane. No other information is available on the reproductive or
developmental effects of 1,2-dichloropropane in humans. (1)
No reproductive effects were noted in several animal inhalation studies. (1)
Developmental effects, such as an increased incidence of delayed ossification of the
bones of the skull, and reproductive effects such as testicular degeneration and increased
incidences of infection of the ovary, uterus, or other organs, have been observed in
animals exposed to 1,2-dichloropropane by gavage. It is not known if the infections
observed were related to 1,2-dichloropropane treatment since controls were also infected.
(1)
Cancer Risk:
No studies are available regarding carcinogenic effects in humans from inhalation or oral
exposure to 1,2-dichloropropane. (1)
An increased incidence of mammary gland tumors in female rats and liver tumors in male
and female mice were reported in studies in which 1,2-dichloropropane was given by
gavage. (1)
EPA has provisionally classified 1,2-dichloropropane as a Group B2, probable human
carcinogen, with an oral cancer slope factor of 6.8 x 10"2 (mg/kg/d)"1. (5)
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Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For dichloropropane: 1 ppm = 4.62 mg/m3.
Health Data from Inhalation Exposure
1,2-Dichloropropcne
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ACGIH STEL - American Conference of Governmental and Industrial Hygienists' short-term
exposure limit; 15-min time-weighted-average exposure that should not be exceeded at any time
during a workday even if the 8-h time-weighted-average is within the threshold limit value.
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ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LC50 (Lethal Concentrationso) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-effect level.
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can
escape from an exposure condition that is likely to cause death or immediate or delayed
permanent adverse health effects or prevent escape from the environment.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c This LOAEL is from the critical study used as the basis for the EPA RfC.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
1,2-Dichloropropane (Draft). Public Health Service, U.S. Department of Health and
Human Services. 1989.
2. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
3. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
4. U.S. Environmental Protection Agency(EPA). Integrated Risk Information System (IRIS)
on 1,2-Dichloropropane. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
5. U.S. Environmental Protection Agency (EPA). Health Effects Assessment Summary
Tables. FY-1997 Update. National Center for Environmental Assessment, Office of
Research and Development, Office of Emergency Response and Remedial Response,
Washington, DC. 1997.
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6. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
7. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
8. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
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1,3-DICHLOROPROPENE
542-75-6
Hazard Summary
1,3-Dichloropropene is used as a component in formulations for soil fumigants. Acute
(short-term) inhalation exposure of humans following a spill caused mucous membrane
irritation, chest pain, and breathing difficulties. Effects on the lung have been observed in
rats acutely exposed to 1,3-dichloropropene by inhalation. Chronic (long-term) dermal
exposure may result in skin sensitization in humans. Damage to the nasal mucosa and
urinary bladder are the primary health effects of rodents chronically exposed to
1,3-dichloropropene by inhalation. A study of male workers engaged in the manufacture
of 1,3-dichloropropene indicated no significant effect on fertility at exposure levels
occurring in the work environment. The only developmental effect seen in animal studies
was fewer fetuses per litter in rats exposed to high levels by inhalation, and no
reproductive effects have been noted. Information on the carcinogenic effects of
1,3-dichloropropene in humans is limited; two cases of histiocytic lymphomas and one
case of leukemia have been reported in humans accidentally exposed by inhalation to
concentrated vapors during cleanup of a tank truck spill. An increased incidence of
bronchioalveolar adenomas has been reported in male mice exposed by inhalation but not
in rats or female mice. The U.S. Environmental Protection Agency (EPA) has classified
1,3-dichloropropene as a Group B2, probable human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on inhalation chronic toxicity of 1,3-dichloropropene and the reference
concentration (RfC), oral chronic toxicity and the reference dose (RfD), and the carcinogenic effects of
1,3-dichloropropene, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile
for 1,3-Dichloropropene.
Physical Properties
The chemical formula for 1,3-dichloropropene is C3H4C12, and its molecular weight is
110.98 g/mol. (1)
1,3-Dichloropropene occurs as a colorless liquid that dissolves in water. (1)
1,3-Dichloropropene has a sweet chloroform-like odor, with an odor threshold of 1 ppm.
(1)
The vapor pressure for 1,3-dichloropropene is 34 to 43 mm Hg at 25 °C, and its log
octanol/water partition coefficient (log Kow) is 1.60. (1)
The half-life of 1,3-dichloropropene in ambient air may range from 7 to 50 hours. (1)
Uses
1,3-Dichloropropene is the predominant component of several formulations used in
agriculture as soil fumigants for parasitic nematodes. (1,4)
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Sources and Potential Exposure
Workers may be occupationally exposed to 1,3-dichloropropene, dermally or by
inhalation, during its manufacture, formulation, or application as a soil fumigant. (1,2)
The general public may be exposed via inhalation near source areas or from the
consumption of contaminated drinking water from wells near some hazardous waste sites.
(1,2)
Assessing Personal Exposure
1,3-Dichloropropene or its breakdown products can be detected in blood and urine to
determine whether or not exposure has occurred. However, metabolites measured in
blood and urine are not specific to 1,3-dichloropropene. (1)
Health Hazard Information
Acute Effects:
Acute inhalation exposure of humans after a tank truck spill resulted in mucous
membrane irritation, cough, chest pain, and breathing difficulties. (1)
Effects on the lung, including emphysema and edema, have been observed in rats acutely
exposed to 1,3-dichloropropene by inhalation. (1)
Lung congestion and hemorrhage, ulcerations of the glandular stomach, hemorrhage of
the small intestine, dark and patchy liver, and hemorrhage of the liver have been observed
in rats acutely exposed to 1,3-dichloropropene in their diet or via gavage. Neurotoxic
effects, including hunched posture, lethargy, ptosis, ataxia, and decreased respiratory rate,
have also been observed in orally exposed rats. (1)
Acute animal tests, such as the LC50 and LD50 tests in rats, mice, and rabbits, have
demonstrated 1,3-dichloropropene to have moderate acute toxicity from inhalation,
moderate to high acute toxicity from oral exposure, and high acute toxicity from dermal
exposure. (3)
Chronic Effects (Noncancer):
Chronic dermal exposure may result in skin sensitization in humans. (1)
Damage to the nasal mucosa and urinary bladder are the primary health effects of rodents
chronically exposed to 1,3-dichloropropene by inhalation. Hyperplastic lesions of the
upper respiratory tract and degeneration of the olfactory epithelium in the nasal turbinates
have been observed in chronically exposed rats and mice. Chronic inhalation exposure of
mice has resulted in changes in the urinary bladder. (1,4,5)
In one study, reversible cloudy swelling of the renal tubular epithelium was reported in
rats chronically exposed by inhalation. (1,4,5)
In rats and mice chronically exposed by inhalation, hyperplasia and hyperkeratosis of the
forestomach have been observed, while hyperplasia of the forestomach and of the urinary
bladder have resulted from chronic oral exposure. (1,4)
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The RfC for 1,3-dichIoropropene is 0.02 mg/m3 based on hypertrophy/hyperplasia of the
nasal respiratory epithelium in mice. The RfC is an estimate (with uncertainty spanning
perhaps an order of magnitude) of a continuous inhalation exposure to the human
population (including sensitive subgroups) that is likely to be without appreciable risk of
deleterious noncancer effects during a lifetime. It is not a direct estimator of risk but
rather a reference point to gauge the potential effects. At exposures increasingly greater
than the RfC, the potential for adverse health effects increases. Lifetime exposure above
the RfC does not imply that an adverse health effect would necessarily occur. (5)
EPA has high confidence in the RfC based on: high confidence in the study on which the
RfC was based because it is a well-designed study using two species of animals (both
sexes) and including detailed histopathological examinations of numerous tissues with
extensive analysis of the respiratory system and corroborative studies performed in both
rats and mice have also shown this to be a sensitive endpoint; and high confidence in the
database because several studies reported similar effects on the respiratory system at
comparable exposure levels, and acute effects observed in humans were similar to the
animal effects. (5)
The RfD for 1,3-dichloropropene is 0.0003 mg/kg/d based on increased organ weights in
rats. (5)
EPA has low confidence in the RfD based on: low confidence in the study on which the
RfD was based because it is of low quality and of short duration (90 days), and low
confidence in the database because of the remaining studies, only two teratology studies
were considered acceptable. (5)
Reproductive/Developmental Effects:
A study of male workers engaged in the manufacture of 1,3-dichloropropene indicated no
significant effect on fertility at exposure levels occurring in the work environment. (4)
No evidence of developmental toxicity was observed in rats or rabbits exposed to
1,3-dichloropropene by inhalation, but significant maternal toxicity was seen in both
species. (4)
In one study of rats exposed by inhalation, fewer fetuses per litter were reported at the
highest exposure concentration. (1)
In other studies, no adverse reproductive effects were observed in rats and mice exposed
by inhalation. (1,5)
Cancer Risk:
Information on the carcinogenic effects of 1,3-dichloropropene in humans is limited. Two
cases of histiocytic lymphomas and one case of leukemia have been reported in
emergency response personnel exposed to concentrated 1,3-dichloropropene vapors
during cleanup of a tank truck spill. (1,4,5)
An increased incidence of bronchioalveolar adenomas has been reported in male mice
exposed by inhalation but not in rats or female mice. (1,4)
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Forestomach, adrenal and thyroid tumors, and liver nodules in rats and forestomach,
urinary bladder, and lung tumors in mice have been observed in rodents exposed to
1,3-dichloropropene via gavage. (1,4,5)
EPA has classified 1,3-dichloropropene as a Group B2, probable human carcinogen. (5)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA has calculated a provisional inhalation unit risk
estimate of 3.7. x 10'5 (jig/m3)'1. (6)
EPA has calculated a provisional oral cancer slope factor of 0.18 (mg/kg/d)"1. (6)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/( 24.45).
For 1,3-dichloropropene: 1 ppm = 4.54 mg/m3.
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Health Data from Inhalation Exposure
1,3-Dichloropr opene
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ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LCso (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-effect level.
NIOSH REL - National Institute of Occupational Safety and Health's recommended exposure
limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure
and/or ceiling.
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NOAEL - No-observed-adverse-effect level.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
0 The LOAEL and NOAEL are from the critical study used as the basis for the EPA RfC.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
1,3-Dichloropropene. Public Health Service, U.S. Department of Health and Human
Services. 1992.
2. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
4. U.S. Environmental Protection Agency (EPA). Health and Environmental Effects Profile
for 1,3-Dichloropropene. ECAO-CIN-G074. Environmental Criteria and Assessment
Office, Office of Health and Environmental Assessment, Office of Research and
Development, Cincinnati, OH. 1989.
5. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on 1,3-Dichloropropene. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
6. U.S. Environmental Protection Agency (EPA). Health Effects Assessment Summary
Tables. FY-1997 Update. National Center for Environmental Assessment, Office of
Research and Development, Office of Emergency and Remedial Response, Washington,
DC. 1997.
7. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
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8. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
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ETHYLENE DIBROMIDE (1,2-DIBROMOETHANE)
106-93-4
Hazard Summary
Exposure to ethylene dibromide primarily occurs from its past use as an additive to
leaded gasoline and as a fumigant. Ethylene dibromide is extremely toxic to humans.
Changes in the liver and kidney have been noted in humans who died from ingestion of
ethylene dibromide. The chronic (long-term) effects of exposure to ethylene dibromide
have not been well documented in humans. Animal studies indicate that chronic exposure
to ethylene dibromide may result in toxic effects to the liver, kidney, and the testis,
irrespective of the route of exposure. Limited data on men occupationally exposed to
ethylene dibromide indicate that long-term exposure to ethylene dibromide can impair
reproduction by damaging sperm cells in the testicles. Animal studies have demonstrated
reproductive and developmental effects from ethylene dibromide exposure. Human data
are considered inadequate in providing evidence of cancer by exposure to ethylene
dibromide. Several animal studies indicate that long-term exposure to ethylene dibromide
increases the incidences of a variety of tumors in rats and mice in both sexes by all routes
of exposure. The U.S. Environmental Protection Agency (EPA) has classified ethylene
dibromide as a Group B2, probable human carcinogen.
Please Note: The main sources of information for this fact sheet EPA's Integrated Risk Information System (IRIS),
which contains information on the carcinogenic effects of ethylene dibromide including the unit cancer risk for
inhalation exposure, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile
for 1,2-Dibromoethane.
Physical Properties
Ethylene dibromide is a colorless liquid with a mild sweet odor, like chloroform. (1,7)
Ethylene dibromide is slightly soluble in water. (1,7)
The chemical formula for ethylene dibromide is C2H4Br2, and it has a molecular weight of
187.88 g/mol. (1,7)
The vapor pressure for ethylene dibromide is 11.0 mm Hg at 25 °C, and it has a log
octanol/water partition coefficient (log Kow) of 86. (1).
Ethylene dibromide reacts with hydroxyl radicals in the atmosphere, with a half-life for
this reaction of approximately 40 days. In water, its half-life ranges from 2.5 to 13.2
years, and in soil it was detected 19 years after it had been applied. (1)
Uses
Ethylene dibromide was used in the past as an additive to leaded gasoline; however, since
leaded gasoline is now banned, it is no longer used for this purpose. (1)
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Ethylene dibromide was used as a fumigant to protect against insects, pests, and
nematodes in citrus, vegetable, and grain crops, and as a fumigant for turf, particularly on
golf courses. In 1984, EPA banned its use as a soil and grain fumigant. (1)
Ethylene dibromide is currently used in the treatment of felled logs for bark beetles and
termites, and control of wax moths in beehives. (1)
Ethylene dibromide is also used as an intermediate for dyes, resins, waxes, and gums. (1)
Sources and Potential Exposure
Possible sources of ethylene dibromide emissions to the ambient air are production and
processing facilities. (1)
Exposure could occur from inhalation of ambient air near industries that use ethylene
dibromide or through the ingestion of contaminated drinking water. (1)
Assessing Personal Exposure
There is no known reliable medical test to determine whether someone has been exposed
to ethylene dibromide. (1)
Health Hazard Information
Acute Effects:
Clinical signs in humans and animals related to acute inhalation exposure to ethylene
dibromide are depression and collapse. Ethylene dibromide is a severe skin irritant that
can cause blistering. (1,2)
Exposure to high concentrations of ethylene dibromide through inhalation, ingestion, or
skin contact can result in death. Changes in the liver and kidney are reported in humans
who died from ingestion of ethylene dibromide. (1,2)
Tests involving acute exposure of animals, such as the LD50 test in rats, have shown
ethylene dibromide to have high acute toxicity from oral exposure, while the LC50 test in
rats has demonstrated moderate acute toxicity from inhalation exposure. (3)
Chronic Effects (Noncancer):
The chronic effects of exposure to ethylene dibromide have not been extensively
documented in humans. In one case in which a worker breathed ethylene dibromide for
several years, he developed bronchitis, headache, and depression. His health improved
after he stopped breathing air contaminated with ethylene dibromide. (1,2)
Animal studies indicate that prolonged exposure to ethylene dibromide may result in
toxic effects to the liver, kidney, and the testis whether by inhalation, ingestion, or skin
contact. (1,2)
EPA has not established a reference dose (RfD) or a reference concentration (RfC) for
ethylene dibromide. (4)
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EPA has calculated a provisional RfC of 0.0002 mg/m3 for ethylene dibromide based on
reproductive effects in humans. The RfC is an estimate (with uncertainty spanning
perhaps an order of magnitude) of a continuous inhalation exposure to the human
population (including sensitive subgroups) that is likely to be without appreciable risk of
deleterious noncancer effects during a lifetime. It is not a direct estimator of risk but
rather a reference point to gauge the potential effects. At exposures increasingly greater
than the RfC, the potential for adverse health effects increases. Lifetime exposure above
the RfC does not imply that an adverse health effect would necessarily occur. The
provisional RfC is a value that has had some form of Agency review, but it does not
appear on IRIS. (5)
Reproductive Effects/Developmental:
Developmental effects have not been documented in humans. Limited data on men
occupationally exposed to ethylene dibromide indicate that long-term exposure to
ethylene dibromide can impair reproduction by damaging sperm cells in the testicles.
(1,2)
Animals that breathed or ate food containing ethylene dibromide for short or long periods
were less fertile than control animals or had abnormal sperm. Pregnant animals that were
sick from exposure to ethylene dibromide have had pups with birth defects. (1,2)
Cancer Risk:
Two cancer studies on workers exposed to ethylene dibromide have been carried out.
Neither study reported a statistically significant increase in cancer mortality; however
these studies are considered inadequate due to confounding factors. (4)
Several animal studies indicate that long-term exposure to ethylene dibromide increases
the incidences of a variety of tumors in rats and mice in both sexes by inhalation, by
gavage, or by administration to the skin. (4)
EPA has classified ethylene dibromide as a Group B2, probable human carcinogen. (4)
EPA uses mathematical models, based on animal studies, to estimate the probability of a
person developing cancer from breathing air containing a specified concentration of a
chemical. EPA has calculated an inhalation unit risk estimate of 2.2 x 10"4 (/ng/m3)"1. EPA
estimates that, if an individual were to continuously breathe air containing ethylene
dibromide at an average of 0.005 j^g/m3 (5 x 10"6 mg/m3) over his or her entire lifetime,
that person would theoretically have no more than a one-in-a-million increased chance of
developing cancer as a direct result of breathing air containing this chemical. Similarly,
EPA estimates that continuously breathing air containing 0.05 /xg/m3 (5 x 10"5 mg/m3)
would result in not greater than a one-in-hundred thousand increased chance of
developing cancer, and air containing 0.5 /xg/m3 (5 x 10"4 mg/m3) would result in not
greater than a one-in-ten thousand increased chance of developing cancer in their lifetime.
For a detailed discussion of confidence in the potency estimates, please see IRIS. (4)
EPA has calculated an oral cancer slope factor of 85 (mg/kg/d)"1. (4)
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Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For ethylene dibromide: 1 ppm 7.7 mg/m3.
To convert from {Jig/m3 to mg/m3: mg/m3 = (fjig/m3) x (1 mg/1,000 fig).
Health Data from Inhalation Exposure
1,2-Dibromoethcne
1000000
100000
10000
1000
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(Lethal Concentrationso) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-affect level.
NIOSH ceiling - National Institute of Occupational Safety and Health's ceiling limit;
NIOSHrecommended 15-min exposure limit, which should not be exceeded.
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NIOSH REL - NIOSH's recommended exposure limit; NIOSH-recommended exposure limit for
an 8- or 10-h time-weighted-average exposure and/or ceiling.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the EPA Provisional RfC.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
1,2-Dibromoethane. Public Health Service, U.S. Department of Health and Human
Services, Atlanta, GA. 1992.
2. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on 1,2-Dibromoethane. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
5. U.S. Environmental Protection Agency (EPA). Health Effects Assessment Summary
Tables. FY-1997 Update. National Center for Environmental Assessment, Office of
Research and Development, Office of Emergency and Remedial Response, Washington,
DC. 1997.
6. The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S.
Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
7. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
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8. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
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ETHYLENE OXIDE
75-21-8
Hazard Summary
The major use for ethylene oxide is as a chemical intermediate in industry. The acute
(short-term) effects of ethylene oxide in humans consist mainly of central nervous system
(CNS) depression and irritation of the eyes and mucous membranes. High concentrations
of ethylene oxide produce weakness, nausea, bronchitis, pulmonary edema, emphysema,
and death. Chronic (long-term) exposure to ethylene oxide in humans can cause irritation
of the eyes, skin, and mucous membranes; and problems in the functioning of the brain
and nerves. Limited evidence in both animal and human studies indicate that inhalation
exposure to ethylene oxide may result in adverse reproductive effects such as an increased
rate of miscarriages. These effects could be seen from acute as well as chronic exposures.
Some human cancer data show an increase in the incidence of leukemia, stomach cancer,
cancer of the pancreas, and Hodgkin's disease in workers exposed to ethylene oxide.
However these data are considered to be limited and inconclusive due to uncertainties in
the studies. Ethylene oxide has been shown to cause lung, gland, and uterine tumors in
laboratory animals. The U.S. Environmental Protection Agency (EPA) has classified
ethylene oxide as a Group Bl, probable human carcinogen.
Please Note: The main source of information for this fact sheet is the Agency for Toxic Substances and Disease
Registry's (ATSDR's) Toxicological Profile for Ethylene Oxide. Other secondary sources include the Hazardous
Substances Data Bank (HSDB), a database of summaries of peer-reviewed literature, and the Registry of Toxic
Effects of Chemical Substances (RTECS), a database of toxic effects that are not peer reviewed.
Physical Properties
Ethylene oxide is a colorless gas with a sweet odor. (1,6)
The chemical formula for ethylene oxide is C2H4O and the molecular weight is 44.1
g/mol. (6)
The vapor pressure for ethylene oxide is 1,095 mm Hg at 20 °C, and it has an
octanol/water partition coefficient (log Kow) of -0.30. (6)
Ethylene oxide is very soluble in water and is flammable. (1)
Ethylene oxide has an odor threshold of 430 ppm. (7)
Ethylene oxide has an estimated half-life in air ranging from 69 to 149 days, while its
half-life in water is about 50 years. (1).
Uses
Ethylene oxide is used mainly as a chemical intermediate in the manufacture of textiles,
detergents, polyurethane foam, antifreeze, solvents, medicinals, adhesives, and other
products. (1)
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Relatively small amounts of ethylene oxide are used as a fumigant, a sterilant for food
(spices) and cosmetics, and in hospital sterilization of surgical equipment and plastic
devices that cannot be sterilized by steam. (1)
Sources and Potential Exposure
Sources of ethylene oxide emissions into the air include uncontrolled emissions or
venting with other gases in industrial settings. (1)
Other sources of ethylene oxide air emissions include automobile exhaust and its release
from commodity-fumigated materials, as well as its use as a sterilizer of medical
equipment. (1)
The general population may be exposed to ethylene oxide through breathing
contaminated air or from smoking tobacco or being in the proximity to someone who is
smoking. Certain occupational groups (e.g., workers in ethylene oxide manufacture or
processing plants, sterilization technicians, and workers involved in fumigation) may be
exposed in the workplace. (1)
Assessing Personal Exposure
There are tests currently available to determine personal exposure to ethylene oxide, such
as the determination of ethylene oxide in the blood or the amount breathed out of the
lungs. (1)
Health Hazard Information
Acute Effects:
Acute inhalation exposure of workers to high levels of ethylene oxide has resulted in
nausea, vomiting, neurological disorders, bronchitis, pulmonary edema, emphysema, and
even death at very high concentrations. (1,2)
Dermal or ocular contact with solutions of ethylene oxide has caused irritation of the eyes
and skin in humans. (1,2)
Tests involving acute exposure of animals, such as the LD50 test in rats, has shown
ethylene oxide to have high acute toxicity from oral exposure. LC50 tests in rats, mice,
dogs, and guinea pigs have also shown high acute toxicity from ethylene oxide exposure.
(3)
Chronic Effects (Noncancer):
Major effects observed in workers exposed to ethylene oxide at low levels for several
years are irritation of the eyes, skin, and mucous membranes and problems in the
functioning of the brain and nerves. (1,2)
There is evidence suggesting that long-term exposure to high levels of ethylene oxide, at
a level of 700 ppm, can result in cataracts in humans. (2)
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EPA has not established a reference dose (RfD) or a reference concentration (RfC) for
ethylene oxide.
The California Environmental Protection Agency (CalEPA) has established a chronic
reference exposure level of 0.005 mg/m3 for ethylene oxide based on hematological
effects in humans. The CalEPA reference exposure level is a concentration at or below
which adverse health effects are not likely to occur. It is not a direct estimator of risk, but
rather a reference point to gauge the potential effects. At lifetime exposures increasingly
greater than the reference exposure level, the potential for adverse health effects
increases. (4)
ATSDR has an established an intermediate inhalation minimal risk level (MRL) of 0.2
mg/m3 (0.09 ppm) based on respiratory effects in humans. The MRL is an estimate of the
daily human exposure to a hazardous substance that is likely to be without appreciable
risk of adverse noncancer health effects over a specified duration of exposure. (1)
Reproductive/Developmental Effects:
Some evidence exists indicating that inhalation exposure to ethylene oxide can cause an
increased rate of miscarriages in female workers. These effects could be seen from acute,
as well as chronic, exposure. (1,2)
Various adverse reproductive effects have been noted in inhalation exposure studies of
animals including decreased number of implantation sites, decreased testicular weights
and sperm concentration, and testicular degeneration. (1,2)
Cancer Risk:
Human occupational studies have shown elevated cases of leukemia, stomach and
pancreatic cancer, and Hodgkin's disease in workers exposed to ethylene oxide by
inhalation. However, the data are considered to be limited and inconclusive due to the
small number of individuals studied and uncertainties about the exposure levels. (1,2)
Animal studies have shown lung, gland, and uterine tumors caused by inhalation
exposure to ethylene oxide. (1,2)
EPA has classified ethylene oxide as a Group Bl, probable human carcinogen. (5)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA has calculated a provisional inhalation unit cancer risk
estimate of 1.0 x 10"4 (jig/m3)"1. A provisional value is one that has not received
Agencywide review. (5)
EPA has calculated a provisional oral cancer slope factor of 1.0 (mg/kg/d)"1. (5)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For ethylene oxide: 1 ppm = 1.8 mg/m3.
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Health Data from Inhalation Exposure
Ethyl ene Oxide
10000
1000
100
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ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
AIHA ERPG - American Industrial Hygiene Association's emergency response planning
guidelines. ERPG 1 is the maximum airborne concentration below which it is believed nearly all
individuals could be exposed up to one hour without experiencing other than mild transient
adverse health effects or perceiving a clearly defined objectionable odor; ERPG 2 is the
maximum airborne concentration below which it is believed nearly all individuals could be
exposed up to one hour without experiencing or developing irreversible or other serious health
effects that could impair their abilities to take protective action.
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LCSO (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-no-adverse-affect level.
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can
escape from an exposure condition that is likely to cause death or immediate or delayed
permanent adverse health effects or prevent escape from the environment.
NIOSH REL - NIOSH's recommended exposure limit; NIOSH-recommended exposure limit for
an 8- or 10-h time-weighted-average exposure and/or ceiling.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the CalEPA chronic reference
exposure level.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Ethylene Oxide. U.S. Public Health Service, U.S. Department of Health and Human
Services. 1990.
2. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
4. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
5. U.S. Environmental Protection Agency (EPA). Health Effects Assessment Summary
Tables. FY1997 Update. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1997.
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6. The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S.
Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
7. I.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds
compared with threshold limit values and volatilities for 214 industrial chemicals in air
and water dilution. Journal of Applied Toxicology, 3(6):272-290. 1983
8. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
9. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
10. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
11. American Industrial Hygiene Association (AIHA). The AIHA 1998 Emergency Response
Planning Guidelines and Workplace Exposure Level Guides Handbook. 1998.
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FORMALDEHYDE
50-00-0
Hazard Summary
Formaldehyde is used mainly to produce resins used in particle board products and as an
intermediate in the synthesis of other chemicals. Exposure to formaldehyde may occur by
breathing contaminated indoor air, tobacco smoke, or ambient urban air. Acute
(short-term) and chronic (long-term) inhalation exposure to formaldehyde in humans can
result in respiratory symptoms, and eye, nose, and throat irritation. Reproductive effects,
such as menstrual disorders and pregnancy problems, have been reported in female
workers exposed to formaldehyde. Limited human studies have reported an association
between formaldehyde exposure and lung and nasopharyngeal cancer. Animal inhalation
studies have reported an increased incidence of nasal squamous cell cancer. The U.S.
Environmental Protection Agency (EPA) has classified formaldehyde as a Group B2,
probable human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Health and Environmental Effects
Profile for Formaldehyde and the Integrated Risk Information System (IRIS), which contains information on oral
chronic toxicity and the reference dose (RfD), and the carcinogenic effects of formaldehyde including the unit
cancer risk for inhalation exposure.
Physical Properties
The chemical formula for formaldehyde is CH2O, and the molecular weight is 30.03
g/mol. (1)
The vapor pressure for formaldehyde is 10 mm Hg at -88 °C, and its log octanol/water
partition coefficient (log Kow) is -0.65. (1)
Formaldehyde is a colorless gas with a pungent, suffocating odor at room temperature;
the odor threshold for formaldehyde is 0.83 ppm. (1,8)
Formaldehyde is readily soluble in water at room temperature. (1)
Commercial formaldehyde is produced and sold as an aqueous solution containing 37 to
50 percent formaldehyde by weight. (1)
Uses
Formaldehyde is used predominantly as a chemical intermediate. It also has minor uses in
agriculture, as an analytical reagent, in concrete and plaster additives, cosmetics,
disinfectants, fumigants, photography, and wood preservation. (1,2)
One of the most common uses of formaldehyde in the U.S. is manufacturing
urea-formaldehyde resins, used in particle board products. (7)
Formaldehyde (as urea formaldehyde foam) was extensively used as an insulating
material until 1982 when it was banned by the U.S. Consumer Product Safety
Commission. (1,2)
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Sources and Potential Exposure
The highest levels of airborne formaldehyde have been detected in indoor air, where it is
released from various consumer products such as building materials and home
furnishings. One survey reported formaldehyde levels ranging from 0.10 to 3.68 ppm in
homes. Higher levels have been found in new manufactured or mobile homes than in
older conventional homes. (1)
Formaldehyde has also been detected in ambient air; the average concentrations reported
in U.S. urban areas were in the range of 11 to 20 ppb. The major sources appear to be
power plants, manufacturing facilities, incinerators, and automobile exhaust emissions.
(7)
Smoking is another important source of formaldehyde. (1)
Formaldehyde may also be present in food, either naturally or as a result of
contamination. (1)
Assessing Personal Exposure
Blood levels of formaldehyde can be measured. However, these measurements are only
useful when exposure by inhalation to relatively large amounts of formaldehyde has
occurred. (2)
Health Hazard Information
Acute Effects:
The major toxic effects caused by acute formaldehyde exposure via inhalation are eye,
nose, and throat irritation and effects on the nasal cavity. (1,2)
Other effects seen from exposure to high levels of formaldehyde in humans are coughing,
wheezing, chest pains, and bronchitis. (1,2)
Ingestion exposure to formaldehyde in humans has resulted in corrosion of the
gastrointestinal tract and inflammation and ulceration of the mouth, esophagus, and
stomach. (1,2)
Acute animal tests, such as the LC50 and LD50 tests in rats and rabbits have shown
formaldehyde to have high acute toxicity from inhalation, oral, and dermal exposure. (3)
Chronic Effects (Noncancer):
Chronic exposure to formaldehyde by inhalation in humans has been associated with
respiratory symptoms and eye, nose, and throat irritation. (1,2,4,5)
Repeated contact with liquid solutions of formaldehyde has resulted in skin irritation and
allergic contact dermatitis. (5)
Animal studies have reported effects on the nasal respiratory epithelium and lesions in the
respiratory system from chronic inhalation exposure to formaldehyde. (1,2,4,5)
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The RfD for formaldehyde is 0.2 mg/kg/d based on a decrease in body weight gain and
effects on the stomach in rats. The RfD is an estimate (with uncertainty spanning perhaps
an order of magnitude) of a daily oral exposure to the human population (including
sensitive subgroups) that is likely to be without appreciable risk of deleterious noncancer
effects during a lifetime. It is not a direct estimator of risk but rather a reference point to
gauge the potential effects. At exposures increasingly greater than the RfD, the potential
for adverse health effects increases. Lifetime exposure above the RfD does not imply that
an adverse health effect would necessarily occur. (6)
EPA has high confidence in the study on which the RfD was based since it consisted of
an adequate number of animals of both sexes, as well as a thorough examination of
lexicological and histological parameters; medium confidence in the database as several
additional chronic bioassays and reproductive and developmental studies support the
critical effect and study; and, consequently, medium confidence in the RfD. (6)
EPA has not established a reference concentration (RfC) for formaldehyde. (6)
The Agency for Toxic Substances and Disease Registry (ATSDR) has established a
chronic inhalation minimal risk level (MRL) of 0.003 ppm (0.004 mg/m3) based on
respiratory effects in humans. The MRL is an estimate of the daily human exposure to a
hazardous substance that is likely to be without appreciable risk of adverse noncancer
health effects over a specified duration of exposure. (7)
Reproductive/Developmental Effects:
An increased incidence of menstrual disorders were observed in female workers using
urea-formaldehyde resins. However, possible confounding factors were not evaluated in
this study. (1,2)
A study of hospital workers who sterilize equipment did not report an association
between formaldehyde exposure and increased spontaneous abortions. (1,2)
Developmental effects, such as birth defects, have not been observed in animal studies
with formaldehyde. (1,2)
Cancer Risk:
Occupational studies have noted statistically significant associations between exposure to
formaldehyde and increased incidence of lung and nasopharyngeal cancer. This evidence
is considered to be "limited," rather than "sufficient," due to possible exposure to other
agents that may have contributed to the excess cancers. (1,6)
Animal studies have reported an increased incidence of nasal squamous cell carcinomas
by inhalation exposure. (1,6)
EPA has classified formaldehyde as a Group Bl, probable human carcinogen. (6)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 1.3 x 10"5
(/-i g/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
formaldehyde at an average of 0.08 fig/in3 (8.0 x 10"5 mg/m3) over his or her entire
lifetime, that person would theoretically have no more than a one-in-a-million increased
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chance of developing cancer as a direct result of breathing air containing this chemical.
Similarly, EPA estimates that breathing air containing 0.8 jitg/m3 (8.0 x 10"4 mg/m3)
would result in not greater than a one-in-a-hundred thousand increased chance of
developing cancer, and air containing 8.0 /ig/m3 (8.0 x 10~3 mg/m3) would result in not
greater than a one-in-ten-thousand increased chance of developing cancer. For a detailed
discussion of confidence in the potency estimates, please see IRIS. (6)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/( 24.45).
For formaldehyde: 1 ppm = 1.23 mg/m3.
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Health Data from Inhalation Exposure
Formddehyde
1000
100
10
Ol
0.1
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experimental animal population.
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health limit; NIOSH recommended exposure limit to ensure that a worker can escape
from an exposure condition that is likely to cause death or immediate or delayed permanent
adverse health effects or prevent escape from the environment.
NIOSH REL - NIOSH's recommended exposure limit; NIOSH recommended exposure limit for
an 8- or 10-h time-weighted average exposure and/or ceiling.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
References
1. U.S. Environmental Protection Agency (EPA). Health and Environmental Effects Profile
for Formaldehyde. EPA/600/X-85/362. Environmental Criteria and Assessment Office,
Office of Health and Environmental Assessment, Office of Research and Development,
Cincinnati, OH. 1988.
2. World Health Organization (WHO). Environmental Health Criteria for Formaldehyde.
Volume 89. World Health Organization, Geneva, Switzerland. 1989.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
4. E.J. Calabrese and E.M. Kenyon. Air Toxics and Risk Assessment. Lewis Publishers,
Chelsea, MI. 1991.
5. U.S. Department of Health and Human Services. Hazardous Substances Databank
(HSDB, online database). National Toxicology Information Program, National Library
of Medicine, Bethesda, MD. 1993.
6. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Formaldehyde. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1999.
7. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Formaldehyde (Draft). Public Health Service, U.S. Department of Health and Human
Services, Atlanta, GA. 1997.
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8. I.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds
compared with threshold limit values and volatilities for 214 industrial chemicals in air
and water dilution. Journal of Applied Toxicology, 3(6):272-290. 1983.
9. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
10. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
11. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29
CFR 1910.1048. 1998.
12. American Industrial Hygiene Association (AfflLA). The AIHA 1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.
1998.
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HEXACHLOROBENZENE
118-74-1
Hazard Summary
Hexachlorobenzene is formed as a byproduct during the manufacture of other chemicals.
It was widely used as a pesticide until 1965. Chronic (long-term) oral exposure to
hexachlorobenzene in humans results in a liver disease with associated skin lesions.
Animal studies have reported effects on the liver, skin, kidneys, immune system, and
blood from chronic oral exposure to hexachlorobenzene. Hexachlorobenzene may cause
developmental effects in humans and has been found to decrease the survival rates of
newborn animals. Epidemiologic studies of persons orally exposed to hexachlorobenzene
have not shown an increased cancer incidence. However, based on animal studies that
have reported cancer of the liver, thyroid, and kidney from oral exposure to
hexachlorobenzene, the U.S. Environmental Protection Agency (EPA) has classified
hexachlorobenzene as a Group B2, probable human carcinogen. Very little inhalation
data are available.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on oral chronic toxicity and the reference dose (RfD), and the carcinogenic
effects of hexachlorobenzene including the unit cancer risk for inhalation exposure, and the Agency for Toxic
Substances and Disease Registry's (ATSDR's) Toxicological Profile for Hexachlorobenzene.
Physical Properties
Hexachlorobenzene is a white crystalline solid that is not very soluble in water. (1)
The odor threshold for hexachlorobenzene is not available.
The chemical formula for hexachlorobenzene is C6C16, and the molecular weight is 284.8
g/mol. (1)
The vapor pressure for hexachlorobenzene is 1.09 x 10'5mm Hg at 20 °C, and it has a log
octanol/water partition coefficient 0ogKow) of 6.18. (1)
Uses
There are currently no commercial uses of hexachlorobenzene in the U.S., (1)
Hexachlorobenzene was used as a pesticide until 1965 and was also used in the
production of rubber, aluminum, and dyes and in wood preservation. (1)
Hexachlorobenzene is currently formed as a byproduct during the manufacture of other
chemicals (mainly solvents) and pesticides. (1)
Sources and Potential Exposure
Inhalation exposure to hexachlorobenzene may occur through proximity to industrial sites
where it is formed as a byproduct or to waste facilities where it is disposed. (1)
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Occupational exposure, via inhalation and dermally, can occur at industries where
hexachlorobenzene is produced as a byproduct. (1)
Exposure to hexachlorobenzene can also occur through consuming foods tainted with
hexachlorobenzene. (1)
Hexachlorobenzene has been listed as a pollutant of concern in EPA's Great Waters
Program due to its persistence in the environment, potential to bioaccumulate, and
toxicity to humans and the environment (2).
Assessing Personal Exposure
Medical tests can measure levels of hexachlorobenzene in the fat or blood. (1)
Health Hazard Information
Acute Effects:
No information is available on the acute (short-term) effects of hexachlorobenzene in
humans. (1,3)
Acute animal tests, such as the LD50 tests in rats and mice, have shown
hexachlorobenzene to have low-to-moderate acute toxicity from oral exposure. (4)
Chronic Effects (Noncancer):
Humans who ingested hexachlorobenzene in heavily contaminated bread during a 4-year
poisoning incident were sickened with a liver disease with associated skin lesions
(porphyria cutanea tarda). (1)
Animal studies have reported effects on the liver, skin, immune system, kidneys, and
blood from chronic oral exposure to hexachlorobenzene. (1,3)
Very little data are available on the health effects of hexachlorobenzene in humans or
animals following inhalation exposure.
EPA has determined that there are inadequate data to establish a reference concentration
(RfC) for hexachlorobenzene. (5)
The California Environmental Protection Agency (CalEPA) has established a chronic
inhalation reference exposure level of 0.003 mg/m3 for hexachlorobenzene. The CalEPA
reference exposure level is a concentration at or below which adverse health effects are
not likely to occur. It is not a direct estimator of risk but rather a reference point to gauge
the potential effects. At lifetime exposures increasingly greater than the reference
exposure level, the potential for adverse health effects increases. (6)
The RfD for hexachlorobenzene is 0.0008 mg/kg/d based on liver effects in rats. The RfD
is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral
exposure to the human population (including sensitive subgroups) that is likely to be
without appreciable risk of deleterious noncancer effects during a lifetime. (5)
EPA has medium confidence in the study used as the basis for the RfD because it had an
unusual dosing scheme making it difficult to determine the true doses received by each
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experimental group; high confidence in the database due to the extensive number of
quality research studies available; and consequently medium confidence in the RfD. (5)
Reproductive/Developmental Effects:
One human study reported abnormal physical development in young children who
ingested contaminated bread during a 4-year poisoning incident. (1)
Hexachlorobenzene has been found to decrease the survival rates of newborn animals and
to cross the placenta and accumulate in fetal tissue in several animal species. (3)
Neurological, teratogenic, liver, and immune system effects have been reported in the
offspring of animals orally exposed to hexachlorobenzene while they were pregnant. (1)
Cancer Risk:
Human data regarding the carcinogenic effects of hexachlorobenzene are inadequate. (5)
Hexachlorobenzene, when administered orally, has been shown to induce tumors of the
liver, thyroid, and kidney in several animal species. (1,3,5)
EPA has classified hexachlorobenzene as a Group B2, probable human carcinogen. (5)
EPA uses mathematical models, based on human and animal studies to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 4.6 x 10"4
(/ig/m3)'1. EPA estimates that, if an individual were to continuously breathe air containing
hexachlorobenzene at an average of 0.002 /ig/m3 (2.0 x 10"6 mg/m3) over his or her entire
lifetime, that person would theoretically have no more than a one-in-a-million increased
chance of developing cancer as a direct result of breathing air containing this chemical.
Similarly, EPA estimates that breathing air containing 0.02 /xg/m3 (2.0 x 10"5 mg/m3)
would result in not greater than a one-in-a-hundred thousand increased chance of
developing cancer, and air containing 0.2 jwg/m3 (2.0 x 10"4 mg/m3) would result in not
greater than a one-in-ten thousand increased chance of developing cancer. For a detailed
discussion of confidence in the potency estimates, please see IRIS. (5)
EPA has calculated an oral cancer slope factor of 1.6 (mg/kg/d)"1. (5)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For hexachlorobenzene: 1 ppm = 11.6 mg/m3.
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Health Data from Inhalation Exposure
Hexochlorobenzene
100000
Regulatory, advisory
numbers'5
Hedth numbers
LC50 (rets) (3,600 mg'rrf)
ft) EPA r eferencs e
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c These cancer risk estimates were derived from oral data and converted to provide the estimated
inhalation risk.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Hexachlorobenzene (Update). Public Health Service, U.S. Department of Health and
Human Services, Atlanta, GA. 1996.
2. U.S. Environmental Protection Agency (EPA). Deposition of Air Pollutants to the Great
Waters. First Report to Congress. EPA-453/R-93-055. Office of Air Quality Planning and
Standards, Research Triangle Park, NC. 1994.
3. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
4. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
5. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Hexachlorobenzene. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
6. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
7. American Conference of Governmental Industrial Hygienists (ACGffl). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
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HYDRAZINE
302-01-2
Hazard Summary
Individuals may be exposed to hydrazine in the workplace or to small amounts in tobacco
smoke. Symptoms of acute (short-term) exposure to high levels of hydrazine may include
irritation of the eyes, nose, and throat, dizziness, headache, nausea, pulmonary edema,
seizures, and coma in humans. Acute exposure can also damage the liver, kidneys, and
central nervous system (CNS) in humans. The liquid is corrosive and may produce
dermatitis from skin contact. Effects to the lungs, liver, spleen, and thyroid have been
reported in animals chronically (long-term) exposed to hydrazine via inhalation.
Exposure of rodents to hydrazine has resulted in fetotoxicity and damage to reproductive
organs. Increased incidences of lung and liver tumors have been observed in mice
exposed to hydrazine. Tumors in the nasal cavity were observed in rats and hamsters
exposed by inhalation. The U.S. Environmental Protection Agency (EPA) has classified
hydrazine as a Group B2, probable human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on the carcinogenic effects of hydrazine including the unit cancer risk for
inhalation exposure, EPA's Health and Environmental Effects Profile for Hydrazine, and the Agency for Toxic
Substances and Disease Registry's (ATSDR's) Toxicological Profile for Hydrazines.
Physical Properties
The chemical formula for hydrazine is H4N2, and its molecular weight is 32.05 g/mol. (6)
Hydrazine occurs as a colorless, oily, flammable liquid that is miscible with water. (6,8)
Hydrazine has a penetrating odor, resembling that of ammonia, with an odor threshold of
3.7 ppm. (8,9)
The vapor pressure for hydrazine is 14.4 mm Hg at 25 °C, and its log octanol/water
partition coefficient (log Kow) is 0.08. (6)
Uses
^
Hydrazine is used in agricultural chemicals (pesticides), chemical blowing agents,
pharmaceutical intermediates, photography chemicals, boiler water treatment for
corrosion protection, textile dyes, and as fuel for rockets and spacecraft. (4,6,8,10)
Sources and Potential Exposure
Individuals may be occupationally exposed to hydrazine in the workplace. (1,2,10)
Accidental discharge into water, air, and soil may occur during storage, handling,
transport, and improper waste disposal. However, hydrazine rapidly degrades in the
environment and is rarely encountered. (2,3)
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Small amounts of hydrazine have been detected in tobacco smoke. (2,10)
Assessing Personal Exposure
Hydrazine may be detected in the blood of exposed individuals. (1,2)
Health Hazard Information
Acute Effects:
Symptoms of acute exposure to high levels of hydrazine include irritation of the eyes,
nose, and throat, temporary blindness, dizziness, headache, nausea, pulmonary edema,
seizures, and coma in humans. Acute exposure can also damage the liver, kidneys, and
the CNS in humans. (2-4)
The liquid is corrosive and may produce chemical bums and severe dermatitis from skin
contact. (1,4)
Acute animal tests, such as the LC50 and LD50 tests in rats, mice, rabbits, and guinea pigs,
have demonstrated hydrazine to have high acute toxicity from inhalation and ingestion
and extreme acute toxicity from dermal exposure. (5)
Chronic Effects (Noncancer):
Information is not available on the chronic effects of hydrazine in humans.
In animals chronically exposed to hydrazine by inhalation, effects on the respiratory
system, liver, spleen, and thyroid have been observed. (10)
EPA has not established a reference concentration (RfC) or a reference dose (RfD) for
hydrazine. (4)
The California Environmental Protection Agency (CalEPA) has calculated a chronic
inhalation reference exposure level of 0.0002 mg/m3 based on liver and thyroid effects in
hamsters. The CalEPA reference exposure level is a concentration at or below which
adverse health effects are not likely to occur. It is not a direct estimator of risk but rather
a reference point to gauge the potential effects. At lifetime exposures increasingly greater
than the reference exposure level, the potential for adverse health effects increases. (11)
ATSDR has calculated an intermediate inhalation minimal risk level (MRL) of 0.005
mg/m3 (0.004 ppm) based on liver effects in mice. The MRL is an estimate of the daily
human exposure to a hazardous substance that is likely to be without appreciable risk of
adverse noncancer health effects over a specified duration of exposure. (10)
Reproductive/Developmental Effects:
Information is not available on the reproductive or developmental effects of hydrazine in
humans.
Data regarding developmental effects in animals are limited to a study in which hydrazine
injected into pregnant rats resulted in fetotoxicity including increased fetal and neonatal
mortality. (6,10)
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Inhalation of hydrazine for a year resulted in effects to the ovaries, endometrium, and
uterus in female rats and to the testes in male hamsters. (10)
Cancer Risk:
Adequate information is not available on the carcinogenic effects of hydrazine in humans.
(4)
Increased incidences of lung and liver tumors have been observed in mice exposed to
hydrazine by inhalation, in their drinking water, via gavage and injection. Tumors in the
nasal cavity were observed in rats and hamsters exposed by inhalation. (4,6,7)
EPA has classified hydrazine as a Group B2, probable human carcinogen. (4)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 4.9 x 10~3
(/ig/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
hydrazine at an average of 0.0002 fig/m3 (2.0 x 10"7 mg/m3) over his or her entire lifetime,
that person would theoretically have no more than a one-in-a-million increased chance of
developing cancer as a direct result of breathing air containing this chemical. Similarly,
EPA estimates that breathing air containing 0.002 ^g/m3 (2.0 x 10"6 mg/m3) would result
in not greater than a one-in-a-hundred thousand increased chance of developing cancer,
and air containing 0.02 jug/m3 (2.0 x 10'5 mg/m3) would result in not greater than a
one-in-ten thousand increased chance of developing cancer. For a detailed discussion of
confidence in the potency estimates, please see IRIS. (4)
EPA has calculated an oral cancer slope factor of 3.0 (mg/kg/d)"1. (4)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For hydrazine: 1 ppm = 1.31 mg/m3.
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Health Data from Inhalation Exposure
Hycfrczme
Regulctory, advisory
numbers6
Heath numbers
LC50 (rets) (747rr&rr?)
LC50(nriCB)(330mg'iT?)
MCSHIDLH(66ma'nrf)
CSHAFELO.Snrn'rr?)
LCX\ELcOiver cndthyrdcj)
(p.Snrn'nr?)
AG3HTLV
(p.OlSma'nrf)
G3 EPA referSTCB ecpcsire
level (0.0002 nr^nrf)
unasr Risk Level
1 inanrillicnrisk
C2x
ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LC50 (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-effect level
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health limit; NIOSH recommended exposure limit to ensure that a worker can escape
from an exposure condition that is likely to cause death or immediate or delayed permanent
adverse health effects or prevent escape from the environment.
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OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the CalEPA chronic reference
exposure level.
References
1. M. Sittig. Handbook of Toxic and Hazardous Chemicals and Carcinogens. 2nd ed. Noyes
Publications, Park Ridge, NJ. 1985.
2. World Health Organization (WHO). Environmental Health Criteria 68: Hydrazine.
Geneva, Switzerland. 1987.
3. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Hydrazine/Hydrazine Sulfate. National Center for Environmental Assessment, Office
of Research and Development, Washington, DC. 1999.
5. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
6. U.S. Environmental Protection Agency (EPA). Health and Environmental Effects Profile
for Hydrazine and Hydrazine Sulfate. EPA/600/X-84/332. Environmental Criteria and
Assessment Office, Office of Health and Environmental Assessment, Office of Research
and Development, Cincinnati, OH. 1984.
7. International Agency for Research on Cancer (IARC). IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Man: Some Aromatic Amines,
Hydrazine and Related Substances, N-Nitroso Compounds and Miscellaneous Alkylating
Agents. Volume 4. World Health Organization, Lyon. 1974.
8. The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S.
Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
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9. J.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds
compared with threshold limit values and volatilities for 214 industrial chemicals in air
and water dilution. Journal of Applied Toxicology, 3(6):272-290. 1983.
10. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Hydrazines. Public Health Service, U.S. Department of Health and Human Services,
Atlanta, GA. 1997.
11. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
12. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
13. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
14. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
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LEAD COMPOUNDS1
Hazard Summary
Lead is used in the manufacture of batteries, metal products, paints, and ceramic glazes.
Exposure to lead can occur from breathing contaminated workplace air or dust or eating
lead-based paint chips or contaminated dirt. Lead is a very toxic element, causing a
variety of effects at low dose levels. Brain damage, kidney damage, and gastrointestinal
distress are seen from acute (short-term) exposure to high levels of lead in humans.
Chronic (long-term) exposure to lead in humans results in effects on the blood, central
nervous system (CNS), blood pressure, kidneys, and Vitamin D metabolism. Children
are particularly sensitive to the chronic effects of lead, with slowed cognitive
development, reduced growth and other effects reported. Reproductive effects, such as
decreased sperm count in men and spontaneous abortions in women, have been
associated with lead exposure. The developing fetus is at particular risk from maternal
lead exposure, with low birth weight and slowed postnatal neurobehavioral development
noted. Human studies are inconclusive regarding lead exposure and cancer, while animal
studies have reported an increase in kidney cancer from lead exposure by the oral route.
The U.S. Environmental Protection Agency (EPA) considers lead to be a Group B2,
probable human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on the carcinogenic effects of lead, and the Agency for Toxic Substances and
Disease Registry's (ATSDR's) Toxicological Profile for Lead.
Physical Properties
Lead is a naturally occurring, bluish-gray metal that is found in small quantities in the
earth's crust. (1,2)
Lead is present in a variety of compounds such as lead acetate, lead chloride, lead
chromate, lead nitrate, and lead oxide. (1,2)
Pure lead is insoluble in water; however, the lead compounds vary in solubility from
insoluble to water soluble. (1,2)
The chemical symbol for lead is Pb, and the atomic weight is 207.2 g/mol. (1)
The vapor pressure for lead is 1.0 mm Hg at 980 °C. (1)
1 Human exposure to lead occurs through a combination of inhalation and oral exposure, with
inhalation generally contributing a greater proportion of the dose for occupationally exposed groups, and
the oral route generally contributing a greater proportion of the dose for the general population. The
effects of lead are the same regardless of the route of exposure (inhalation or oral) and are correlated
with internal exposure as blood lead levels. For this reason, this fact sheet will not discuss the exposure
in terms of route but will present it in terms of blood lead levels.
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Uses
The primary use of lead is in the manufacture of batteries. (1)
Lead is also used in the production of metal products, such as sheet lead, solder (but no
longer in food cans), and pipes, and in ceramic glazes, paint, ammunition, cable covering,
and other products. (1)
Tetraethyl lead was used in gasoline to increase the octane rating until lead additives were
phased out and eventually banned from use in gasoline by the EPA beginning in 1973. (1)
Sources and Potential Exposure
The largest source of lead in the atmosphere has been from leaded gasoline combustion,
but with the phase down of lead in gasoline, air lead levels have decreased considerably.
Other airborne sources include combustion of solid waste, coal, and oils, emissions from
iron and steel production and lead smelters, and tobacco smoke. (1,2)
Exposure to lead can also occur from food and soil. Children are at particular risk to lead
exposure since they commonly put hands, toys, and other items in their mouths, which
may come in contact with lead-containing dust and dirt. (1,2)
Lead-based paints were commonly used for many years and flaking paint, paint chips, and
weathered paint powder may be a major source of lead exposure, particularly for children.
(1,2)
Lead in drinking water is due primarily to the presence of lead in certain pipes, solder,
and fixtures. (1,2)
Exposure to lead may also occur in the workplace, such as lead smelting and refining
industries, steel and iron factories, gasoline stations, and battery manufacturing plants.
(1,2)
Lead has been listed as a pollutant of concern to EPA's Great Waters Program due to its
persistence in the environment, potential to bioaccumulate, and toxicity to humans and
the environment. (3)
Assessing Personal Exposure
The amount of lead in the blood can be measured to determine if exposure to lead has
occurred. (1,2)
The level of lead in the blood is measured in jiig/dL.
The Centers for Disease Control concluded in 1993 that blood lead concentrations at or
around 10 (ig/dL present a public health risk to sensitive populations.
Exposure to lead can also be evaluated by measuring erythrocyte protoporphyrin (EP), a
component of red blood cells known to increase when the amount of lead in the blood is
high. This method was commonly used to screen children for potential lead poisoning.
(1,2)
Methods to measure lead in teeth or bones by X-ray fluorescence techniques are not
widely available. (1)
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Health Hazard Information
Acute Effects:
Death from lead poisoning may occur in children who have blood lead levels greater than
125 ptg/dL, and brain and kidney damage have been reported at blood lead levels of
approximately 100 /ig/dL in adults and 80 yttg/dL in children. (1,2)
Gastrointestinal symptoms, such as colic, have also been noted in acute exposures at
blood lead levels of approximately 60 jug/dL in adults and children. (1,2)
Short-term (acute) animal tests, such as the LC50test in rats, have shown lead to have
moderate to high acute toxicity. (4)
Chronic Effects (Noncancer):
Chronic exposure to lead in humans can affect the blood. Anemia has been reported in
adults at blood lead levels of 50 to 80 jWg/dL, and in children at blood lead levels of 40 to
70/ig/dL.(l,2)
Lead also affects the nervous system. Neurological symptoms have been reported in
workers with blood lead levels of 40 to 60 /ttg/dL, and slowed nerve conduction in
peripheral nerves in adults occurs at blood lead levels of 30 to 40 /^g/dL. (1,2)
Children are particularly sensitive to the neurotoxic effects of lead. A greatly expanded
body of research has shown that even low levels of lead exposure can result in
neurobehavioral changes, such as lowered IQ, in developing children. There is evidence
that blood lead levels of 10 to 30 ptg/dL, or lower, may affect the hearing threshold and
growth in children. (1,2)
Other effects from chronic lead exposure in humans include effects on blood pressure and
kidney function, and interference with vitamin D metabolism. (1,2,5)
Animal studies have reported effects similar to those found in humans, with effects on the
blood, kidneys, and nervous, immune, and cardiovascular systems noted. (1,2,5)
EPA has not established a reference concentration (RfC) or a reference dose (RfD) for
elemental lead or inorganic lead compounds. (6)
EPA has established an RfD for tetraethyl lead (an organometallic form of lead) of 1 x
10"7 mg/kg/d based on effects in the liver and thymus of rats. The RfD is an estimate
(with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the
human population (including sensitive subgroups) that is likely to be without appreciable
risk of deleterious noncancer effects during a lifetime. It is not a direct estimator of risk,
but rather a reference point to gauge the potential effects. At exposures increasingly
greater than the RfD, the potential for adverse health effects increases. Lifetime exposure
above the RfD does not imply that an adverse health effect would necessarily occur. (7)
EPA has medium to low confidence in the RfD due to: medium to low confidence in the
study on which the RfD for tetraethyl lead was based because, although only a few
animals per sex per dose level were tested, a good histopathologic exam was conducted
and a dose-severity was observed; and medium to low confidence in the database because
some supporting information was available. (7)
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The EPA has set a national ambient air quality standard (NAAQS) for lead at 1.5 |U.g/m3
as a quarterly average concentration. The NAAQS was set on the basis of evidence that
numerous health effects were associated with lead exposure, including impairment of
heme synthesis, and in recognition that young children (age 1-5 years) were a particularly
sensitive group to lead effects. (11,12)
Reproductive/Developmental Effects:
Studies on male lead workers have reported severe depression of sperm count and
decreased function of the prostate and/or seminal vesicles at blood lead levels of 40 to 50
jLtg/dL. These effects may be seen from acute as well as chronic exposures. (1,5)
Occupational exposure to high levels of lead has been associated with a high likelihood of
spontaneous abortion in pregnant women. However, the lowest blood lead levels at
which this occurs has not been established. These effects may be seen from acute as well
as chronic exposures. (1,5)
Exposure to lead during pregnancy produces toxic effects on the human fetus, including
increased risk of preterm delivery, low birth weight, and impaired mental development.
These effects have been noted at maternal blood lead levels of 10 to 15 jug/dL, and
possibly lower. Decreased IQ scores have been noted in children at blood lead levels of
approximately 10 to 50 /xg/dL. (1,2)
Human studies are inconclusive regarding the association between lead exposure and
other birth defects, while animal studies have shown a relationship between high lead
exposure and birth defects. (1,5)
Cancer Risk:
Human studies are inconclusive regarding lead exposure and an increased cancer risk.
Four major human studies of workers exposed to lead have been carried out; two studies
did not find an association between lead exposure and cancer, one study found an
increased incidence of respiratory tract and kidney cancers, and the fourth study found
excesses for lung and stomach cancers. However, all of these studies are limited in
usefulness because the route(s) of exposure and levels of lead to which the workers were
exposed were not reported. In addition, exposure to other chemicals probably occurred.
(1,2,6)
Animal studies have reported kidney tumors in rats and mice exposed to lead via the oral
route. (1,2,5,6)
EPA considers lead to be a Group B2, probable human carcinogen. (6)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For lead: 1 ppm = 8.5 mg/m3.
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Health Data from Inhalation Exposure
Lead
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ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LCSO (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
NIOSH REL - National Institute of Occupational Safety and Health's recommended exposure
limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure
and/or ceiling.
NIOSH IDLH - NIOSH's immediately dangerous to life or health concentration; NIOSH
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recommended exposure limit to ensure that a worker can escape from an exposure condition that
is likely to cause death or immediate or delayed permanent adverse health effects or prevent
escape from the environment.
NAAQS - National Ambient Air Quality Standard. NAAQS set by EPA for pollutants that are
considered to be harmful to public health and the environment; the NAAQS for lead is 1.5 /xg/m3,
maximum arithmetic mean averaged over a calendar quarter.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Lead (Update). Draft for Public Comment. Public Health Service, U.S. Department of
Health and Human Services, Atlanta, GA. 1997.
2. Agency for Toxic Substances and Disease Registry (ATSDR). Case Studies in
Environmental Medicine, Lead Toxicity. Public Health Service, U.S. Department of
Health and Human Services, Atlanta, GA. 1992.
3. U.S. Environmental Protection Agency (EPA). Deposition of Air Pollutants to the Great
Waters. First Report to Congress. EPA-453/R-93-055. Office of Air Quality Planning
and Standards, Research Triangle Park, NC. 1994.
4. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
5. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
6. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Lead and Compounds (Inorganic). National Center for Environmental Assessment,
Office of Research and Development, Washington, DC. 1999.
7. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Tetraethyl Lead. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1999.
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8. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
9. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29
CFR 1910.1025. 1998.
10. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
11. U.S. Environmental Protection Agency (EPA). National Ambient Air Quality Standard
for Lead. 43 FR 46246, October 5, 1978.
12. U.S. Environmental Protection Agency (EPA). Review of the National Ambient Air
Quality Standards for Lead: Assessment of Scientific and Technical Information. Office
of Air Quality Planning and Standards, Research Triangle Park, NC 27711. EPA-450/2-
89-022. December 1990.
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MANGANESE COMPOUNDS
Hazard Summary
Manganese is naturally ubiquitous in the environment. Manganese is essential for normal
physiologic functioning in humans and animals. Health effects in humans have been
associated with both deficiencies and excess intakes of manganese. Chronic (long-term)
exposure to low levels of manganese in the diet is considered to be nutritionally essential
in humans, with a recommended daily allowance of 2 to 5 mg/d. Chronic exposure to
high levels of manganese by inhalation in humans results primarily in central nervous
system (CNS) effects. Visual reaction time, hand steadiness, and eye-hand coordination
were affected in chronically-exposed workers. A syndrome named manganism may result
from chronic exposure to higher levels; manganism is characterized by feelings of
weakness and lethargy, tremors, a mask-like face, and psychological disturbances.
Respiratory effects have also been noted in workers chronically exposed by inhalation.
Impotence and loss of libido have been noted in male workers afflicted with manganism
attributed to high-level inhalation exposures to manganese. No studies are available
regarding the carcinogenic effects of manganese in humans, and animal studies are
inadequate. The U.S. Environmental Protection Agency (EPA) has classified manganese
as a Group D, not classifiable as to carcinogenicity in humans.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on inhalation chronic toxicity of manganese and the reference concentration
(RfC), oral chronic toxicity and the reference dose (RfD), and the Agency for Toxic Substances and Disease
Registry's (ATSDR's) Toxicologlcal Profile for Manganese.
Physical Properties
Manganese is a silver-colored metal that forms compounds in the environment with
chemicals such as oxygen, sulfur, and chlorine. (1)
Manganese compounds are solids that do not evaporate; however, small dust particles can
become suspended in air. (1)
Manganese can dissolve in water. (1)
The chemical symbol for manganese is Mn, and elemental manganese has an atomic
weight of 54.94 g/mol. (1)
Some manganese compounds are: manganese dioxide (MnO2), manganese tetraoxide
(Mn3O4), manganese salts (chloride, sulfate, carbonate, and nitrate), manganese silicate,
and potassium permanganate (KMnO4).
Uses
Metallic manganese is used primarily in steel production to improve hardness, stiffness,
and strength. It is also used in carbon steel, stainless steel, and high-temperature steel,
along with cast iron and superalloys. (1)
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Manganese compounds have a variety of uses. Manganese dioxide is used in the
production of dry-cell batteries, matches, fireworks, and the production of other
manganese compounds. (1)
Manganese chloride is used as a catalyst in the chlorination of organic compounds, in
animal feed, and in dry-cell batteries, while manganese sulfate is used as a fertilizer,
livestock nutritional supplement, in glazes and varnishes, and in ceramics. (1)
Potassium permanganate is used for water purification purposes in water and
waste-treatment plants. (1)
Sources and Potential Exposure
Manganese is a naturally occurring substance found in many types of rock and soil; it is
ubiquitous in the environment and found in low levels in water air, soil, and food. (1)
Manganese can also be released into the air by iron and steel production plants, power
plants, and coke ovens. (1)
The average manganese levels in various media are as follows: levels in drinking water
are approximately 0.004 ppm; average air levels are approximately 0.02 jug/m3; levels in
soil range from 40 to 900 ppm; the average daily intake from food ranges from 1 to 5
mg/d. (1)
People who work in factories where manganese metal is produced from manganese ore or
where manganese compounds are used to make steel or other products are most likely to
be exposed through inhalation to higher than normal levels of manganese. (1)
Assessing Personal Exposure
Several tests are available for measuring manganese in blood, urine, hair, or feces. As
manganese is naturally present in the body, some manganese is always found in these
materials. In addition, excess manganese is usually removed from the body within a few
days, making it difficult to measure past exposure to manganese. (1)
Health Hazard Information
Acute Effects:
No reports of effects in humans following acute (short-term) effects of exposure to
manganese are available.
Effects to the lung have been reported following acute exposure of rats to manganese via
inhalation. (1)
Manganese is considered to have moderate acute toxicity based on short-term tests, such
as the LD50 test given by gavage in rats. However, other animal tests in which manganese
has been given orally have indicated that manganese has low acute oral toxicity. (1)
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Chronic Effects (Noncancer):
Chronic exposure to manganese at low levels is nutritionally essential in humans. The
recommended daily intake of manganese is 2 to 5 mg/d for adults and adolescents. (1)
No cases of manganese deficiency have been observed in the general population.
However, manganese deficiency in animals has been associated with impaired growth,
skeletal abnormalities, impaired reproductive function in females, and testicular
degeneration in males. (1)
Chronic inhalation exposure of humans to manganese results primarily in effects on the
nervous system. Slower visual reaction time, poorer hand steadiness, and impaired
eye-hand coordination were reported in several studies of workers occupationally exposed
to manganese dust in air. (1,3)
Chronic inhalation exposure of humans to high levels may result in a syndrome called
manganism and typically begins with feelings of weakness and lethargy and progresses to
other symptoms such as gait disturbances, clumsiness, tremors, speech disturbances, a
mask-like facial expression, and psychological disturbances. (1,3)
Other chronic effects reported in humans from inhalation exposure to manganese are
respiratory effects such as an increased incidence of cough, bronchitis, dyspnea during
exercise, and an increased susceptibility to infectious lung disease. (1,3)
The RfC for manganese is 0.00005 mg/m3 based on impairment of neurobehavioral
function in humans. The RfC is an estimate (with uncertainty spanning perhaps an order
of magnitude) of a continuous inhalation exposure to the human population (including
sensitive subgroups) that is likely to be without appreciable risk of deleterious noncancer
effects during a lifetime. It is not a direct estimator of risk but rather a reference point to
gauge the potential effects. At exposures increasingly greater than the RfC, the potential
for adverse health effects increases. Lifetime exposure above the RfC does not imply that
an adverse health effect would necessarily occur. (3)
EPA has medium confidence in the RfC due to medium confidence in the principal
studies on which the RfC was based and medium confidence in the database. Neither of
the principal studies identified a no-observed-adverse-effect level (NOAEL) for
neurobehavioral effects, nor did either study directly measure particle size or provide
information on the particle size distribution. These limitations of the studies are mitigated
by the fact that the principal studies found similar indications of neurobehavioral
dysfunction, and these findings were consistent with the results of other human studies.
EPA has medium confidence in the database because the duration of exposure was
relatively limited in the principal and supporting studies, the majority of studies did not
specify the species of manganese, and the reproductive and developmental effects have
not been adequately studied. (3)
EPA has established a RfD for manganese of 0.14 mg/kg/d based on CNS effects in
humans. The RfD is estimated to be an intake for the general population that is not
associated with adverse health effects; this is not meant to imply that intakes above the
RfD are necessarily associated with toxicity. Some individuals may, in fact, consume a
diet that contributes more than 10 mg Mn/day without any cause for concern. When
assessing risk from manganese in drinking water or soil, a modified RfD of 0.05 mg/kg/d
is recommended. (3)
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EPA has medium confidence in the RfD due to medium confidence in the studies on
which the RfD for manganese was based; and medium confidence in the database. (3)
Reproductive/Developmental Effects:
Reproductive effects, such as impotence and loss of libido, have been noted in male
workers afflicted with manganism attributed to occupational exposure to high levels of
manganese by inhalation. No information is available on developmental effects of
manganese in humans. (1,3)
Animal studies have reported degenerative changes in the seminiferous tubules leading to
sterility from intratracheal instillation of high doses of manganese (experimentally
delivering the manganese directly to the trachea). In young animals exposed to
manganese orally, decreased testosterone production and retarded growth of the testes
were reported. (1)
Decreased activity levels and a decrease in average pup weight have been noted in the
offspring of mice exposed to manganese by inhalation. (1)
Cancer Risk:
No studies are available regarding carcinogenic effects in humans or animals from
inhalation exposure to manganese. (1,3)
No studies are available regarding cancer in humans from oral exposure to manganese.
Oral animal studies on manganese sulfate are inadequate, with several studies reporting
negative results, one study reporting an increased incidence of thyroid gland follicular cell
adenomas and hyperplasia, and one study noting an increased incidence of pancreatic
tumors. (1,3)
EPA has classified manganese as a Group D, not classifiable as to carcinogenicity in
humans. (3)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/( 24.45).
For manganese: 1 ppm = 2.25 mg/m3.
To convert from fJig/m3 to mg/m3: mg/m3 = (ng/m3) x (1 mg/1,000 fig).
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Health Data from Inhalation Exposure
Mcngcnese
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ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LOAEL - Lowest-observed-adverse-effect level.
NIOSH REL - National Institute of Occupational Safety and Health's recommended exposure
limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure
and/or ceiling.
NIOSH IDLH - NIOSH's immediately dangerous to life or health concentration; NIOSH
recommended exposure limit to ensure that a worker can escape from an exposure condition that
is likely to cause death or immediate or delayed permanent adverse health effects or prevent
escape from the environment.
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OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
OSHA ceiling - OSHA's short-term exposure limit ceiling; an exposure that should not be
exceeded at any time during a workday even if the 8-h time-weighted-average is within the
threshold limit value.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
0 This LOAEL is from the critical study used as the basis for the EPA RfC.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Manganese (Update). Draft for Public Comment. U.S. Public Health Service, U.S.
Department of Health and Human Services, Altanta, GA. 1997.
2. National Academy of Sciences (NAS). Drinking Water and Health. Volume 3. National
Academy Press, Washington, DC. 1989.
3. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Manganese. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
4. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29
CFR 1910.1000. 1998.
5. E.J. Calabrese and E.M. Kenyon. Air Toxics and Risk Assessment. Lewis Publishers,
Chelsea, MI. 1991.
6. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
7. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
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MERCURY COMPOUNDS
Hazard Summary
Mercury exists in three forms: elemental mercury, inorganic mercury compounds
(primarily mercuric chloride), and organic mercury compounds (primarily methyl
mercury). All forms of mercury are quite toxic, and each form exhibits different health
effects.
Acute (short-term) exposure to high levels of elemental mercury in humans results in
central nervous system (CNS) effects such as tremors, mood changes, and slowed sensory
and motor nerve function. High inhalation exposures can also cause kidney damage.
Effects on the gastrointestinal tract and respiratory system have also been noted in
humans from acute inhalation exposure. Chronic (long-term) exposure to elemental
mercury in humans also affects the CNS, with effects such as erethism (increased
excitability), irritability, excessive shyness, and tremors. Human studies are inconclusive
regarding elemental mercury and cancer. The U.S. Environmental Protection Agency
(EPA) has classified elemental mercury as a Group D, not classifiable as to human
carcinogenicity.
Acute exposure to inorganic mercury by the oral route may result in effects such as
nausea, vomiting, and severe abdominal pain. The major effect from chronic exposure to
inorganic mercury is kidney damage. Animal studies have reported effects such as
alterations in testicular tissue, increased resorption rates, and abnormalities of
development. Mercuric chloride (an inorganic mercury compound) exposure has been
shown to result in forestomach, thyroid, and renal tumors in experimental animals. EPA
has classified inorganic mercury as Group C, possible human carcinogen.
Acute exposure of humans to very high levels of methyl mercury results in CNS effects
such as blindness, deafness, and impaired level of consciousness. Chronic exposure to
methyl mercury in humans also affects the CNS with symptoms such as paresthesia (a
sensation of pricking on the skin), blurred vision, malaise, speech difficulties, and
constriction of the visual field. Methyl mercury exposure, via the oral route, has led to
significant developmental effects. Infants born to women who ingested high levels of
methyl mercury exhibited mental retardation, ataxia, constriction of the visual field,
blindness, and cerebral palsy. No human studies are available on the carcinogenic effects
of methyl mercury, and one animal study reported renal tumors in mice. EPA has
classified methyl mercury as Group C, possible human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on inhalation chronic toxicity and the reference concentration (RfC) for
elemental mercury, oral chronic toxicity and the reference dose (RfD) for inorganic and methyl mercury, EPA's
Mercury Study Report to Congress, and the Agency for Toxic Substances and Disease Registry's (ATSDR's)
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Toxicological Profile for Mercury. Other secondary sources include the World Health Organization's Environmental
Health Criteria Documents on Methyl Mercury and Inorganic Mercury.
Physical Properties
Elemental mercury is a silver-white metal with an atomic weight of 200.59 g/mol. (1)
Mercury is a liquid at room temperature and has a vapor pressure of 0.002 mm Hg at 25
°C.(1)
Mercury can exist in three oxidation states elemental, mercurous, and mercuric and
it can be part of both inorganic and organic compounds. (1)
Inorganic mercury compounds include mercuric chloride, mercuric sulfide, mercurous
chloride. Organic mercury compounds include mercuric acetate, methylmercuric
chloride, dimethyl mercury, and phenylmercuric acetate. (1)
Uses
Elemental Mercury
Elemental mercury is used in thermometers, barometers, and pressure-sensing devices. It
is also used in batteries, lamps, industrial processes, refining, lubrication oils, and dental
amalgams. (1)
Inorganic Mercury
Inorganic mercury was used in the past in laxatives, skin-lightening creams and soaps,
and in latex paint. In 1990, EPA canceled registration for all interior paints that contained
mercury. Mercury use in exterior paint was discontinued after 1991. (1)
Methyl Mercury
Methyl mercury has no industrial uses; it is formed in the environment from the
methylation of the inorganic mercurial ion. (1)
Sources and Potential Exposure
Elemental Mercury
A major source of exposure for elemental mercury is through inhalation in occupational
settings. (1,3,4)
Another source of exposure to low levels of elemental mercury in the general population
is elemental mercury released in the mouth from dental amalgam fillings. (3-5)
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Inorganic Mercury
The general population is usually not exposed to inorganic mercury compounds to any
significant extent today, as most products containing these compounds have now been
banned. Limited exposure could occur through the use of old cans of latex paint, which
until 1990, could contain mercury compounds to prevent bacterial and fungal growth.
(1,4)
Methyl Mercury
The most important organic mercury compound, in terms of human exposure, is methyl
mercury. Methyl mercury exposure occurs primarily through the diet, with fish and fish
products as the dominant source. Sources of past exposure to methyl mercury include
fungicide-treated grains and meat from animals fed such grain. However, fungicides
containing mercury are banned in the U.S. today, and this source of exposure is now
negligible. (1)
Mercury has been listed as a pollutant of concern to EPA's Great Waters Program due to
its persistence in the environment, potential to bioaccumulate, and toxicity to humans and
the environment. (6)
Assessing Personal Exposure
Laboratory tests can detect mercury in blood, urine, and hair samples. (1)
Health Hazard Information
Acute Effects:
Elemental Mercury
The major systems impacted by human inhalation of elemental mercury are the kidneys
and CNS. Acute exposure to high levels of elemental mercury in humans results in CNS
effects, such as tremors, irritability, insomnia, memory loss, neuromuscular changes,
headaches, slowed sensory and motor nerve function, and reduction in cognitive function.
(1,2)
Acute inhalation exposure of humans to high concentrations has resulted in kidney effects
ranging from mild transient proteinuria to acute renal failure. (1,2)
Gastrointestinal effects and respiratory effects, such as chest pains, dyspnea, cough,
pulmonary function impairment, and interstitial pneumonitis have also been noted from
human inhalation exposure to elemental mercury. (1,2)
Inorganic Mercury
Symptoms noted after acute oral exposure to inorganic mercury compounds include a
metallic taste in the mouth, nausea, vomiting, and severe abdominal pain. (1,2,7)
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The acute lethal dose for most inorganic mercury compounds for an adult is 1 to 4 g or 14
to 57 mg/kg for a 70-kg person. (1,7)
Methyl Mercury
Acute inhalation exposure to high levels of methyl mercury, which is extremely rare, has
resulted in severe CNS effects, including blindness, deafness, impaired level of
consciousness, and death. (8)
It has been estimated that the minimum lethal dose of methyl mercury for a 70-kg person
ranges from 20 to 60 mg/kg. (8)
Chronic Effects (Noncancer):
Elemental Mercury
The CNS is the major target organ for elemental mercury toxicity in humans. Effects
noted include erethism (increased excitability), irritability, excessive shyness, insomnia,
severe salivation, gingivitis, and tremors. (1,2,9)
Chronic exposure to elemental mercury also affects the kidney in humans, with the
development of proteinuria. (1,2,9)
Acrodynia is a rare syndrome found in children exposed to elemental mercury
compounds. It is characterized by severe leg cramps, irritability, paresthesia (a sensation
of prickling on the skin), and painful pink fingers and peeling hands, feet, and nose. (1,2)
EPA has not established an RfD for elemental mercury. (11)
The RfC for elemental mercury is 0.0003 mg/m3 based on CNS effects in humans. The
RfC is an estimate (with uncertainty spanning perhaps an order of magnitude) of a
continuous inhalation exposure to the human population (including sensitive subgroups)
that is likely to be without appreciable risk of deleterious noncancer effects during a
lifetime. It is not a direct estimator of risk but rather a reference point to gauge the
potential effects. At exposures increasingly greater than the RfC, the potential for adverse
health effects increases. Lifetime exposure above the RfC does not imply that an adverse
health effect would necessarily occur. (11)
EPA has medium confidence in the RfC due to: medium confidence in the studies on
which the RfC was based because there were sufficient number of human subjects,
inclusion of appropriate control groups, and exposure levels in a number of the studies
had to be extrapolated from blood mercury levels; and medium confidence in the database
due to a lack of human or multispecies reproductive/developmental studies. (11)
Inorganic Mercury
The primary effect from chronic exposure to inorganic mercury is kidney damage,
primarily due to mercury-induced autoimmune glomerulonephritis (induction of an
immune response to the body's kidney tissue). (1,2,9,10)
Acrodynia may also occur from exposure to inorganic mercury compounds. (1,2,9,10)
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The RfD for inorganic mercury (mercuric chloride) is 0.0003 mg/kg/d based on
autoimmune effects in rats. (12)
EPA has high confidence in the RfD based on the weight of evidence from the studies
using Brown-Norway rats and the entirety of the mercuric chloride database. (12)
EPA has not established an RfC for inorganic mercury. (12)
Methyl Mercury
The primary effect from chronic exposure to methyl mercury in humans is damage to the
CNS. The earliest effects are symptoms such as paresthesia, blurred vision, and malaise.
Effects at higher doses include deafness, speech difficulties, and constriction of the visual
field. (1,2,8)
The RfD for methyl mercury is 0.0001 mg/kg/d based on CNS effects in humans. (13)
EPA has medium confidence in the RfD due to: (1) medium confidence in the studies on
which the RfD was based because the benchmark dose approach allowed use of the entire
dose-response assessment, and the results of laboratory studies with nonhuman primates
support the quantitative estimate of the no-observed-adverse-effect level (NOAEL)/
lowest-observed-adverse-effect level (LOAEL) range of the benchmark dose that was
indicated by the human studies; and (2) medium confidence in the database. (13)
EPA has not established an RfC for methyl mercury. (13)
Reproductive/Developmental Effects:
Elemental Mercury
Studies on the reproductive and developmental effects of elemental mercury in humans
have shown mixed results. One study did not see an association between mercury
exposure and miscarriages, while another revealed an increase in the rate of spontaneous
abortions. Another study showed a higher than expected frequency of birth defects, which
was not confirmed in a fourth study. (1,9)
Inorganic Mercury
No information is available on the reproductive or developmental effects of inorganic
mercury in humans.
Animal studies have reported effects including alterations in testicular tissue, increased
resorption rates, and abnormalities of development. (1,7,9)
Methyl Mercury
A large number of human studies on the systemic effects of methyl mercury have been
carried out. This is the result of two large scale poisoning incidents in Japan and Iraq and
several epidemiologic studies investigating populations that consume large quantities of
fish. (1,2)
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Oral exposure to methyl mercury has been observed to produce significant developmental
effects in humans. Infants born to women who ingested high concentrations of methyl
mercury exhibited CNS effects, such as mental retardation, ataxia, deafness, constriction
of the visual field, blindness, and cerebral palsy. At lower methyl mercury concentrations,
developmental delays and abnormal reflexes were noted. (1,2,8)
Considerable new data on the health effects of methyl mercury are becoming available.
Large studies of fish and marine mammal consuming populations in Seychelles and Faroe
Islands are being carried out. Smaller scale studies also describe effects around the U.S.
Great Lakes. (1,2)
Cancer Risk:
Elemental Mercury
Several studies have been carried out regarding elemental mercury and cancer in humans.
These studies are inconclusive due to lack of valid exposure data and confounding
factors. (1,2,9)
EPA has classified elemental mercury as a Group D, not classifiable as to human
carcinogenicity. (12)
Inorganic Mercury
No studies are available on the carcinogenic effects of inorganic mercury in humans.
A chronic study on mercuric chloride in rats and mice reported an increased incidence of
forestomach and thyroid tumors in rats, and an increased incidence of renal tumors in
mice.(14)
EPA has classified inorganic mercury as Group C, possible human carcinogen. (12)
Methyl Mercury
No studies are available on the carcinogenic effects of methyl mercury in humans, and the
one available animal study reported renal tumors in mice. (1,2,13)
EPA has classified methyl mercury as Group C, possible human carcinogen. (13)
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Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For elemental mercury: 1 ppm = 8.2 mg/m3. For mercuric chloride: 1 ppm = 11.1 mg/m3. For
methyl mercuric chloride: 1 ppm = 10.3 mg/m1.
Health Data from Inhalation Exposure
Mercury
Regulaory, advisory
numbers"
Heath numbers
NCBHIDLH (dl exaspt crgncdkyl)
NCSHIDLH(crgrcdkyl)
AO3H TLV(ayl) NCSH REL (dl exaspf
crgnodkyl)(p.l
NC6H REL (dl exa=p* crgredkyl)
(0.05 nrg'rTf)
LO&RC(CNS)
(P.025 rrgfrtf)
C8HAPELAG3H
TLV MC8H REL
(crgno-
dkyl)
(P.01
rrg/rr?)
RfOgerrerttd)
(0.0003 nroTrf)
0.0001
ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effect.
NIOSH IDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health value; the maximum environmental concentration of a contaminant from which
one could escape within 30 min without any escape-impairing symptoms or irreversible health
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effects.
NIOSH REL - National Institute of Occupational Safety and Health's recommended exposure
limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure
and/or ceiling.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the EPA RfC for elemental mercury.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Mercury. Public Health Service, U.S. Department of Health and Human Services,
Atlanta, GA. 1999.
2. U.S. Environmental Protection Agency (EPA). Mercury Study Report to Congress.
Volume V: Health Effects of Mercury and Mercury Compounds. Office of Air Quality
Planning and Standards, Office of Research and Development. 1997
3. U.S. Environmental Protection Agency (EPA). Locating and Estimating Air Emissions
from Sources of Mercury and Mercury Compounds. EPA-453/R-93-023. Office of Air
Quality Planning and Standards, Research Triangle Park, NC. 1993.
4. U.S. Environmental Protection Agency (EPA). National Emissions Inventory of Mercury
and Mercury Compounds: Interim Final Report. EPA-453/R-93-048. Office of Air
Quality Planning and Standards, Research Triangle Park, NC. 1993.
5. U.S. Public Health Service. Dental Amalgams: A Public Health Service Strategy for
Research, Education, and Regulation. Final Report. Committee to Coordinate
Environmental Health and Related Programs, Washington, DC. 1993.
6. U.S. Environmental Protection Agency (EPA). Deposition of Air Pollutants to the Great
Waters. First Report to Congress. EPA-453/R-93-055. Office of Air Quality Planning
and Standards, Research Triangle Park, NC. 1994.
7. U.S. Environmental Protection Agency (EPA). Summary Review of Health Effects
Associated with Mercuric Chloride: Health Issue Assessment. EPA/600/R-92/199. Office
of Health and Environmental Assessment, Washington, DC. 1994.
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8. World Health Organization (WHO). Methyl Mercury. Volume 101. Distribution and Sales
Service, International Programme on Chemical Safety, Geneva, Switzerland. 1990.
9. World Health Organization (WHO). Inorganic Mercury. Volume 118. Distribution and
Sales Service, International Programme on Chemical Safety, Geneva, Switzerland. 1991.
10. U.S. Environmental Protection Agency (EPA). Drinking Water Criteria Document for
Inorganic Mercury. (Final). PB 89-19A 2207. Environmental Criteria and Assessment
Office, Cincinnati, OH. 1988.
11. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Elemental Mercury. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
12. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Mercuric chloride. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1999.
13. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Methyl mercury. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1999.
14. National Toxicology Program (NTP). Toxicology and Carcinogenesis Studies of
Mercuric Chloride in F344 Rats and B6C3FI Mice (Gavage Studies). U.S. Department
of Health and Human Services, Public Health Service, National Institutes of Health,
Bethesda,MD. 1991.
15. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
16. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
17. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
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METHYLENE CHLORIDE
75-09-2
Hazard Summary
Methylene chloride is predominantly used as a solvent. The acute (short-term) effects of
methylene chloride inhalation in humans consist mainly of nervous system effects
including decreased visual, auditory, and motor functions, but these effects are reversible
once exposure ceases. The effects of chronic (long-term) exposure to methylene chloride
suggest that the central nervous system (CNS) is a potential target in humans and
animals. Limited animal studies have reported developmental effects. Human data are
inconclusive regarding methylene chloride and cancer. Animal studies have shown
increases in liver and lung cancer and benign mammary gland tumors following the
inhalation of methylene chloride. The U.S. Environmental Protection Agency (EPA) has
classified methylene chloride as a Group B2, probable human carcinogen.
Please Note: The main sources of information for this fact sheet are the Agency for Toxic Substances and Disease
Registry's (ATSDR's) Toxicological Profile for Methylene Chloride and EPA's Integrated Risk Information System
(ERIS), which contains information on oral chronic toxicity and the reference dose (RfD), and the carcinogenic
effects of methylene chloride including the unit cancer risk for inhalation exposure.
Physical Properties
A common synonym for methylene chloride is dichloroethane. (1,4)
Methylene chloride is a colorless liquid with a sweetish odor. (1,6)
The chemical formula for methylene chloride is CH2C12, and the molecular weight is
84.93 g/mol. (1)
The vapor pressure for methylene chloride is 349 mm Hg at 20 °C, and it has an
octanol/water coefficient (log Kow) of 1.30. (1)
Methylene chloride has an odor threshold of 250 ppm. (7)
Methylene chloride is slightly soluble in water and is nonflammable. (1,6)
Uses
Methylene chloride is predominantly used as a solvent in paint strippers and removers; as
a process solvent in the manufacture of drugs, pharmaceuticals, and film coatings; as a
metal cleaning and finishing solvent in electronics manufacturing; and as an agent in
urethane foam blowing. (1)
Methylene chloride is also used as a propellant in aerosols for products such as paints,
automotive products, and insect sprays. (1)
It is used as an extraction solvent for spice oleoresins, hops, and for the removal of
caffeine from coffee. However, due to concern over residual solvent, most decaffeinators
no longer use methylene chloride. (1)
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Methylene chloride is also approved for use as a postharvest fumigant for grains and
strawberries and as a degreening agent for citrus fruit. (1)
Sources and Potential Exposure
The principal route of human exposure to methylene chloride is inhalation of ambient air.
(1)
Occupational and consumer exposure to methylene chloride in indoor air may be much
higher, especially from spray painting or other aerosol uses. People who work in these
places can breathe in the chemical or it may come in contact with the skin. (1)
Methylene chloride has been detected in both surface water and groundwater samples
taken at hazardous waste sites and in drinking water at very low concentrations. (1)
Assessing Personal Exposure
Several tests exist for determining exposure to methylene chloride. These tests include
measurement of methylene chloride in the breath, blood, and urine. It is noted that
smoking and exposure to other chemicals may affect the results of these tests. (1)
Health Hazard Information
Acute Effects:
Case studies of methylene chloride poisoning during paint stripping operations have
demonstrated that inhalation exposure to extremely high levels can be fatal to humans.
(1,2)
Acute inhalation exposure to high levels of methylene chloride in humans has resulted in
effects on the CNS including decreased visual, auditory, and psychomotor functions, but
these effects are reversible once exposure ceases. Methylene chloride also irritates the
nose and throat at high concentrations. (1,2)
Tests involving acute exposure of animals, such as the LD50 and LC50 tests in rats, have
shown methylene chloride to have moderate acute toxicity from oral and inhalation
exposure. (3)
Chronic Effects (Noncancer):
The major effects from chronic inhalation exposure to methylene chloride in humans are
effects on the CNS, such as headaches, dizziness, nausea, and memory loss. (1,2)
Animal studies indicate that the inhalation of methylene chloride causes effects on the
liver, kidney, CNS, and cardiovascular system. (1,2)
EPA has calculated a provisional reference concentration (RfC) of 3 mg/m3 based on liver
effects in rats. The RfC is an estimate (with uncertainty spanning perhaps an order of
magnitude) of a continuous inhalation exposure to the human population (including
sensitive subgroups) that is likely to be without appreciable risk of deleterious noncancer
effects during a lifetime. It is not a direct estimator of risk but rather a reference point to
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gauge the potential effects. At exposures increasingly greater than the RfC, the potential
for adverse health effects increases. Lifetime exposure above the RfC does not imply that
an adverse health effect would necessarily occur. (5)
The RfD for methylene chloride is 0.06 mg/kg/d based on liver toxicity in rats. (4)
EPA has medium confidence in the RfD based on: high confidence in the study on which
the RfD is based because a large number of animals of both sexes were tested in four dose
groups, with a large number of controls, many effects were monitored, and a dose-related
increase in severity was observed; and medium to low confidence in the database because
only a few studies support the no-observed-adverse-effect level (NOAEL). (4)
Reproductive/Developmental Effects:
No studies were located regarding developmental or reproductive effects in humans from
inhalation or oral exposure. (1,2)
Animal studies have demonstrated that methylene chloride crosses the placental barrier,
and minor skeletal variations and lowered fetal body weights have been noted. (1,2)
Cancer Risk:
Several studies did not report a statistically significant increase in deaths from cancer
among workers exposed to methylene chloride. (1,2)
Animal studies have shown an increase in liver and lung cancer and benign mammary
gland tumors following inhalation exposure to methylene chloride. (1,2,4)
EPA has classified methylene chloride as a Group B2, probable human carcinogen. (4)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 4.7 x 10"7
(/ig/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
methylene chloride at an average of 2.0 /ig/m3 (0.002 mg/m3) over his or her entire
lifetime, that person would theoretically have no more than a one-in-a-million increased
chance of developing cancer as a direct result of breathing air containing this chemical.
Similarly, EPA estimates that breathing air containing 20 /tig/m3 (0.02 mg/m3) would
result in not greater than a one-in-a-hundred thousand increased chance of developing
cancer, and air containing 200 /ig/m3 (0.2 mg/m3) would result in not greater than a
one-in-ten thousand increased chance of developing cancer. For a detailed discussion of
confidence in the potency estimates, please see IRIS. (4)
EPA calculated an oral cancer slope factor of 7.5 x 10"3 (mg/kg/d)'1. (4)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For methylene chloride: 1 ppm = 3.5 mg/m3. To convert from fig/m3 to mg/m3: mg/m3 = (fJ-g/m3)
x(lmg/l,000ng).
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Health Data from Inhalation Exposure
Methyl ene Chloride
1000000
100000
10000
_ 1000
Ol
£
c
CB8,000 rrgftrf)
LC50 (rricE) (350,020 rrg/rr?)
MCSHIDLH(7980m^nr?)
Al HA ERPG2 C2602 rrgfrrf)
AIHAERPG-l(694rr^rr?)
AO3HTLV(174rT#nr?)
CSHAPEL<388rrtfrT?)
Rcw'sicna RfC
Qrrg/rr?)
QnoEr Risk L&J&
1 inam'llicnrisk
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NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can
escape from an exposure condition that is likely to cause death or immediate or delayed
permanent adverse health effects or prevent escape from the environment.
NOAEL - No-observed-adverse-effects level.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average: the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The NOAEL is from the critical study used as the basis for the provisional RfC.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Methylene Chloride (Update). Draft for Public Comment. Public Health Service, U.S.
Department of Health and Human Services, Atlanta, GA. 1998.
2. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database), National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Methylene Chloride. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
5. U.S. Environmental Protection Agency (EPA). Health Effects Assessment Summary
Tables. FY1997 Update. Solid Waste and Emergency Response, Office of Emergency
and Remedial Response, Cincinnati, OH. EPA/540/R-97-036. 1997.
6. The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S.
Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
7. I.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds
compared with threshold limit values and volatilities for 214 industrial chemicals in air
and water dilution. Journal of Applied Toxicology, 3(6):272-290. 1983.
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8. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
9. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29
CFR 1910.1052. 1998.
10. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
11. American Industrial Hygiene Association (AfflLA). The AIHA 1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.
1998.
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NICKEL COMPOUNDS
Hazard Summary
Nickel occurs naturally in the environment at low levels. Nickel is an essential element
in some animal species, and it has been suggested it may be essential for human
nutrition. Nickel dermatitis, consisting of itching of the fingers, hands, and forearms, is
the most common effect in humans from chronic (long-term) skin contact with nickel.
Respiratory effects have also been reported in humans from inhalation exposure to
nickel. No information is available regarding the reproductive or developmental effects
of nickel in humans, but animal studies have reported reproductive and developmental
effects. The U.S. Environmental Protection Agency (EPA) has not evaluated soluble salts
of nickel as a class of compounds for potential human carcinogenicity. Human and
animal studies have reported an increased risk of lung and nasal cancers from exposure to
nickel refinery dusts and nickel subsulfide. EPA has classified nickel refinery dust and
nickel subsulfide as Group A, human carcinogens. Animal studies of soluble nickel
compounds (i.e., nickel carbonyl) have reported lung tumors. EPA has classified nickel
carbonyl as a Group B2, probable human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on oral chronic toxicity and the reference dose (RfD), and the carcinogenic
effects of nickel including the unit cancer risk for inhalation exposure, EPA's Health Assessment Document for
Nickel, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for Nickel.
Physical Properties
Nickel is a silvery-white metal that is found in nature as a component of silicate, sulfide,
or arsenide ores. (1)
In the environment, nickel is found primarily combined with oxygen or sulfur as oxides
or sulfides. (1)
Each form of nickel exhibits different physical properties. (1,6)
Soluble nickel salts include nickel chloride, nickel sulfate, and nickel nitrate. (6)
Nickel carbonyl, a highly unstable form, is not found naturally and decomposes rapidly.
(1)
The chemical symbol for nickel is Ni, and it has an atomic weight of 58.71 g/mol. (1)
Uses
Nickel is used for nickel alloys, electroplating, batteries, coins, industrial plumbing, spark
plugs, machinery parts, stainless-steel, nickel-chrome resistance wires, and catalysts. (1,6)
Nickel carbonyl has severely limited use in nickel refining. (1)
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Sources and Potential Exposure
Nickel is a natural element of the earth's crust; therefore, small amounts are found in
food, water, soil, and air. (6)
Food is the major source of nickel exposure, with an average intake for adults estimated
to be approximately 100 to 300 /ig/d. (1,6)
Individuals also may be exposed to nickel in occupations involved in its production,
processing, and use, or through contact with everyday items such as nickel-containing
jewelry and stainless steel cooking and eating utensils, and by smoking tobacco. (1)
Nickel is found in ambient air at very low levels as a result of releases from oil and coal
combustion, nickel metal refining, sewage sludge incineration, manufacturing facilities,
and other sources. (2,6)
Given its high instability, nickel carbonyl exposure is extremely rare.
Assessing Personal Exposure
Laboratory tests can detect nickel in blood, urine, feces, and hair samples. (1,6)
Health Hazard Information
Acute Effects:
One person exposed to an extremely high level of nickel by inhalation suffered severe
damage to the lungs and kidneys. (6)
Gastrointestinal distress (e.g., nausea, vomiting, diarrhea) and neurological effects were
reported in workers who drank water on one shift that was contaminated with nickel as
nickel sulfate and nickel chloride. (1,6)
Pulmonary fibrosis and renal edema were reported in humans and animals following
acute (short-term) exposure to nickel carbonyl. (1)
Acute animal tests, such as the LD50 test in rats, have shown nickel compounds to exhibit
acute toxicity values ranging from low to high. The soluble compounds, such as nickel
acetate, were the most toxic, and the insoluble forms, such as nickel powder, were the
least toxic. (6)
Chronic Effects (Noncancer):
Dermatitis is the most common effect in humans from chronic dermal exposure to nickel.
Cases of nickel dermatitis have been reported following occupational and
non-occupational exposure, with symptoms of eczema (rash, itching) of the fingers,
hands, wrists, and forearms. (1,2,6,7)
Chronic inhalation exposure to nickel in humans also results in respiratory effects,
including a type of asthma specific to nickel, decreased lung function, and bronchitis.
(6,7)
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Animal studies have reported effect on the lungs and immune system from inhalation
exposure to soluble and insoluble nickel compounds (nickel oxide, subsulfide, sulfate
heptahydrate). (1,6)
Soluble nickel compounds are more toxic to the respiratory tract than less soluble
compounds. (6)
EPA has not established a reference concentration (RfC) for nickel. (2-5)
The RfD for nickel (soluble salts) is 0.02 mg/kg/d based on decreased body and organ
weights in rats. The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of a daily oral exposure to the human population (including sensitive
subgroups) that is likely to be without appreciable risk of deleterious noncancer effects
during a lifetime. It is not a direct estimator of risk, but rather a reference point to gauge
the potential effects. At exposures increasingly greater than the RfD, the potential for
adverse health effects increases. Lifetime exposure above the RfD does not imply that an
adverse health effect would necessarily occur. (5)
EPA has medium confidence in the RfD due to: low confidence in the study on which the
RfD for nickel (soluble salts) was based because, although it was properly designed and
provided adequate toxicological endpoints, high mortality occurred in the controls; and
medium confidence in the database because it provided adequate supporting subchronic
studies, one by gavage and the other in drinking water, but inadequacies in the remaining
reproductive data. (5)
Nickel is an essential nutrient for some mammalian species and has been suggested to be
essential for human nutrition. By extrapolation from animal data, it is estimated that a
70-kg person would have a daily requirement of 50 ^g per kg diet of nickel. (6)
The California Environmental Protection Agency (CalEPA) has calculated a chronic
inhalation reference exposure level of 0.00005 mg/m3 for nickel based on respiratory and
immune system effects reported in rats exposed to a soluble nickel salt. The CalEPA
reference exposure level is a concentration at or below which adverse health effects are
not likely to occur. (7)
ATSDR has calculated a chronic-duration inhalation minimal risk level (MRL) of 0.0002
mg/m3 for nickel based on respiratory effects reported in rats exposed to a soluble nickel
salt. The MRL is an estimate of the daily human exposure to a hazardous substance that is
likely to be without appreciable risk of adverse noncancer health effects over a specified
duration of exposure. (6)
Reproductive/Developmental Effects:
No information is available regarding the reproductive or developmental effects of nickel
in humans. (6)
Animal studies have reported reproductive and developmental effects, such as a
decreased number of live pups per litter, increased pup mortality, and reduction in fetal
body weight, and effects to the female from oral exposure to soluble salts of nickel. (5,6)
Sperm abnormalities and decreased sperm count have been reported in animals exposed
to nickel nitrate orally and nickel oxide by inhalation, respectively. (6)
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Cancer Risk:
Nickel Salts
Nickel sulfate via inhalation and nickel acetate in drinking water were not carcinogenic in
either rats or mice. (6)
EPA has not evaluated soluble salts of nickel as a class of compounds for potential
human carcinogenicity. (5)
Nickel Refinery Dust and Nickel Subsulfide
Human studies have reported an increased risk of lung and nasal cancers among nickel
refinery workers exposed to nickel refinery dust. Nickel refinery dust is a mixture of
many nickel compounds, with nickel subsulfide being the major constituent. (3,4,6)
Animal studies have also reported lung tumors from inhalation exposure to nickel
refinery dusts and to nickel subsulfide. (3,4)
EPA has classified nickel refinery dust and nickel subsulfide as Group A, human
carcinogens. (3,4)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA calculated an inhalation unit risk estimate of 2.4 x 10"4
(jug/rn3)"1 for nickel refinery dusts. EPA estimates that, if an individual were to
continuously breathe air containing nickel refinery dusts at an average of 0.004 jug/m3 (4
x 10"6 mg/m3) over his or her entire lifetime, that person would theoretically have no more
than a one-in-a-million increased chance of developing cancer as a direct result of
breathing air containing this chemical. Similarly, EPA estimates that continuously
breathing air containing 0.04 jug/m3 would result in not greater than a one-in-a-hundred
thousand increased chance of developing cancer, and air containing 0.4 /u.g/m3 would
result in not greater than a one-in-ten thousand increased chance of developing cancer.
For a detailed discussion of confidence in the potency estimates, please see IRIS. (3)
For nickel subsulfide, EPA calculated an inhalation unit risk estimate of 4.8 x 10"4
(ptg/m3)"1. EPA estimates that, if an individual were to continuously breathe air containing
this nickel compound at an average of 0.002 /xg/m3 (2 x 10"6 mg/m3) over his or her entire
lifetime, that person would theoretically have no more than a one-in-a-million increased
chance of developing cancer as a direct result of breathing air containing this chemical.
Similarly, EPA estimates that continuously breathing air containing 0.02 /ig/m3 would
result in not greater than a one-in-a-hundred thousand increased chance of developing
cancer, and air containing 0.2 /xg/m3 would result in not greater than a one-in-ten
thousand increased chance of developing cancer. (4)
Nickel Carbonyl
Nickel carbonyl has been reported to produce lung tumors in rats exposed via inhalation.
(2)
EPA has classified nickel carbonyl as a Group B2, probable human carcinogen. (2)
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Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For nickel: 1 ppm = 2.4 mg/m3.
To convert from fJtg/m3 to mg/m3: mg/m3 - (ng/m3) x (1 mg/1,000 p.g).
Nickel
Health Data from Inhalation Exposure
100 -
Regulctory, advisory
numbers6
Hedth numbers
NCSHIDLH(10nnc/rTf)
AO3H TLV(nretd crrrpcux*)0.5 m^nf)
CBHAPEL (rrefd ojrpancfe)(l rrg/rr?)
A03HTLV(sdJdenickel)(p.] rrg/rr?)
AQ3H TLVflnsdJderickel)
NIC8H REL (msta
NCW£LcresprcTcry effects
CBHAPEL,
NICSHREL
(rickel ccr-
bcnyl)(p.007
mg'rrf)
ATSCRdTanicM2L
Cb EPA r efe ence ecfXBU e
Risk Le/d
1 inanrillicnrisk
(rickelrefina-ydjsts
Ctncs-Risk
Le/d 1 in a
mllicnrisk
(rickd sUDBJficfe
G2x l&rrgfrrf)
0.00001
0.000001
ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
NIOSH REL - National Institute of Occupational Safety and Health's recommended exposure
limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure
and/or ceiling.
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NIOSHIDLH - NIOSH's immediately dangerous to life or health concentration; NIOSH
recommended exposure limit to ensure that a worker can escape from an exposure condition that
is likely to cause death or immediate or delayed permanent adverse health effects or prevent
escape from the environment.
NOAEL - No-observed-adverse-effect level.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
0 The NOAEL is from the critical study used as the basis for both the ATSDR chronic MRL and
CalEPA chronic reference exposure level.
References
1. U.S. Environmental Protection Agency (EPA). Health Assessment Document for Nickel.
EPA/600/8-83/012F. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1986.
2. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Nickel Carbonyl. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1999.
3. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Nickel Refinery Dust. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Nickel Subsulfide. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1999.
5. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Nickel, Soluble Salts. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
6. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Nickel (Update). Public Health Service, U.S. Department of Health and Human Services,
Altanta, GA. 1997.
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1. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
8. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
9. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
10. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29
CFR 1910.1000. 1998.
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POLYCHLORINATED BIPHENYLS (PCBs)
1336-36-3
Hazard Summary
PCBs are a group of chemicals that contain 209 individual compounds (known as
congeners) with varying harmful effects. Information on specific congener toxicity is very
limited. Most toxicity testing has been done on specific commercial mixtures; however,
PCB mixtures found in the environment will differ in composition from the commercial
mixtures because of biotransformation and bioaccumulation. The U.S. Environmental
Protection Agency (EPA) treats all PCBs as being potentially hazardous based on results
from some formulations. However, this can have large uncertainty for any given mixture
situation.
PCBs are no longer produced or used in the U.S. today; the major source of exposure to
PCBs today is the redistribution of PCBs already present in soil and water. No
information is available on the acute (short-term) effects of PCBs in humans, and animal
studies have reported effects on the liver, kidney, and central nervous system (CNS) from
oral exposure to PCBs. Chronic (long-term) exposure to some PCB formulations by
inhalation in humans results in respiratory tract symptoms, gastrointestinal effects, mild
liver effects, and effects on the skin and eyes such as chloracne, skin rashes, and eye
irritation. Epidemiological studies suggest an association between dietary PCB exposures
and developmental effects; human reproductive studies are inconclusive. Human studies
provide inconclusive, yet suggestive, evidence of an association between PCBs exposure
and liver cancer. Animal studies have reported an increase in liver tumors in rats and
mice exposed orally to some PCB formulations. EPA has classified PCBs as a Group B2,
probable human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on the carcinogenic effects of PCBs including the unit cancer risk for oral
exposure, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for PCBs.
Physical Properties
PCBs are a class of industrial chemicals that contain 209 individual compounds or
congeners. (1)
PCBs made in the U.S. were marketed under the trade name Aroclor and are identified by
a four-digit numbering code in which the first two digits indicate that the parent molecule
is a biphenyl and for the 1200 series Aroclors the last two digits indicate the chlorine
content by weight. For example, Aroclor 1260 has 60 percent chlorine. (1)
Commercial trade names for PCBs not manufactured in the U.S. include Kanechlor,
Clophen, Fenclor, and Phenoclor. (1)
PCBs are either oily liquids or solids and are colorless to light yellow in color with no
known smell or taste. (1)
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The molecular weight for one particular PCB (Aroclor 1260) is 375.7 g/mol; the vapor
pressure is 4.05 x 10"5 mm Hg at 25 °C; the octanol/water partition coefficient (log Kow)
is 6.8. (1)
PCB mixtures found in environmental media (air, water, sediment, foods) will differ in
composition from the commercial mixtures due to differential biotransformation and
bioaccumulation among the individual compounds. (1)
Uses
Before 1974, PCBs were used in capacitors, transformers, plasticizers, surface coatings,
inks, adhesives, pesticide extenders, and carbonless duplicating paper. After 1974, use of
PCBs was restricted to the production of capacitors and transformers, and after 1979
PCBs were no longer used in the production of capacitors and transformers. (1)
Sources and Potential Exposure
PCBs are no longer produced in the U.S. and are no longer used in the manufacture of
new products; the major source of air exposure to PCBs today is the redistribution of
PCBs already present in soil and water. Smaller amounts of PCBs may be released to the
air from disposal sites containing transformers, capacitors, and other PCB wastes,
incineration of PCB-containing wastes, and improper disposal of the compounds to open
areas. (1)
PCBs have been detected in indoor air at concentrations of an order of magnitude greater
than ambient air. It has been suggested that certain electrical appliances and devices, such
as fluorescent lighting ballasts, which have PCB-containing components, may emit PCBs
to the indoor air. (1)
In the past, PCBs were released to wastewater from its industrial uses. Today, PCBs are
still detected in water due to the environmental recycling of the compound. Most of the
PCBs in water are bound to the soil and sediments and may be released to the water
slowly over a long period of time. (1)
PCBs have been detected in food; they bioaccumulate through the food chain, with some
of the highest concentrations found in fish. (1)
PCBs have been listed as a pollutant of concern to EPA's Great Waters Program due to
their persistence in the environment, potential to bioaccumulate, and toxicity to humans
and the environment. (3)
Assessing Personal Exposure
Laboratory analyses can detect PCBs in blood, body fat, and breast milk. (1)
Health Hazard Information
Acute Effects:
No reports of effects in humans following acute exposure to PCBs are available. (1)
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Animal studies have reported acute effects on the liver, kidney, and CNS from oral
exposure to PCBs. (1)
Acute animal tests, such as the LD50 test in rats, have shown PCBs to have moderate
acute toxicity from oral exposure. (1,4)
Chronic Effects (Noncancer):
Chronic inhalation exposure of workers to PCBs has been reported to result in respiratory
tract symptoms, such as cough and tightness of the chest, gastrointestinal effects
including anorexia, weight loss, nausea, vomiting, and abdominal pain, mild liver effects,
and effects on the skin and eyes, such as chloracne, skin rashes, and eye irritation. (1,5)
EPA has not established a reference concentration (RfC) or a reference dose (RfD) for all
PCB mixtures. (6)
The RfD for Aroclor 1016 is 0.00007 mg/kg/d based on reduced birth weights in
monkeys. The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of a daily oral exposure to the human population (including sensitive
subgroups) that is likely to be without appreciable risk of deleterious noncancer effects
during a lifetime. It is not a direct estimator of risk, but rather a reference point to gauge
the potential effects. At exposures increasingly greater than the RfD, the potential for
adverse health effects increases. Lifetime exposure above the RfD does not imply that an
adverse health effect would necessarily occur. (7)
EPA has medium confidence in the RfD based on: medium confidence in the study on
which the RfD was based because this was a well-conducted study, but only one group of
monkeys was examined; and medium confidence in the database because an extensive
amount of data are available but mixtures of PCBs in the environment do not match the
pattern of congeners found in Aroclor 1016. (7)
The RfD for Aroclor 1254 is 0.00002 mg/kg/d based on immunological effects in
monkeys. (8)
EPA has medium confidence in the RfD based on: (1) medium confidence in the study on
which the RfD was based because groups of monkeys were tested at four dose levels and
a lowest-observed-adverse-effect level (LOAEL) was established; and (2) medium
confidence in the database because an extensive number of laboratory animal and human
studies were available for review, but human data are available for PCB mixtures in
general but not specifically for Aroclor 1254. (8)
EPA has not established an RfC for Aroclor 1016 or Aroclor 1254. (7,8)
Reproductive/Developmental Effects:
An epidemiological study of women occupationally exposed to high levels of PCBs
suggested a relationship between PCB exposure and reduced birth weight and shortened
gestational age of their babies; however, limitations of the study limit the strength of the
conclusion. (1)
Two human studies that investigated exposure to PCBs through the consumption of
contaminated fish suggest that exposure to PCBs may cause developmental effects in
humans. Both studies reported an association between consumption of fish with high
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PCB levels by pregnant women and an increased incidence of neurodevelopmental
effects, such as motor deficits at birth, impaired psychomotor index, impaired visual
recognition, and deficits in short-term memory in infants. (1)
Human studies are not conclusive on the reproductive effects of PCBs. One study of men
who were occupationally exposed to PCBs showed no fertility abnormalities, while
another study of men with low sperm counts found elevated levels of PCBs in the blood
and an association between certain PCB compounds in semen and decreased sperm
motility. (1)
Animal studies have reported developmental effects, such as learning deficits, impaired
immune functions, focal liver necrosis, and cellular alterations of the thyroid, in the
offspring of animals exposed orally to PCBs. Reproductive effects, such as decreased
fertility, decreased conception, and prolonged menstruation have also been noted in
animal studies of dietary PCB exposures. (1)
Cancer Risk:
Human studies provide inconclusive, yet suggestive evidence of an association between
PCBs' exposure and liver cancer. Several studies have reported an increase in liver cancer
among persons occupationally exposed to some PCB formulations. However, the studies
are inconclusive due to confounding exposures and lack of exposure quantification. (1,6)
Oral exposure studies in animals show an increase in liver tumors in rats and mice
exposed to several commercial mixtures of PCBs and to several specific congeners. (1,6)
No animal inhalation studies are available on PCBs. (1)
EPA has classified PCBs as a Group B2, probable human carcinogen. (6)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from ingesting water containing a specified
concentration of a chemical. EPA calculated an upper bound inhalation unit cancer risk
estimate of 1.0 x 10"4 (jug/m3)"1 for inhalation of evaporated PCB congeners. EPA
estimates that, if an individual were to continuously breathe air containing PCBs at an
average of 0.01 /ig/m3 (1 x 10"5 mg/m3) over his or her entire lifetime, that person would
theoretically have no more than a one-in-a-million increased chance of developing cancer
as a direct result of breathing air containing this chemical. Similarly, EPA estimates that
breathing air containing 0.1 /tg/m3 (1 x 10"4 mg/m3) would result in not greater than a
one-in-a-hundred thousand increased chance of developing cancer, and air containing 1.0
/ig/m3 (1 x 10"3 mg/m3) would result in not greater than a one-in-ten thousand increased
chance of developing cancer. For a detailed discussion of confidence in the potency
estimates, please see IRIS. (6)
EPA has calculated an upperbound oral cancer slope factor of 0.4 (mg/kg/d)"1 for
ingestion of water soluble congeners, an upperbound oral cancer slope factor of 2.0
(mg/kg/d)"1 for food chain exposure, and an upperbound oral cancer slope factor of 0.07
(mg/kg/d)"1 for PCB exposures where congeners with more than 4 chlorines comprise less
than 5 percent of the total. (6)
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Conversion Factors:
To convert from ppm to mg/m3: mg/m3 (ppm) x (molecular weight of the compound)/(24.45).
For Arodor 1260:1 ppm = 15.4 mg/m3. To convert from ng/m3 to mg/m3: mg/m3 = (fig/m3) x (1
mg/1,000
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Health Data from Inhalation Exposure
Pd ychl or i nded bi phenyl s
100
10
01
£
c
o
"*5
re
u
£
O
U
Hedth numbers0
Regulctory, advisory
nurrbers6
C8HA PEL, AQ3H TLV(42% chcrine) (1
C8HAPELA03HTLV
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a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Poly chlorinated Biphenyls. Public Health Service, U.S. Department of Health and Human
Services, Atlanta, GA. 1997.
2. U.S. Environmental Protection Agency (EPA). Workshop Report on Toxicity Equivalence
forPCB Congeners. EPA/625/3-91/020. 1991.
3. U.S. Environmental Protection Agency (EPA). Deposition of Air Pollutants to the Great
Waters. First Report to Congress. EPA-453/R-93-055. Office of Air Quality Planning
and Standards, Research Triangle Park, NC. 1994.
4. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
5. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
6. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on PCBs. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
7. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Aroclor 1016. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
8. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Aroclor 1254. National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
9. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
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10. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
11. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
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POLYCYCLIC ORGANIC MATTER (POM)1
Hazard Summary
The term POM defines a broad class of compounds that includes the polycyclic aromatic
hydrocarbon compounds (PAHs), of which benzo[a]pyrene is a member. POM
compounds are formed primarily from combustion and are present in the atmosphere
predominantly in particulate form with a smaller amount as vapor. Sources of air
emissions are diverse and include cigarette smoke, vehicle exhaust, home heating, laying
tar, and grilling meat. Skin exposures to mixtures of carcinogenic PAHs cause skin
disorders in humans and animals. No information is available on the reproductive or
developmental effects of POM in humans, while animal studies have reported that
benzofajpyrene, via oral exposure, causes reproductive and developmental effects. Cancer
is the major concern from exposure to POM. Epidemiologic studies have reported an
increase in lung cancer in humans exposed to coke oven emissions, roofing tar emissions,
and cigarette smoke; all of these mixtures contain POM compounds. Animal studies have
reported respiratory tract tumors from inhalation exposure to benzo[a]pyrene and
forestomach tumors, leukemia, and lung tumors from oral exposure to benzofajpyrene.
The U.S. Environmental Protection Agency (EPA) has classified seven PAHs
(benzo[a]pyrene, benz[a]anthracene, chrysene, benzo[b]fluoranthene,
benzo[k]fluoranthene, dibenz[a,h]anthracene, and indeno[l,2,3-cd]pyrene) as Group B2,
probable human carcinogens.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on the carcinogenic effects of benzo(a)pyrene including the unit cancer risk for
oral exposure, and the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for
Polycyclic Aromatic Hydrocarbons (PAHs).
Physical Properties
The term POM generally defines a broad class of compounds that includes all organic
structures having two or more fused aromatic rings (i.e., rings that share a common
border), and that have a boiling point greater than or equal to 212 °F (100 °C). The 1990
Amendments to the Clean Air Act describes POM as including "organic compounds with
more than one benzene ring, and which have a boiling point greater than or equal to 100
degrees C." (11)
POM has been identified with up to seven fused rings and, theoretically, millions of POM
compounds could be formed; however, only about 100 species have been identified and
studied. (11)
1 Polycyclic organic matter consists of polycyclic aromatic hydrocarbons (PAHs),
including benzo(a)pyrene (CAS#50-32-8), their nitrogen analogs, and a small number of
oxygen-containing polycyclic organic matter compounds.
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Eight major categories of compounds have been defined by the EPA to constitute the
class known as POM. The most common category is the polycyclic aromatic
hydrocarbons (PAHs), also known as polynuclear aromatics, which include
benzo[a]pyrene. (11)
Most POM compounds are solids with high melting and boiling points, and are extremely
insoluble in water. The PAHs are primarily planar, nonpolar compounds with melting
points considerably over 212 °F (100 °C). Phenanthrene, with a melting point of 214 °F
(101 °C), and benzo[c]phenanthrene, with a melting point of 154 °F (68 °C), are two
exceptions. (11)
POM is present in the atmosphere predominantly in the paniculate form with a smaller
amount in the vapor phase. (11)
The chemical formula for benzo[a]pyrene is C20H]2, and the molecular weight is 252.3
g/mol. (1)
The vapor pressures of POM compounds vary, depending upon the ring size and
molecular weight, from 6.8 x 10"4 mm Hg for phenanthrene, to 1.5 x 10"12 for coronene.
The vapor pressure for benzo[a]pyrene is 5.6 x 10"9 mm Hg at 25 °C, and it has a log
octanol/water partition coefficient (log Kow) of 6.06. (1,11)
Uses
The majority of the polycyclic organic compounds have no commercial uses. (11)
Solutions containing mixtures of some PAHs are used to treat some skin disorders in
humans. (1)
Sources and Potential Exposure
The primary source of POM is formation during combustion. A less significant formation
mechanism is the volatilization of lightweight POM compounds, which occurs in the
production and use of naphthalene. (11)
Polycyclic organic compounds have been detected in ambient air from sources including
cigarette smoke, vehicle exhausts, asphalt road paving, coal burning, application of coal
tar, agricultural burning, residential wood burning, and hazardous waste sites. The
compounds present in POM and their relative amounts differ among different sources
(e.g, POM from diesel exhaust is chemically different than POM from wood burning).
(1,2)
Benzo[a]pyrene, one of the more commonly monitored PAHs, has been detected in urban
air at levels approximately twice as high as those in rural areas (e.g., 0.6 ng/m3 versus 0.3
ng/m3). Seasonal variations have also been observed from monitoring in the Northeast
U.S. during the early 1980's, with mean benzo[a]pyrene concentrations during the winter
more than an order of magnitude greater than during the summer. (11)
PAHs have been found in some drinking water supplies. (1)
Cooking meat or other foods at high temperatures increases the amount of PAHs in the
food. (1)
Occupational exposure to PAHs may occur in coal tar production plants, coking plants,
coal-gasification sites, smokehouses, municipal trash incinerators, and other facilities. (1)
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POM has been listed as a pollutant of concern in EPA's Great Waters Program due to its
persistence in the environment, potential to bioaccumulate, and toxicity to humans and
the environment (2).
Assessing Personal Exposure
PAHs or their breakdown products can be measured in urine, blood, or body tissues. (1)
Health Hazard Information
Acute Effects:
No reports of effects to humans following acute (short-term) exposure to POM are
available.
Acute animal tests, such as the LD50 test in rats, have shown benzo[a]pyrene to have high
acute toxicity from oral exposure. (3)
Chronic Effects (Noncancer):
Skin exposures to mixtures of carcinogenic PAHs cause skin disorders in humans and
animals, and adverse skin effects have been noted in humans and animals following
application of solutions containing benzo[a]pyrene. (1)
An epidemiological study of workers exposed by inhalation to benzo[a]pyrene and other
particulate matter reported some respiratory effects. The role of benzo[a]pyrene in this
association, however, is unclear. (1)
Animal studies have reported effects on the blood and liver from oral exposure to
benzo[a]pyrene and a slight hypersensitivity response from dermal exposure to
benzo[a]pyrene. (1)
EPA has not established a reference concentration (RfC) or a reference dose (RfD) for
POM or for benzo[a]pyrene. (4,5)
Reproductive/Developmental Effects:
No information is available on the reproductive or developmental effects of POM in
humans.
Animal studies have indicated that benzo[a]pyrene, via oral exposure, induces
reproductive toxicity, including a reduced incidence of pregnancy and decreased fertility.
Developmental effects, such as a reduced viability of litters and reduced mean pup
weight, have also been noted from oral exposure to benzo[a]pyrene in animals. (1,6)
Cancer Risk:
Epidemiologic studies have reported an increase in lung cancer in humans exposed to
coke oven emission, roofing tar emissions, and cigarette smoke. Each of these mixtures
contains a number of POM compounds (e.g., certain PAHs). (1,6)
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Animal studies have reported respiratory tract tumors from inhalation exposure to
benzo(a)pyrene and forestomach tumors, leukemia, and lung tumors from oral exposure
to benzo[a]pyrene. (1,5,7)
EPA has classified seven PAHs (benzo[a]pyrene, benz[a]anthracene, chrysene,
benzo[b]fluoranthene, benzo[k]fluoranthene, dibenz[a,h]anthracene, and
indeno[l,2,3-cd]pyrene) as Group B2, probable human carcinogens. (4,5,12-17)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from ingesting water containing a specified
concentration of a chemical. Although a quantitative cancer risk estimate for the mixture
of POM has not been derived, EPA has calculated an oral cancer slope factor of 7.3
(mg/kg/d)"1 for benzo[a]pyrene, one of the many constituents of POM. For a detailed
discussion of the confidence in the potency estimates, please see IRIS. (5)
The California Environmental Protection Agency (CalEPA) has calculated an inhalation
unit risk estimate of 1.1 x 10~3 (/ng/m3)"1 for benzo[a]pyrene, one of the many constituents
of POM. (7)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For benzo(a)pyrene: 1 ppm = 10.3 mg/m3.
To convert from fJ-g/m3 to mg/m3: mg/m3 = (fjig/m3) x (1 mg/1,000 [Jig).
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Health Data from Inhalation Exposure
Coal Tar Pitch Volatiles*
1000000
100000
10000
_ 1000
Regulatory, advisory
number^
£
o
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100
10
NIOSH IDLH (coal tar pitch volatiles,
benzo(a)pyrene)(80 mg/m3)
OSHA PEL and ACGIH TLV (coal tar pitch
volatiles-benzene soluble) (0.2 mg/m3)
NIOSH REL (coal tar pitch
volatiles, benzo(a)pyrene)
(0.1 mg/m3)
0.1
0.01
0.001
ACGIH TLV - American Conference of Governmental and Industrial Hygienists1 threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
NIOSH REL - National Institute of Occupational Safety and Health's recommended exposure
limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure
and/or ceiling.
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NIOSHIDLH - NIOSH's recommended exposure limit; NIOSH-recommended immediately
dangerous to health level.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effects averaged over a normal 8-h workday or a 40-h
workweek.
a These chemicals, a subset of POM, are emitted from the application of hot coal tar pitch.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Poly cyclic Aromatic Hydrocarbons (PAHs). Public Health Service, U.S. Department of
Health and Human Services, Atlanta, GA. 1995.
2. U.S. Environmental Protection Agency (EPA). Deposition of Air Pollutants to the Great
Waters. First Report to Congress. EPA-453/R-93-055. Office of Air Quality Planning
and Standards, Research Triangle Park, NC. 1994.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Polycyclic Organic Matter. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
5. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Benzo(a)pyrene. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1999.
6. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
7. California Environmental Protection Agency (CalEPA). Air Toxics Hot Spots Program
Risk Assessment Guidelines: Technical Support Document for Determining Cancer
Potency Factors. Draft for Public Comment. Office of Environmental Health Hazard
Assessment, Berkeley, CA. 1997
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8. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
9. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29
CFR 1910.1000. 1998.
10. American Conference of Governmental Industrial Hygienists (ACGIH). 7999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
11. U.S. Environmental Protection Agency (EPA). Locating and Estimating Air Emissions
from Sources ofPolycyclic Organic Matter. EPA-454/R-98-014. Office of Air Quality
Planning and Standards, Research Triangle Park, NC. 1998.
12. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System
(IRIS) on Benz[aJanthracene. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
13. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System
(IRIS) on Benzo[b]fluoranthene. National Center for Environmental Assessment, Office
of Research and Development, Washington, DC. 1999.
14. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System
(IRIS) on Benzofkjfluoranthene. National Center for Environmental Assessment, Office
of Research and Development, Washington, DC. 1999.
15. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System
(IRIS) on Chrysene. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1999.
16. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System
(IRIS) on Dibenz[a,h]anthracene. National Center for Environmental Assessment,
Office of Research and Development, Washington, DC. 1999.
17. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System
(IRIS) on Indeno[I,2,3-cd]pyrene. National Center for Environmental Assessment,
Office of Research and Development, Washington, DC. 1999.
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QUINOLINE
91-22-5
Hazard Summary
Quinoline is used mainly as an intermediate in the manufacture of other products.
Potential exposure to quinoline may occur from the inhalation of cigarette smoke and, to
a much lesser extent, ambient air contaminated by emissions from the petroleum and coal
industries. Acute (short-term) inhalation exposure to quinoline vapors irritates the eyes,
nose, and throat and may cause headaches, dizziness, and nausea in humans. Information
on the chronic (long-term), reproductive, developmental, or carcinogenic effects of
quinoline in humans is not available. Liver damage has been observed in rats chronically
exposed to quinoline by ingestion. An increased incidence of liver vascular tumors has
been observed in rats and mice orally exposed to quinoline. The U.S. Environmental
Protection Agency (EPA) has provisionally classified quinoline as a Group C, possible
human carcinogen.
Please Note: The main source of information for this fact sheet is EPA's Health and Environmental Effects Profile
for Quinoline. Other secondary sources include the Hazardous Substances Data Bank (HSDB), a database of
summaries of peer-reviewed literature, and the Registry of Toxic Effects of Chemical Substances (RTECS), a
database of toxic effects that are not peer reviewed.
Physical Properties
The chemical formula for quinoline is Cc>H7N, and it has a molecular weight of 129.15
g/mol.(7)
Quinoline occurs as a colorless, hygroscopic liquid that darkens with age and is sparingly
soluble in water but is more easily soluble in hot water. (3,7)
Quinoline has a penetrating, pungent odor. (3,7)
The vapor pressure of quinoline is 0.0091 mm Hg at 25 °C and its log octanol/water
partition coefficient (log Kow) is 2.03. (3)
Uses
Quinoline is used mainly as an intermediate in the manufacture of other products. (3)
Quinoline is also used as a catalyst, a corrosion inhibitor, in metallurgical processes, in
the manufacture of dyes, as a preservative for anatomical specimens, in polymers and
agricultural chemicals, and as a solvent for resins and terpenes. It is also used as an
antimalarial medicine. (2,3,7)
Sources and Potential Exposure
Workers in certain industries may be occupationally exposed to quinoline by inhalation,
ingestion of particulates, or dermal contact. (1,2)
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A potential source of very low exposure to quinoline includes the inhalation of ambient
air contaminated by emissions from petroleum refining, coal mining, quenching and
coking, and release in shale oil, synthetic coal conversion wastewaters, and wood
preservative wastewaters. Levels of 2-7 jug/m3 have been measured in ambient air. (1,3)
Quinoline is found at higher levels in cigarette smoke (1-20 jug/cigarette). (1,3)
Underground coal gasification has been a source of quinoline contamination of
groundwater. Individuals may be exposed by consumption of contaminated water. (1)
Assessing Personal Exposure
No information was located regarding the measurement of personal exposure to
quinoline.
Health Hazard Information
Acute Effects:
Acute inhalation exposure to quinoline vapor irritates the eyes, nose, and throat, and may
cause headaches, dizziness, and nausea, and, at high concentrations, coma in humans. (3)
Tests involving acute exposure of animals, such as the LD50 test in rats and rabbits, have
demonstrated quinoline to have high acute toxicity by oral or dermal exposure. (4)
Chronic Effects (Noncancer):
Information on the chronic effects of quinoline in humans is not available. (3)
Liver damage has been observed in rats chronically exposed to quinoline by ingestion. (3)
EPA has not established a reference concentration (RfC) or reference dose (RfD) for
quinoline. (5)
Reproductive/Developmental Effects:
No information is available on the reproductive or developmental effects of quinoline in
humans or animals. (3)
Cancer Risk:
No human studies are available on the carcinogenicity of quinoline. (3)
An increased incidence of liver hemangioendotheliomas (liver vascular tumors) has been
observed in rats and mice orally exposed to quinoline. (3)
EPA has provisionally classified quinoline as a Group C, possible human carcinogen.
(3,6)
EPA has calculated a provisional oral cancer slope factor of 12 (mg/kg/d)"1. A
provisional value is one which has not received Agency-wide review. (6)
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Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For quinoline: 1 ppm = 5.3 mg/m3.
Note: There are very few health numbers or regulatory/advisory numbers for quinoline; thus, a
graph has not been prepared for this compound.
References
1. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
2. G.D. Clayton and F.E. Clayton, Eds. Patty's Industrial Hygiene and Toxicology. Volume
HA, 3rd revised ed. John Wiley & Sons, New York. 1981.
3. U.S. Environmental Protection Agency (EPA). Health and Environmental Effects Profile
for Quinoline. EPA/600/X-85/355. Environmental Criteria and Assessment Office, Office
of Health and Environmental Assessment, Office of Research and Development,
Cincinnati, OH. 1985.
4. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
5. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System
(IRIS). National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
6. U.S. Environmental Protection Agency (EPA). Health Effects Assessment Summary
Tables. FY1997 Update. Office of Research and Development, Office of Emergency
and Remedial Response, Washington, DC. EPA/540/R-97-036. 1997.
7. The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S.
Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
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2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN(2,3,7,8-TCDD)
1746-01-6
Hazard Summary
2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) js formed as an unintentional
by-product of incomplete combustion. It may be released to the environment during the
combustion of fossil fuels and wood, and during the incineration of municipal and
industrial wastes. It causes chloracne in humans, a severe acne-like condition, and has
been shown to be very toxic in animals studies. It is known to be a developmental
toxicant in animals, causing skeletal deformities, kidney defects, and weakened immune
responses in the offspring of animals exposed to 2,3,7,8-TCDD during pregnancy. Human
studies have shown an association between 2,3,7,8-TCDD and soft-tissue sarcomas,
lymphomas, and stomach carcinomas. The U.S. Environmental Protection Agency (EPA)
has classified 2,3,7,8- TCDD as a Group B2, probable human carcinogen.
Please Note: The main source of information for this fact sheet is the Agency for Toxic Substances and Disease
Registry's (ATSDR's) Toxicological Profile for Chlorinated Dibenzo-p-Dioxins.
Physical Properties
2,3,7,8-TCDD is a colorless solid with no distinguishable odor. (1)
The chemical formula for 2,3,7,8-TCDD is C12H4C14O2, and the molecular weight is 322
g/mol. (1)
The vapor pressure for 2,3,7,8-TCDD is 7.4 x 10'10 at 25 °C, and it has an octanol/water
partition coefficient (log Kow) of 6.8 - 7.58. (1)
Uses
2,3,7,8-TCDD is not intentionally produced by industry. It can be inadvertently produced
in very small amounts as an impurity during the incineration of municipal and industrial
wastes and during the manufacture of certain chemicals. (1)
The only present use for 2,3,7,8-TCDD is in chemical research. (1)
Sources and Potential Exposure
2,3,7,8-TCDD may be formed during the chlorine bleaching process used by pulp and
paper mills, and as a by-product from the manufacture of certain chlorinated organic
chemicals, such as chlorinated phenols. (1)
2,3,7,8-TCDD is primarily released to the environment during the combustion of fossil
fuels (including motor vehicles) and wood, and during incineration processes. (1)
Very low levels of 2,3,7,8-TCDD are found throughout the environment, including air,
food, and soil. (1)
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Most of the exposure of the general population to 2,3,7,8-TCDD is from food, mainly
meat, dairy products, and fish. (1)
Assessing Personal Exposure
Body fat, blood, and breast milk may be analyzed for 2,3,7,8-TCDD. (1)
Health Hazard Information
Acute Effects:
The major acute (short-term) effect from exposure of humans to high levels of
2,3,7,8-TCDD in air is chloracne, a severe acne-like condition that can develop within
months of first exposure. (1,2)
Acute animal tests, such as the LD50 test in dogs, monkeys, and guinea pigs, have shown
2,3,7,8-TCDD to have extreme toxicity from oral exposure. (1)
Chronic Effects (Noncancer):
Chloracne is also the major effect seen from chronic (long-term) exposure to
2,3,7,8-TCDD. (1)
Animal studies have reported hair loss, loss of body weight, and a weakened immune
system from oral exposure to 2,3,7,8-TCDD. (1)
EPA has not established a reference concentration (RfC) or a reference dose (RfD) for
2,3,7,8-TCDD.
ATSDR has calculated a chronic oral minimal risk level (MRL) of 1 x 10"9 mg/kg/d based
on neurological effects in monkeys. The MRL is an estimate of daily exposure to a dose
of a chemical that is likely to be without appreciable risk of adverse noncancerous effects
over a specified duration of exposure. Exposure to a level above the MRL does not mean
that adverse effects will occur. The MRL is used by public health professionals as a
screening tool. (1)
Reproductive/Developmental Effects:
The results of available reproductive and developmental studies in humans are
inconclusive. (1)
Animal studies have reported developmental effects, such as skeletal deformities, kidney
defects, and weakened immune responses in the offspring of animals exposed to
2,3,7,8-TCDD during pregnancy. (1)
Reproductive effects, including altered levels of sex hormones, reduced production of
sperm, and increased rates of miscarriages, have been seen in animals exposed to
2,3,7,8-TCDD. (1)
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Cancer Risk:
Human studies, primarily of workers occupationally exposed to 2,3,7,8-TCDD by
inhalation, have found an association between 2,3,7,8-TCDD and lung cancer, soft-tissue
sarcomas, lymphomas, and stomach carcinomas, although for malignant lymphomas, the
increase in risk is not consistent. (1)
No information is available on the carcinogenic effects of 2,3,7,8-TCDD in animals
following inhalation exposure. (1)
Animal studies have reported tumors of the liver, lung, tongue, thyroid, and nasal
turbinates from oral exposure to 2,3,7,8-TCDD. (1)
EPA has classified 2,3,7,8-TCDD as a Group B2, probable human carcinogen. (2,3)
EPA has calculated a provisional inhalation cancer slope factor of l.SxlO5 (mg/kg/d)"1
and an inhalation unit risk estimate of 3.3 x 10'5 (pg/m3)'1 for 2,3,7,8-TCDD. The
provisional slope factor is a value that has had some form of Agency review, but it does
not appear on IRIS. (2,3)
EPA has calculated a provisional oral cancer slope factor of 1.5 x 105 (mg/kg/d)"1 and an
oral unit risk factor of 4.5 (/ig/L)'1 for 2,3,7,8-TCDD. (2,3)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24,45).
For 2,3,7,8-TCDD: 1 ppm = 13.2 mg/m3.
Note: There are very few health numbers or regulatory/advisory numbers for 2,3,7,8-TCDD;
thus, a graph has not been prepared for this compound.
References
I. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Chlorinated Dibenzo-p-Dioxins. Public Health Service, U.S. Department of Health and
Human Services, Atlanta, GA. 1998.
2. U.S. Environmental Protection Agency (EPA). Health Effects Assessment Summary
Tables. FY1997 Update. Environmental Criteria and Assessment Office, Office of
Health and Environmental Assessment, Office of Research and Development, Cincinnati,
OH. 1997.
3. U.S. Environmental Protection Agency (EPA). Health Assessment Document for
Poly chlorinated Dibenzo-p-Dioxin. Environmental Criteria and Assessment Office,
Office of Health and Environmental Assessment, Office of Research and Development,
Cincinnati, OH. EPA 600/8-84-014F. 1985.
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1,1,2,2-TETRACHLOROETHANE
79-34-5
Hazard Summary
As 1,1,2,2-tetrachloroethane is no longer used much in the U.S., current air emissions
predominantly result from its use as a chemical intermediate during the manufacture of
other chemicals. Low levels have been detected in air. The main effects of
1,1,2,2-tetrachloroethane are liver and neurological effects. Acute (short-term) inhalation
exposure to very high levels of 1,1,2,2-tetrachloroethane has resulted in effects on the
liver and respiratory, central nervous, and gastrointestinal systems in humans. Chronic
(long-term) inhalation exposure to 1,1,2,2-tetrachloroethane in humans results in jaundice
and an enlarged liver, headaches, tremors, dizziness, numbness, and drowsiness. Animal
studies have shown a significantly increased incidence of liver tumors in mice orally
exposed to 1,1,2,2-tetrachloroethane. The U.S. Environmental Protection Agency (EPA)
has classified 1,1,2,2-tetrachloroethane as a Group C possible human carcinogen.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on the carcinogenic effects of 1,1,2,2-tetrachloroethane, and the Agency for
Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for 1,1,2,2-Tetrachloroethane.
Physical Properties
1,1,2,2-Tetrachloroethane is a colorless, dense liquid that has a sweet, chloroform like
odor. (1,6)
The odor threshold for 1,1,2,2-tetrachloroethane is 1.5 ppm. (6)
The chemical formula for 1,1,2,2-tetrachloroethane is C2H9C14, and the molecular weight
is 167.85 g/mol. (1,2)
The vapor pressure for 1,1,2,2-tetrachloroethane is 5.95 mm Hg at 25 °C, and it has a log
octanol/water partition coefficient (log Kow) of 2.39. (1)
The half-life in air is about 60 days. (1)
Uses
The production of 1,1,2,2-tetrachloroethane has decreased significantly in the U.S. (1)
In the past, 1,1,2,2-tetrachloroethane was used in large amounts to produce
trichloroethylene, tetrachloroethylene, and 1,2,-dichloroethylene. (1)
It was also used as a solvent, in cleaning and degreasing metals, in paint removers,
varnishes and lacquers, in photographic films, as an extractant for oils and fats, and in
pesticides. (1)
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Sources and Potential Exposure
As it is no longer used much in the U.S., present sources of 1,1,2,2-tetrachloroethane are
chemical production activities in which it is an intermediate product. (1)
Low levels of 1,1,2,2-tetrachloroethane can be present in both indoor and outdoor air. In
the early 1980s, average ambient air concentrations were around 0.005 ppb, and average
concentrations in the indoor air of several homes measured 1.8 ppb. (1)
1,1,2,2-Tetrachloroethane has been found, in trace amounts, in adhesives, oils, greases,
and lubricants; these household products may contaminate indoor air. (1)
Limited occupational exposure to 1,1,2,2-tetrachloroethane may occur through inhalation
of the vapors or through skin contact due to spills or accidents in the workplace. (1)
1,1,2,2-Tetrachloroethane has been detected in surface water and groundwater; however,
a nationwide survey of drinking water supplies in the 1980s did not find any supplies
containing 1,1,2,2-tetrachloroethane. (1)
Assessing Personal Exposure
No specific medical tests are available to determine exposure to 1,1,2,2-tetrachloroethane.
(1)
Health Hazard Information
Acute Effects:
Acute exposure to very high levels of 1,1,2,2-tetrachloroethane has caused death in
humans; the autopsies revealed severe liver destruction. (1,2)
Respiratory and eye irritation, dizziness, nausea, and vomiting have been noted in humans
exposed to fumes in the workplace. (1)
Animal studies have reported effects on the liver, eyes, and central nervous system (CNS)
from acute inhalation exposure to 1,1,2,2,-tetrachloroethane. (1)
Tests involving acute exposure of animals, such as the LC50 and LD50 tests in rats and
mice, have shown 1,1,2,2-tetrachloroethane to have moderate acute toxicity. (3)
Chronic Effects (Noncancer):
Chronic exposure of humans to high levels of 1,1,2,2-tetrachloroethane results in effects
on the liver (jaundice and an enlarged liver), central and peripheral nervous system
(headaches, tremors, dizziness, and drowsiness), and gastrointestinal effects (pain,
nausea, vomiting, and loss of appetite). (1)
Liver effects have also been observed in animals exposed via inhalation. (1)
EPA has not established a reference concentration (RfC) or reference dose (RfD) for
1,1,2,2-tetrachloroethane. (4)
ATSDR has calculated an intermediate-duration inhalation minimal risk level (MRL) of
0.4 ppm (3 mg/m3) for 1,1,2,2-tetrachloroethane based on liver effects in rats. The MRL
is an estimate of the daily human exposure to a hazardous substance that is likely to be
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without appreciable risk of adverse noncancer health effects over a specified duration of
exposure. Exposure to a level above the MRL does not mean that adverse health effects
will occur. The MRL is intended to serve as a screening tool. (1)
Reproductive/Developmental Effects:
No studies are available regarding developmental or reproductive effects in humans from
inhalation or oral exposure to 1,1,2,2-tetrachloroethane. (1)
Animal studies have not reported reproductive effects from inhalation exposure to
1,1,2,2-tetrachloroethane, while an oral study in rats reported histopathological changes in
the testes. (1)
No effects to the offspring of male rats exposed to 1,1,2,2-tetrachloroethane via
inhalation were reported. (1)
Cancer Risk:
Oral exposure to 1,1,2,2-tetrachloroethane in mice resulted in an increased incidence of
hepatocellular carcinomas, while no increase in tumors was reported in rats. (1,4)
EPA has classified 1,1,2,2-tetrachloroethane as a Group C, possible human carcinogen.
(4)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA has calculated an inhalation unit risk estimate of 5.8 x
10"5 (/zg/m3)"1. EPA estimates that, if an individual were to continuously breathe air
containing 1,1,2,2-tetrachloroethane at an average of 0.02 /^cg/m3 (2.0 x 10"5 mg/m3) over
his or her entire lifetime, that person would theoretically have no more than a
one-in-a-million increased chance of developing cancer as a direct result of breathing air
containing this chemical. Similarly, EPA estimates that continuously breathing air
containing 0.2 /ig/m3 (2.0 x 10"4 mg/m3) would result in not greater than a
one-in-a-hundred thousand increased chance of developing cancer over a lifetime, and air
containing 2.0 Mg/m3 (2.0 x 10~3 mg/m3) would result in not greater than a one-in-ten
thousand increased chance of developing cancer. For a detailed discussion of confidence
in the potency estimates, please see IRIS. (4)
EPA has also calculated an oral cancer slope factor of 0.2 (mg/kg/d)'1. (4)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For 1,1,2,2-tetrachloroethane: 1 ppm = 6.86 mg/m3.
To convert from (JLg/tri* to mg/m3: mg/m3 = (fJLg/m3) x (1 mg/1,000
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Health Data from Inhalation Exposure
1,1,2,2-Tetrochloroethcne
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ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LC50 (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-no-adverse-affect level.
NIOSH REL - National Institute of Occupational Safety and Health's recommended exposure
limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure
and/or ceiling.
NIOSH IDLH - NIOSH's immediately dangerous to life or health concentration; NTOSH
recommended exposure limit to ensure that a worker can escape from an exposure condition that
is likely to cause death or immediate or delayed permanent adverse health effects or prevent
escape from the environment.
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OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average: the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c These cancer risk estimates were derived from oral data and converted to provide the estimated
inhalation risk.
d The LOAEL is from the critical study used as the basis for the ATSDR intermediate MRL.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
1,1,2,2-Tetrachloroethane (Update). U.S. Public Health Service, U.S. Department of
Health and Human Services, Atlanta, GA. 1996.
2. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on 1,1,2,2-Tetrachloroethane. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
5. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29
CFR 1910.1000. 1998.
6. I.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds
compared with threshold limit values and volatilities for 214 industrial chemicals in air
and water dilution. Journal of Applied Toxicology, 3(6):272-290. 1983.
7. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
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8. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
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TETRACHLOROETHYLENE(PERCHLOROETHYLENE)
127-18-4
Hazard Summary
Tetrachloroethylene is widely used for dry-cleaning fabrics and metal degreasing
operations. The main effects of tetrachloroethylene in humans are neurological, liver, and
kidney effects following acute (short-term) and chronic (long-term) inhalation exposure.
Dizziness, sleepiness, and impaired coordination have been reported. Some adverse
reproductive effects, such as menstrual disorders and spontaneous abortions, have been
reported from occupational exposure to tetrachloroethylene; however, no definite
conclusions can be made because of the limitations of the studies. Results from
epidemiological studies of tetrachloroethylene and cancer incidence have been mixed;
some studies reported an increased incidence of a variety of tumors, while other studies
did not report any carcinogenic effects. Animal studies have reported an increased
incidence of liver cancer in mice, via inhalation and gavage, and kidney and mononuclear
cell leukemia in rats. The U.S. Environmental Protection Agency (EPA) considers
trichloroethylene as intermediate between a probable and possible human carcinogen
(Group B/C). The Agency is currently reassessing its potential carcinogenicity.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System
(IRIS), which contains information on oral chronic toxicity and the reference dose (RfD), and the Agency for Toxic
Substances and Disease Registry's (ATSDR's) lexicological Profile for Tetrachloroethylene. Another secondary
source is EPA's Health Effects Assessment for Tetrachloroethylene.
Physical Properties
Tetrachloroethylene is a nonflammable colorless liquid with a sharp sweet odor; the odor
threshold is 1 ppm. (1)
The chemical formula for tetrachloroethylene is C2C14, and the molecular weight is
165.83 g/mol. (1)
The vapor pressure for tetrachloroethylene is 18.47 mm Hg at 25 °C, and it has a log
octanol/water partition coefficient (log Kovv) of 3.40. (1)
Uses
Tetrachloroethylene is used for dry cleaning and textile processing, as a chemical
intermediate, and for vapor degreasing in metal-cleaning operations. (1)
Sources and Potential Exposure
Prior to 1981, tetrachloroethylene was detected in ambient air at average levels of 0.16
ppb in rural and remote areas, 0.79 ppb in urban and suburban areas, and 1.3 ppb in areas
near emission sources. (1)
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Tetrachloroethylene has also been detected in drinking water; one survey prior to 1984 of
water supplies from groundwater sources reported a median concentration of 0.75 ppb for
the samples in which tetrachloroethylene was detected, with a maximum level of 69 ppb.
(1)
Occupational exposure to tetrachloroethylene may occur, primarily in dry cleaning
establishments and at industries manufacturing or using the chemical. (1)
Assessing Personal Exposure
Tetrachloroethylene can be measured in the breath, and breakdown products of
tetrachloroethylene can be measured in the blood and urine. (1)
Health Hazard Information
Acute Effects:
Acute exposure to very high levels of tetrachloroethylene in humans has caused death.
Effects noted from short-term, inhalation exposure to tetrachloroethylene vapors include
irritation of the upper respiratory tract and eyes, kidney dysfunction, and at lower
concentrations, neurological effects, such as reversible mood and behavioral changes,
impairment of coordination, dizziness, headache, sleepiness, and unconsciousness. (1)
Animal studies have reported effects on the liver, kidney, and central nervous system
(CNS) from acute inhalation exposure to tetrachloroethylene. (1)
Acute animal tests, such as the LC50 and LD50 tests in mice have shown
tetrachloroethylene to have low toxicity from inhalation and oral exposure. (1)
Chronic Effects (Noncancer):
The major effects from chronic inhalation exposure to tetrachloroethylene in humans are
neurological effects, including headaches, and impairment of memory, concentration, and
intellectual function. Other effects noted in humans include cardiac arrhythmia, liver
damage, and possible kidney effects. (1,5)
Animal studies have reported effects on the liver, kidney, and CNS from chronic
inhalation exposure to tetrachloroethylene. (1,5)
EPA has not established a reference concentration (RfC) for tetrachloroethylene. (4)
The RfD for tetrachloroethylene is 0.01 mg/kg/d based on hepatotoxicity in mice and
weight gain in rats. The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of a daily oral exposure to the human population (including sensitive
subgroups) that is likely to be without appreciable risk of deleterious noncancer effects
during a lifetime. It is not a direct estimator of risk, but rather a reference point to gauge
the potential effects. At exposures increasingly greater than the RfD, the potential for
adverse health effects increases. Lifetime exposure above the RfD does not imply that an
adverse health effect would necessarily occur. (4)
EPA has medium confidence in the RfD based on low confidence in the study on which
the RfD was based due to the lack of complete histopathological examination at the
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no-observed-adverse-effect level (NOAEL) in the mouse; and medium confidence in the
database because it is relatively complete but lacks studies of reproductive and teratology
endpoints subsequent to oral exposure. (4)
ATSDR has calculated a chronic-duration inhalation minimal risk level (MRL) of 0.04
ppm (0.3 mg/m3) for tetrachloroethylene based on neurological effects in humans. The
MRL is an estimate of the daily human exposure to a hazardous substance that is likely to
be without appreciable risk of adverse noncancer health effects over a specified duration
of exposure. (1)
Repeated skin contact may cause irritation. (1)
Reproductive/Developmental Effects:
Some adverse reproductive effects, such as menstrual disorders and spontaneous
abortions, have been reported in women occupationally exposed to tetrachloroethylene.
However, no definitive conclusions can be made because of the limitations of the studies.
(1)
In a study of residents exposed to drinking water contaminated with solvents, including
tetrachloroethylene, there was a suggestion that birth defects were associated with
exposure. However, no firm conclusions can be drawn from this study due to multiple
chemical exposures and problems with the analysis. (1)
Increased fetal resorptions and effects to the fetus have been reported in animals exposed
to high levels of tetrachloroethylene by inhalation. (1)
Cancer Risk:
Epidemiological studies of dry cleaning workers exposed to tetrachloroethylene and other
solvents have shown mixed results; some studies reported an increased incidence of a
variety of tumors, while other studies did not show any carcinogenic effects. All of these
studies are complicated by potential exposure to numerous chemicals. (1,5,6)
One human study reported that there was a potential association between drinking water
contaminated with tetrachloroethylene and other chemicals and an increased risk of
childhood leukemia. Other studies reexamined the data and did not agree with the
association because the people were exposed to multiple chemicals and the statistical
significance of the incidence of leukemia has not been resolved. (1)
Animal studies have reported an increased incidence of liver tumors in mice, from
inhalation and gavage exposure, and kidney and mononuclear cell leukemias in rats, via
inhalation exposure. (1,5,6)
Regardless of exposure route, less than 5 percent of absorbed tetrachloroethylene is
metabolized by humans to trichloroacetic acid (TCA), with the remainder being exhaled
unchanged. Trichloroacetic acid is classified as a Group C, possible human carcinogen
based on limited evidence of liver tumors in mice (but not rats). (4,7)
EPA considers trichloroethylene as intermediate between a probable and possible human
carcinogen (Group B/C). The Agency is currently reassessing its potential
carcinogenicity. (10)
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EPA uses mathematical models, based on animal studies, to estimate the probability of a
person developing cancer from breathing air containing a specified concentration of a
chemical. EPA has calculated a provisional inhalation unit risk estimate of 5.8 x 10"7
(/-tg/m3)"1. A provisional value is one which has not received Agency-wide review. (7)
EPA has calculated a provisional oral cancer slope factor of 0.051 (mg/kg/d)"1. (5)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For tetrachloroethylene: 1 ppm = 6.78 mg/m3.
To convert from [ig/m3 to mg/m3: mg/m3 = (fig/m3) x (1 mg/1,000
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Health Data from Inhalation Exposure
T ef rcrhloroef hyf ene
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10000
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LCSO (rriCB) (35,268 nrg/nrf)
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numbers"
A1HAERFG2 (1360 rrg/rr?)
NCBHIDLH0020nr9'rr?)
CSHA PEL, A03H STEL (686 rr&rr?)
A/HAERPG-I
(680 rrg/rr?)
A03HTLV
0.1
AIHA ERPG - American Industrial Hygiene Association's emergency response planning
guidelines. ERPG 1 is the maximum airborne concentration below which it is believed nearly all
individuals could be exposed up to one hour without experiencing other than mild transient
adverse health effects or perceiving a clearly defined objectionable odor; ERPG 2 is the
maximum airborne concentration below which it is believed nearly all individuals could be
exposed up to one hour without experiencing or developing irreversible or other serious health
effects that could impair their abilities to take protective action.
ACGIH STEL - American Conference of Governmental and Industrial Hygienists' short-term
exposure limit; 15-min time-weighted-average exposure that should not be exceeded at any time
during a workday even if the 8-h time-weighted-average is within the threshold limit value.
ACGIH TLV - American Conference of Governmental and Industrial Hygienists' threshold
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limit value expressed as a time-weighted average; the concentration of a substance to which most
workers can be exposed without adverse effects.
LC50 (Lethal Concentration^) - A calculated concentration of a chemical in air to which
exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-no-adverse-affect level.
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can
escape from an exposure condition that is likely to cause death or immediate or delayed
permanent adverse health effects or prevent escape from the environment.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the ATSDR chronic inhalation MRL.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Tetrachloroethylene (Update). U.S. Public Health Service, U.S. Department of Health
and Human Services, Atlanta, GA. 1997.
2. American Conference of Governmental and Industrial Hygienists (ACGIH). 7999 TLVs
and BEIs: Threshold Limit Values for Chemical Substances and Physical Agents,
Biological Exposure Indices. Cincinnati, OH. 1999.
3. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29
CFR 1910.1000. 1998.
4. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Tetrachloroethylene. National Center for Environmental Assessment, Office of
Research and Development, Washington, DC. 1999.
5. U.S. Environmental Protection Agency (EPA). Health Effects Assessment for
Tetrachloroethylene. EPA/600/8-89-096. Environmental Criteria and Assessment Office,
Office of Health and Environmental Assessment, Office of Research and Development,
Cincinnati, OH. 1988.
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6. U.S. Environmental Protection Agency (EPA). Updated Health Assessment Document for
Tetrachloroethylene. EPA/600/8-82/005B. Environmental Criteria and Assessment
Office, Office of Health and Environmental Assessment, Office of Research and
Development, Cincinnati, OH. 1988.
7. U.S. Environmental Protection Agency (EPA). Risk Assessment Issue Paper for
Carcinogenicity Information for Tetrachloroethylene (Perchloroethylene, PERC)
(CASRN127-18-4). Superfund Technical Support Center, National Center for
Environmental Assessment, Cincinnati, OH. nd.
8. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
9. American Industrial Hygiene Association (AHA). The AIHA 1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.
1998.
10. U.S. Environmental Protection Agency (EPA). National Emission Standards for
Hazardous Air Pollutants: Wood Furniture Manufacturing Operations. Federal Register
63 FR 34336-346. June 24,1998.
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TRICHLOROETHYLENE
79-01-6
Hazard Summary
Most of the trichloroethylene (TCE) used in the U.S. is released into the atmosphere from
industrial degreasing operations. Acute (short-term) and chronic (long-term) inhalation
exposure to trichloroethylene can affect the human central nervous system (CNS), with
symptoms such as dizziness, headaches, confusion, euphoria, facial numbness, and
weakness. High, short-term exposures of humans by inhalation also have been associated
with effects on the liver, kidneys, gastrointestinal system, and skin. Although several
epidemiological studies have investigated a possible link between trichloroethylene
exposure and reproductive or developmental effects, no conclusive evidence has been
identified. Similarly, the existence of a relationship between trichloroethylene exposure
and cancer is also not clear from the epidemiological studies that have been performed.
Animal studies have reported increases in lung, liver, and testicular tumors, via inhalation
exposure. The U.S. Environmental Protection Agency (EPA) considers trichloroethylene
as intermediate between a probable and possible human carcinogen (Group B/C). The
Agency is currently reassessing its potential carcinogenicity.
Please Note: The main source of information for this fact sheet is the Agency for Toxic Substances and Disease
Registry's (ATSDR's) Toxicological Profile for Trichloroethylene. Another secondary source used is EPA's Health
Assessment Document for Trichloroethylene.
Physical Properties
Trichloroethylene is a nonflammable colorless liquid with a sweet odor similar to ether or
chloroform. (1)
The odor threshold for trichloroethylene is 28 ppm. (6)
The chemical formula for trichloroethylene is C2HC13, and the molecular weight is 131.40
g/mol. (1)
The vapor pressure for trichloroethylene is 74 mm Hg at 25 °C, and it has a log
octanol/water partition coefficient (log Kow) of 2.42. (1)
Trichloroethylene is not a persistent chemical in the atmosphere; its half-life in air is
about 7 days. (1)
Uses
The main use of trichloroethylene is in the vapor degreasing of metal parts. (1)
Trichloroethylene is also used as an extraction solvent for greases, oils, fats, waxes, and
tars, a chemical intermediate in the production of other chemicals, and as a refrigerant. (1)
Trichloroethylene is used in consumer products such as typewriter correction fluids, paint
removers/strippers, adhesives, spot removers, and rug-cleaning fluids. (1)
Trichloroethylene was used in the past as a general anesthetic. (1)
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Sources and Potential Exposure
Trichloroethylene has been detected in ambient air at levels less than 1 ppb. (1)
Drinking water supplies relying on contaminated groundwater sources may contain
trichloroethylene. A monitoring study in the early 1980s of drinking water systems
relying groundwater sources detected TCE in 10 percent of the systems sampled. The
median level among the systems where detected was 1 ppb. (1)
Workers may be exposed to trichloroethylene in the factories where it is manufactured or
used. In addition, persons breathing air around these factories may be exposed to
trichloroethylene. (1)
Persons may also be exposed to trichloroethylene through the use of products containing
the chemical and from evaporation and leaching from waste disposal sites. (1)
Assessing Personal Exposure
Trichloroethylene can be measured in the breath, and breakdown products of
trichloroethylene can be measured in urine or blood. (1)
Health Hazard Information
Acute Effects:
Acute exposure to extremely high levels of trichloroethylene (approximately 10,000 ppm)
in humans has caused death. A few of these reports have cited cardiac arrhythmias as the
cause of death, and one report noted massive liver damage. (1)
CNS effects are the primary effects noted from acute inhalation exposure to
trichloroethylene in humans, with symptoms including sleepiness, fatigue, headache,
confusion, and feelings of euphoria. Effects on the liver, kidneys, gastrointestinal system,
and skin have also been noted. (1)
Neurological, lung, kidney, and heart effects have been reported in animals acutely
exposed to trichloroethylene. (1)
Tests involving acute exposure of animals, such as the LC50 and LD50 tests in rats and
mice, have shown trichloroethylene to have low toxicity from inhalation exposure and
moderate toxicity from oral exposure. (1,2)
Chronic Effects (Noncancer):
As with acute exposure, chronic exposure to trichloroethylene by inhalation also affects
the human CNS. Case reports of intermediate and chronic occupational exposures
included effects such as dizziness, headache, sleepiness, nausea, confusion, blurred
vision, facial numbness, and weakness. (1)
Studies have shown that simultaneous alcohol consumption and trichloroethylene
inhalation increases the toxicity of trichloroethylene in humans. (1)
Neurological, liver, and kidney effects were reported in chronically-exposed animals. (1)
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EPA has not calculated a reference concentration (RfC) or reference dose (RfD) for
trichloroethylene. (3)
ATSDR has calculated an intermediate-duration inhalation minimal risk level (MRL) of
0.1 ppm (0.5 mg/m3) for trichloroethylene based on neurological effects in rats. The
MRL is an estimate of the daily human exposure to a hazardous substance that is likely to
be without appreciable risk of adverse noncancer health effects over a specified duration
of exposure. Exposure to a level above the MRL does not mean that adverse health
effects will occur. The MRL is intended to serve as a screening tool. (1)
The California Environmental Protection Agency (CalEPA) has calculated a chronic
inhalation reference exposure level of 0.6 mg/m3 based on neurological effects in humans.
The CalEPA reference exposure level is a concentration at or below which adverse health
effects are not likely to occur. (5)
Reproductive/Developmental Effects:
A study of nurses occupationally exposed by inhalation to trichloroethylene along with
other chemicals in operating rooms, and another epidemiological study of women
exposed occupationally or nonoccupationally to trichloroethylene and other solvents,
have reported increases in the incidence of miscarriages. The presence of other chemicals,
however, limits the ability to draw conclusions specific to trichloroethylene. (1)
An epidemiological study of 2,000 male and female workers exposed to trichloroethylene
via inhalation found no increase in malformations in babies born following exposure. (1)
Several studies have evaluated and not found an association between adverse
reproductive effects in humans and exposure to trichloroethylene in contaminated
drinking water. An association was found between the occurrence of congenital heart
disease in children and a drinking water supply contaminated with trichloroethylene and
other similar chemicals; however, no causal relationship with trichloroethylene could be
concluded. (1)
In one animal study, an increase in abnormal sperm morphology was observed following
very high inhalation exposures of mice; however, other animal studies have not reported
reproductive or developmental effects from either inhalation or ingestion exposures. (1,4)
Cancer Risk:
Several human studies have investigated the relationship between inhalation exposure to
trichloroethylene and cancer, some finding weak relationships and others finding none;
however, each has limitations that restrict its usefulness. None of the studies found strong
evidence of an association between trichloroethylene exposure and cancer incidence. (1,4)
The existence of a relationship between oral exposure to trichloroethylene and cancer
incidence is also not clear. One human study reported that there was a potential
association between drinking water contaminated with trichloroethylene and an increased
risk of childhood leukemia. Other studies reexamined the data and did not agree with the
association because the people were exposed to chemicals other than trichloroethylene,
and the statistical significance of the incidence of leukemia has not been resolved. (1)
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Animal studies, via inhalation exposure, have" reported increases in lung, liver, and
testicular tumors and increases in liver tumors via gavage. (1,4)
EPA considers trichloroethylene as intermediate between a probable and possible human
carcinogen (Group B/C). The Agency is currently reassessing its potential
carcinogenicity. (11)
EPA uses mathematical models, based on animal studies, to estimate the probability of a
person developing cancer from continuously breathing air containing a specified
concentration of a chemical. EPA has calculated a provisional inhalation unit risk
estimate of 1.7 x 10-6 (pcg/m3)"1. A provisional value is one which has not received
Agency-wide review. (10)
EPA has also calculated a provisional oral cancer slope factor of 0.011 (mg/kg/d)"1. (10)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 = (ppm) x (molecular weight of the compound)/(24.45).
For trichloroethylene: 1 ppm = 5.37 mg/m3. To convert from fJig/m3 to mg/m3: mg/m3 = (ng/m3) x
(1 mg/1,000
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Health Data from Inhalation Exposure
Trichloroefhylene
1000000
100000
10000
Ol
e
c
o
01
u
I
1000
100
10
Regulatory, crivisory
numbers15
Heath numbers
LC50(rc*s)(67,778nrp'rr?)
LC50 (nrice) (45.412 rrQ/rrf)
AIHAERPG2
NIC8HIDLH (5370nrn'nr?)
CSHAPEL,
AO3HSTEL,
AIHAERPS1
La\ELc(nardog
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exposure for a specific length of time is expected to cause death in 50% of a defined
experimental animal population.
LOAEL - Lowest-observed-adverse-affect level
NIOSHIDLH - National Institute of Occupational Safety and Health's immediately dangerous
to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can
escape from an exposure condition that is likely to cause death or immediate or delayed
permanent adverse health effects or prevent escape from the environment.
OSHA PEL - Occupational Safety and Health Administration's permissible exposure limit
expressed as a time-weighted average; the concentration of a substance to which most workers
can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.
a Health numbers are toxicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the ATSDR intermediate MRL.
d The LOAEL is from the critical study used as the basis for the CalEPA chronic reference
exposure level.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Trichloroethylene (Update). U.S. Public Health Service, U.S. Department of Health and
Human Services, Atlanta, GA. 1997.
2. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
3. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System (IRIS)
on Trichloroethylene. National Center for Environmental Assessment, Office of Research
and Development, Washington, DC. 1999.
4. U.S. Environmental Protection Agency (EPA). Health Assessment Document for
Trichloroethylene. EPA7600/8-82/006F. Environmental Criteria and Assessment Office,
Office of Health and Environmental Assessment, Office of Research and Development.
1985.
5. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
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6. J.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds
compared with threshold limit values and volatilities for 214 industrial chemicals in air
and water dilution. Journal of Applied Toxicology, 3(6):272-290. 1983.
7. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to
Chemical Hazards. U.S. Department of Health and Human Services, Public Health
Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
8. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEIs. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
9. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29
CFR 1910.1000. 1998.
10. U.S. Environmental Protection Agency (EPA). Risk Assessment Issue Paper for
Carcinogenicity Information for Trichloroethylene (TCE) (CASRN 79-01-6). Superfund
Technical Support Center, National Center for Environmental Assessment, Cincinnati,
OH. nd.
11. U.S. Environmental Protection Agency (EPA). National Emission Standards for
Hazardous Air Pollutants: Wood Furniture Manufacturing Operations. Federal Register
63 FR 34336-346. June 24,1998.
12. American Industrial Hygiene Association (AIHA). The AIHA 1998 Emergency Response
Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.
1998.
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VINYL CHLORIDE
75-01-4
Hazard Summary
Most vinyl chloride is used to make polyvinyl chloride (PVC) plastic and vinyl products.
Acute (short-term) exposure to high levels of vinyl chloride in air has resulted in central
nervous system(CNS) effects, such as dizziness, drowsiness, and headaches in humans.
Chronic (long-term) exposure to vinyl chloride through inhalation and oral exposure in
humans has resulted in liver damage. There are positive human and animal studies
showing adverse effects which raise a concern about potential reproductive and
developmental hazards to humans from exposure to vinyl chloride. Cancer is a major
concern from exposure to vinyl chloride via inhalation, as vinyl chloride exposure has
been shown to increase the risk of a rare form of liver cancer in humans. The U.S.
Environmental Protection Agency (EPA) has classified vinyl chloride as a Group A,
human carcinogen.
Please Note: The main sources of information for this fact sheet are the Agency for Toxic Substances and Disease
Registry's (ATSDR's) Toxicological Profile for Vinyl Chloride and Case Studies in Environmental Medicine. Vinyl
Chloride Toxicity.
Physical Properties
Vinyl chloride is a colorless gas with a mild, sweet odor. (1)
The odor threshold for vinyl chloride is 3,000 ppm. (5)
Vinyl chloride is slightly soluble in water and is quite flammable. (1)
The chemical formula for vinyl-chloride is C2H3C1, and the molecular weight is 62.5
g/mol. (1)
The vapor pressure for vinyl chloride is 2,600 mm Hg at 25 °C, and it has a log
octanol/water partition coefficient (log Kow) of 1.36. (1)
The half-life of vinyl chloride in air is a few hours. (1)
Uses
Most of the vinyl chloride produced in the U.S. is used to make polyvinyl chloride (PVC),
a material used to manufacture a variety of plastic and vinyl products including pipes,
wire and cable coatings, and packaging materials. (1)
Smaller amounts of vinyl chloride are used in furniture and automobile upholstery, wall
coverings, housewares, and automotive parts. (1)
Vinyl chloride has been used in the past as a refrigerant. (1)
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Sources and Potential Exposure
Ambient air concentrations of vinyl chloride are generally quite low, with exposure
occurring from the discharge of exhaust gases from factories that manufacture or process
vinyl chloride, or evaporation from areas where chemical wastes are stored. (1,2)
Air inside new cars may contain vinyl chloride at higher levels than detected in ambient
air because vinyl chloride may outgas into the air from the new plastic parts. (1,2)
Drinking water may contain vinyl chloride released from contact with polyvinyl pipes.
(1,2)
Vinyl chloride is a microbial degradation product of trichloroethylene in groundwater,
and thus can be found in groundwater affected by trichloroethylene contamination. (3)
Occupational exposure to vinyl chloride may occur in those workers concerned with the
production, use, transport, storage, and disposal of the chemical. (1,2)
Assessing Personal Exposure
Vinyl chloride can be detected in urine and body tissues, but the tests are not reliable
indicators of total exposure. (1,2)
Health Hazard Information
Acute Effects:
Acute exposure of humans to high levels of vinyl chloride via inhalation in humans has '
resulted in effects on the CNS, such as dizziness, drowsiness, headaches, and giddiness.
(1,2)
Vinyl chloride is reported to be slightly irritating to the eyes and respiratory tract in
humans. (1,2)
Acute exposure to extremely high levels of vinyl chloride has caused loss of
consciousness, lung and kidney irritation, and inhibition of blood clotting in humans and
cardiac arrhythmias in animals. (1)
Tests involving acute exposure of animals, such as the LC50 test in mice, have shown
vinyl chloride to have high acute toxicity from inhalation exposure. (5)
Chronic Effects (Noncancer):
Liver damage may result in humans from chronic exposure to vinyl chloride, through
both inhalation and oral exposure. (1,2)
A small percentage of individuals occupationally exposed to high levels of vinyl chloride
in air have developed a set of symptoms termed "vinyl chloride disease," which is
characterized by Raynaud's phenomenon (fingers blanch and numbness and discomfort
are experienced upon exposure to the cold), changes in the bones at the end of the fingers,
joint and muscle pain, and scleroderma-like skin changes (thickening of the skin,
decreased elasticity, and slight edema). (1,2)
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CNS effects (including dizziness, drowsiness, fatigue, headache, visual and/or hearing
disturbances, memory loss, and sleep disturbances) as well as peripheral nervous system
symptoms (peripheral neuropathy, tingling, numbness, weakness, and pain in fingers)
have also been reported in workers exposed to vinyl chloride. (1)
Animal studies have reported effects on the liver, kidney, and CNS from-chronic
exposure to vinyl chloride. (1,6)
EPA has not established a reference concentration (RfC) or a reference dose (RfD) for
vinyl chloride. (8)
ATSDR has calculated an intermediate-duration inhalation minimal risk level (MRL) of
0.03 ppm (0.08 mg/m3) for vinyl chloride based on liver effects in rats. The MRL is an
estimate of the daily human exposure to a hazardous substance that is likely to be without
appreciable risk of adverse noncancer health effects over a specified duration of exposure.
Exposure to a level above the MRL does not mean that adverse health effects will occur.
The MRL is intended to serve as a screening tool. (1)
The California Environmental Protection Agency (CalEPA) has calculated a chronic
inhalation reference exposure level of 0.005 mg/m3 based on liver effects in humans. The
CalEPA reference exposure level is a concentration at or below which adverse health
effects are not likely to occur. (15)
Reproductive/Developmental Effects:
Several case reports suggest that male sexual performance may be affected by vinyl
chloride. However, these studies are limited by lack of quantitative exposure information
and possible co-occurring exposure to other chemicals. (1)
Several epidemiological studies have reported an association between vinyl chloride
exposure in pregnant women and an increased incidence of birth defects, while other
studies have not reported similar findings. (1,2)
Epidemiological studies have suggested an association between men occupationally
exposed to vinyl chloride and miscarriages in their wives' pregnancies although other
studies have not supported these findings. (1,2)
Testicular damage and decreased male fertility have been reported in rats exposed to low
levels for up to 12 months. (1)
Animal studies have reported decreased fetal weight and birth defects at levels that are
also toxic to maternal animals in the offspring of rats exposed to vinyl chloride through
inhalation. (1)
Cancer Risk:
Inhaled vinyl chloride has been shown to increase the risk of a rare form of liver cancer
(angiosarcoma of the liver) in humans. (1,2,6)
Vinyl chloride exposure, through inhalation, has also been associated with cancer of the
brain, CNS, lung, respiratory tract, and the lymphatic/hematopoietic system in humans.
(1,2)
Animal studies have shown that vinyl chloride, via inhalation, increases the incidence of
angiosarcoma of the liver and cancer of the liver and brain. (1,2,6)
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Several rat studies show a pronounced early-life susceptibility to the carcinogenic effect
of vinyl chloride, i.e., early exposures are associated with higher cancer incidence than
much longer exposures that occur after maturity. (1)
EPA has classified vinyl chloride as a Group A, human carcinogen. (8)
EPA uses mathematical models, based on human and animal studies, to estimate the
probability of a person developing cancer from breathing air containing a specified
concentration of a chemical. EPA has calculated a provisional inhalation unit risk
estimate of 8.4 x 10"5 (/ig/m3)"1 for vinyl chloride. A provisional value is one which has
not received Agency-wide review. (8)
EPA has calculated a provisional oral cancer slope factor of 1.9 (mg/kg/d)'1 for vinyl
chloride. (8)
Conversion Factors:
To convert from ppm to mg/m3: mg/m3 - (ppm) x (molecular weight of the compound)/(24.45).
For vinyl chloride: 1 ppm = 2.6 mg/m3.
To convert from fig/m3 to mg/m3: mg/m3 = (fig/m3) x (1 mg/1,000
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Health Data from Inhalation Exposure
Vinyl Chloride
10000
1000
100
Ol
c
o
c
01
u
10
Reguiaory, advisory
numbers"
Hedth numbers0
L(3Krcfct)ts) ($88 nr^m)
LC50 (price) (299 rrgfm)
LCAELcfliver)(26nra'm)
AOSHTLVCBHAcBling
GSnrp'nrf)
LO\ELd(!rver)(4nrQ'ni9
ATSDRinfermBdcte
VRL (P.08 rr^nr?)
CaEPA reference
0
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Report to Congress
a Health numbers are lexicological numbers from animal testing or risk assessment values
developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while
advisory numbers are nonregulatory values provided by the Government or other groups as
advice.
c The LOAEL is from the critical study used as the basis for the ATSDR intermediate-duration
inhalation MRL.
d The LOAEL is from the critical study used as the basis for the CalEPA chronic inhalation
reference exposure level.
References
1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Vinyl Chloride (Update). Public Health Service, U.S. Department of Health and Human
Services, Atlanta, GA. 1997.
2. Agency for Toxic Substances and Disease Registry (ATSDR). Case Studies in
Environmental Medicine. Vinyl Chloride Toxicity. Public Health Service, U.S.
Department of Health and Human Services, Atlanta, GA. 1990.
3. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for
Trichloroethylene. Public Health Service, U.S. Department of Health and Human
Services, Atlanta, GA. 1992.
4. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical
Substances (RTECS, online database). National Toxicology Information Program,
National Library of Medicine, Bethesda, MD. 1993.
5. J.E. Amoore and E. Hautala. Odor as an aid to chemical safety: Odor thresholds
compared with threshold limit values and volatilities for 214 industrial chemicals in air
and water dilution. Journal of Applied Toxicology, 3(6):272-290. 1983.
6. U.S. Department of Health and Human Services. Hazardous Substances Data Bank
(HSDB, online database). National Toxicology Information Program, National Library of
Medicine, Bethesda, MD. 1993.
7. U.S. Environmental Protection Agency (EPA). Integrated Risk Information System
(IRIS). National Center for Environmental Assessment, Office of Research and
Development, Washington, DC. 1999.
8. U.S. Environmental Protection Agency (EPA). Health Effects Assessment Summary
Tables. FY1997 Update. Environmental Criteria and Assessment Office, Office of Health
and Environmental Assessment, Office of Research and Development, Cincinnati, OH.
1997.
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9. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and
BEls. Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH. 1999.
10. Occupational Safety and Health Administration (OSHA). Occupational Safety and
Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29
CFR 1910.1017. 1998.
11. California Environmental Protection Agency (CalEPA). Technical Support Document for
the Determination ofNoncancer Chronic Reference Exposure Levels. Draft for Public
Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
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TECHNICAL REPORT DATA
(Please read Instructions on reverse before completing)
1. REPORT NO. 2.
EPA-453/R-99.-007
4. TITLE AND SUBTITLE
National Air Toxics Program: The Integrated Urban Strategy
Report to Congress
7. AUTHOR(S)
9. PERFORMING ORGANIZATION NAME AND ADDRESS
U.S. Environmental Protection Agency
Office of Air Quality Planning and Standards
Research Triangle Park, NC 27711
12. SPONSORING AGENCY NAME AND ADDRESS
Director
Office of Air Quality Planning and Standards
Office of Air and Radiation
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
3. RECIPIENT'S ACCESSION NO.
5. REPORT DATE
2000
6. PERFORMING ORGANIZATION CODE
8. PERFORMING ORGANIZATION REPORT NO.
10. PROGRAM ELEMENT NO.
11. CONTRACT/GRANT NO.
13. TYPE OF REPORT AND PERIOD COVERED
14. SPONSORING AGENCY CODE
EPA/200/04
15. SUPPLEMENTARY NOTES
16. ABSTRACT
The report is the first one of two that are required by section 112(k) of the Clean Air Act. It summarizes
EPA's strategy to reduce risk to public health posed by the release of hazardous air pollutants from area
sources. The report contains information similar to that provided in the Federal Register notice titled
National Air Toxics Program: The Integrated Urban Strategy ("Strategy") that was published on July 19,
1999. However, this report contains more details on the information and assessments conducted to comple
the Strategy. Furthermore, the report summarizes existing information on risk assessments which have be(
conducted in various urban areas and provides a detailed description of 13 research needs to carry out the
goals of the Strategy.
17. KEY WORDS AND DOCUMENT ANALYSIS
a. DESCRIPTORS
Air Toxics
Hazardous Air Pollutants ,
18. DISTRIBUTION STATEMENT
Release Unlimited
b. IDENTIFIERS/OPEN ENDED TERMS
Air Pollution control
. * * a
19. SECURITY CLASS (Report) .-_.,.
Unclassified
20. SECURITY CLASS (Page)
Unclassified
c. COSATI Field/Group
21. NO OF PAGES
22. PRICE
EPA Form 2220-1 (Rer. 4-77) PREVIOUS EDITION IS OBSOLETE
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