National Primary Drinking Water Regulations; Arsenic and
Clarifications to Compliance and New Source Contaminants Monitoring
[Federal Register: June 22, 2000 (Volume 65, Number 121)]
[Proposed Rules]
[Page 38887-38983]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr22jn00-30]
[[Page 38887]]
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Part II
Environmental Protection Agency
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40 CFR Parts 141 and 142
National Primary Drinking Water Regulations; Arsenic and Clarifications
to Compliance and New Source Contaminants Monitoring; Proposed Rule
[[Page 38888]]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Parts 141 and 142
[WH-FRL-6707-2]
RIN 2040-AB75
National Primary Drinking Water Regulations; Arsenic and
Clarifications to Compliance and New Source Contaminants Monitoring
AGENCY: Environmental Protection Agency (EPA).
ACTION: Notice of proposed rulemaking.
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SUMMARY: The Environmental Protection Agency (EPA) is proposing a
drinking water regulation for arsenic, as required by the 1996
amendments to the Safe Drinking Water Act (SDWA). The proposed health-
based, non-enforceable goal, or Maximum Contaminant Level Goal (MCLG),
for arsenic is zero, and the proposed enforceable standard, or maximum
contaminant level (MCL), for arsenic is 0.005 mg/L. EPA is also
requesting comment on 0.003 mg/L, 0.010 mg/L and 0.020 mg/L for the
MCL. EPA is listing technologies that will meet the MCL, including
affordable compliance technologies for three categories of small
systems serving less than 10,000 people. This proposal also includes
monitoring, reporting, public notification, and consumer confidence
report requirements and State primacy revisions for public drinking
water programs affected by the arsenic regulation.
In addition, in this proposal the Agency is clarifying compliance
for State-determined monitoring after exceedances for inorganic,
volatile organic, and synthetic organic contaminants. Finally, EPA is
proposing that States will specify the time period and sampling
frequency for new public water systems and systems using a new source
of water to demonstrate compliance with the MCLs. The requirement for
new systems and new source monitoring will be effective for inorganic,
volatile organic, and synthetic organic contaminants.
DATES: EPA must receive public comments, in writing, on the proposed
regulations by September 20, 2000. EPA will hold a public meeting on
this proposed regulation this summer. EPA will publish a notice of the
meeting, providing date and location, in the Federal Register, as well
as post it on EPA's Office of Ground Water and Drinking Water web site
at http://www.epa.gov/safewater.
ADDRESSES: You may send written comments to the W-99-16 Arsenic
Comments Clerk, Water Docket (MC-4101); U.S. Environmental Protection
Agency; 1200 Pennsylvania Ave., NW, Washington, DC 20460. Comments may
be hand-delivered to the Water Docket, U.S. Environmental Protection
Agency; 401 M Street, SW; EB-57; Washington, DC 20460; (202) 260-3027
between 9 a.m. and 3:30 p.m. Eastern Time, Monday through Friday.
Comments may be submitted electronically to ow-docket@epamail.epa.gov.
See SUPPLEMENTARY INFORMATION for file formats and other information
about electronic filing and docket review. The proposed rule and
supporting documents, including public comments, are available for
review in the Water Docket at the above address.
FOR FURTHER INFORMATION CONTACT: Regulatory information: Irene Dooley,
(202) 260-9531, email: dooley.irene@epa.gov. Benefits: Dr. John B.
Bennett, (202) 260-0446, email: bennett.johnb@epa.gov General
information about the regulation: Safe Drinking Water Hotline, phone:
(800) 426-4791, or (703) 285-1093, email: hotline.sdwa@epa.gov.
SUPPLEMENTARY INFORMATION:
Regulated Entities
A public water system, as defined in 40 CFR 141.2, provides water
to the public for human consumption through pipes or other constructed
conveyances, if such system has ``at least fifteen service connections
or regularly serves an average of at least twenty-five individuals
daily at least 60 days out of the year.'' A public water system is
either a community water system (CWS) or a non-community water system
(NCWS). A community water system, as defined in Sec. 141.2, is ``a
public water system which serves at least fifteen service connections
used by year-round residents or regularly serves at least twenty-five
year-round residents.'' The definition in Sec. 141.2 for a non-
transient, non-community water system [NTNCWS] is ``a public water
system that is not a [CWS] and that regularly serves at least 25 of the
same persons over 6 months per year.'' EPA has an inventory totaling
over 54,000 community water systems and approximately 20,000 non-
transient, non-community water systems nationwide. Entities potentially
regulated by this action are community water systems and non-transient,
non-community water systems. The following table provides examples of
the regulated entities under this rule.
Table of Regulated Entities
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Examples of potentially regulated
Category entities
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Industry..................... Privately owned/operated community water
supply systems using ground water or
mixed ground water and surface water.
State, Tribal, and Local State, Tribal, or local government-owned/
Government. operated water supply systems using
ground water or mixed ground water and
surface water.
Federal Government........... Federally owned/operated community water
supply systems using ground water or
mixed ground water and surface water.
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The table is not intended to be exhaustive, but rather provides a
guide for readers regarding entities likely to be regulated by this
action. This table lists the types of entities that EPA is now aware
could potentially be regulated by this action. Other types of entities
not listed in this table could also be regulated. To determine whether
your facility is regulated by this action, you should carefully examine
the applicability criteria in Secs. 141.11 and 141.62 of the rule. If
you have any questions regarding the applicability of this action to a
particular entity, consult Irene Dooley, the regulatory information
person listed in the FOR FURTHER INFORMATION CONTACT section.
Additional Information for Commenters
Please submit an original and three copies of your comments and
enclosures (including references). To ensure that EPA can read,
understand, and therefore properly respond to comments, the Agency
would prefer that comments cite, where possible, the paragraph(s) or
sections in the notice or supporting documents to which each comment
refers. Commenters should use a separate paragraph for each issue
discussed. Electronic comments must be submitted as a WordPerfect 5.1,
WP6.1
[[Page 38889]]
or WP8 file or as an ASCII file avoiding the use of special characters.
Comments and data will also be accepted on disks in WP5.1, WP6.1 or
WP8, or ASCII file format. Electronic comments on this Notice may be
filed online at many Federal Depository Libraries. Commenters who want
EPA to acknowledge receipt of their comments should include a self-
addressed, stamped envelope. No facsimiles (faxes) will be accepted.
Availability of Docket
The docket for this rulemaking has been established under number W-
99-16, and includes supporting documentation as well as printed, paper
versions of electronic comments. The docket is available for inspection
from 9 a.m. to 4 p.m., Monday through Friday, excluding legal holidays,
at the Water Docket; EB 57; U.S. EPA; 401 M Street, SW; Washington,
D.C. For access to docket materials, please call (202) 260-3027 to
schedule an appointment.
Abbreviations Used in This Proposed Rule
>--greater than
³--greater than or equal to
--less than
£--less than or equal to
Sec. --Section
ACWA--Association of California Water Agencies
AA--activated alumina
As (III)--trivalent arsenic. Common inorganic form in water is arsenite
As (V)--pentavalent arsenic. Common inorganic form in water is arsenate
ATSDR--Agency for Toxic Substances and Disease Registry, U.S.
Department of Health & Human Services
ASTM--American Society for Testing and Materials
ASV--anodic stripping voltammetry
AWQC--Ambient Water Quality Criterion
AWWA--American Water Works Association
BAT--best available technology
BFD--Blackfoot disease
BOD--biochemical oxygen demand
BOSC--Board of Scientific Counselors, ORD
CASRN--Chemical Abstracts Service registration number
CCA--chromated copper arsenate
CCR--consumer confidence report
CDC--Centers for Disease Control and Prevention
CFR--Code of Federal Regulations
CPI--Consumer Price Index
CSFII--Continuing Survey of Food Intakes by Individuals
CV--coefficient of variation=standard deviation divided by the mean x
100
CWS--community water system
CWSS--Community Water System Survey
DBPs--disinfection byproducts
DBPR--Disinfectants/Disinfection By-products Rule
DMA--Di-methyl arsinic acid, cacodylic acid,
(CH3)2HAsO2
DSMA--Disodium methanearsonate
DWSRF--Drinking Water State Revolving Fund
DNA--Deoxyribonucleic acid
EB--East Tower Basement
EDL--Estimated Detection Limit
EDR--Electrodialysis Reversal
e.g.--such as
EJ--Environmental Justice
EO--Executive Order
EPA--U.S. Environmental Protection Agency
FDA--Food and Drug Administration
FR--Federal Register
FTE--full-time equivalents (employees)
GDP--Gross Domestic Product
GFAA--Graphite Furnace Atomic Absorption
GHAA--Gaseous Hydride Atomic Absorption
GI--gastrointestinal
gw--ground water
HRRCA--Health Risk Reduction and Cost Analysis
IARC--International Agency for Research on Cancer
ICP-MS--Inductively Coupled Plasma Mass Spectroscopy
i.e.--that is
ICP-AES--Inductively Coupled Plasma-Atomic Emission Spectroscopy
IESWTR--Interim Enhanced Surface Water Treatment Rule
IOCs--inorganic contaminants
IRFA--Initial Regulatory Flexibility Analysis
IRIS--Integrated Risk Information System
IX--Ion exchange
K--thousands
kg--kilogram, which is one thousand grams
L--Liter, also referred to as lower case ``l'' in older citations
LC50--The concentration of a chemical in air or water which
is expected to cause death in 50% of test animals living in that air or
water
LCP--laboratory certification program
LD50--The dose of a chemical taken by mouth or absorbed by
the skin which is expected to cause death in 50% of the test animals so
treated
LOAEL--Lowest-observed-adverse-effect level
LS--lime softening
LT2ESWTR--Long-Term 2 Enhanced Surface Water Treatment Rule
M--millions
m3--Cubic meters
MCL--maximum contaminant level
MCLG--maximum contaminant level goal
MDL--method detection limit
Metro--Metropolitan Water District of Southern California
mg--Milligrams--one thousandth of gram, 1 milligram = 1,000 micrograms
mg/kg--milligrams per kilogram
mg/m3--Milligrams per cubic meter
microgram (µg)--One-millionth of gram (3.5 x 10-8
oz., 0.000000035 oz.)
µg/L--micrograms per liter
M/DBP--Microbial/Disinfection By-product
MMA--Mono-methyl arsenic, arsonic acid,
CH3H2AsO3
MOS--margin of safety
MSMA--Monosodium methanearsonate
NAOS--National Arsenic Occurrence Survey
NAS--National Academy of Sciences
NAWQA--National Ambient Water Quality Assessment, USGS
NCI--National Cancer Institute
NCWS--non-community water system
NDWAC--National Drinking Water Advisory Council
NELAC--National Environmental Laboratory Accreditation Council
NIRS--National Inorganic and Radionuclide Survey
NIST--National Institute of Standards and Technology
NOAEL--No-observed-adverse-effect level
NODA--notice of data availability
NOEL--No-observed-effect level
NPDWR--National Primary Drinking Water Regulation, OGWDW
NRC--National Research Council, the operating arm of NAS
NTNCWS--non-transient non-community water system
NTTAA--National Technology Transfer and Advancement Act of 1995
NWIS--National Water Information System
O&M--operational and maintenance
OGWDW--Office of Ground Water and Drinking Water
PBMS--Performance-Based Measurement System
PE--performance evaluation, studies to certify laboratories for EPA
drinking water testing
P.L.--Public Law
PNR--Public notification rule
POD--point of departure
POE--Point-of-entry treatment devices
POU--Point-of-use treatment devices
ppb--Parts per billion. Also, µg/L or micrograms per liter
ppm--Parts per million. Also, mg/L or milligrams per liter
PQL--Practical quantitation level
PRA--Paperwork Reduction Act
PT--performance testing
PWS--Public water systems
PWSS--Public Water Systems Supervision
RCRA--Resource Conservation and Recovery Act
[[Page 38890]]
REFs--relative exposure factors
RFA--Regulatory Flexibility Act
RfD--Reference dose
RIA--Regulatory Impact Analysis
RMCL--Recommended Maximum Contaminant Level
RO--reverse osmosis
RWS--Rural Water Survey
SAB--Science Advisory Board
SBA--Small Business Administration
SBREFA--Small Business Regulatory and Enforcement Flexibility Act, SBA
SDWA--Safe Drinking Water Act of 1974, as amended
SDWIS--Safe Drinking Water Information System
SER--Small Entity Representative for SBREFA
SISNOSE--Substantial impact on a significant number of small entities,
SBREFA
SM--Standard Methods for the Examination of Water and Wastewater
SMRs--Standardized mortality ratios, comparing deaths in test areas to
deaths in unexposed areas
SSCTs--Small System Compliance Technologies
STP-GFAA--Stabilized Temperature Platform Graphite Furnace Atomic
Absorption
SW--Office of Solid Waste publication or test method
SW-846--Solid Waste publication #846, Test Methods for Solid and
Hazardous Waste
TC--toxicity characteristic
TDS--total dissolved solids
TNC--transient, non-community
TOC--total organic carbon
µg--Microgram, 1000 micrograms = 1 milligram
UMRA--Unfunded Mandates Reform Act
U.S.--United States
USDA--U.S. Department of Agriculture
USGS--U.S. Geological Survey
USPHS--U.S. Public Health Service
VSL--Value of Statistical Life
WESTCAS--Western Coalition of Arid States
WHO--World Health Organization
WITAF--Water Industry Technical Action Fund
WS--water supply
WTP--Willingness to pay
Table of Contents
I. Summary of Regulation
II. Background
A. What is the Statutory Authority for the Arsenic Drinking
Water Regulation?
B. What is arsenic?
C. What are the sources of arsenic exposure?
1. Natural Sources of Arsenic
2. Industrial Sources of Arsenic
3. Dietary Sources
4. Environmental Sources
D. What is the regulatory history for arsenic?
1. Earliest U.S. Arsenic Drinking Water Standards
2. EPA's 1980 Guidelines
3. Research and Regulatory Work
E. EPA's Arsenic Research Plan
III. Toxic Forms and Health Effects of Arsenic
A. What are the toxic forms of arsenic?
B. What are the effects of acute toxicity?
C. What cancers are associated with arsenic?
1. Skin Cancer
2. Internal Cancers
D. What non-cancer effects are associated with arsenic?
E. What are the recent developments in health effects research?
1. Funding of Health Effects Research
2. Expert Panel on Arsenic Carcinogenicity
3. NAS Review of EPA's Risk Assessment
4. May 1999 Utah Mortality Study
5. 1999 Review of health effects
6. Study of Bladder and Kidney Cancer in Finland
F. What did the National Academy of Sciences/National Research
Council report?
1. The National Research Council and its Charge
2. Exposure
3. Essentiality
4. Metabolism and Disposition
5. Human Health Effects and Variations in Sensitivity
6. Modes of Action
7. Risk Considerations
8. Risk Characterization
IV. Setting the MCLG
A. How did EPA approach it?
B. What is the MCLG?
C. How will a health advisory protect potentially sensitive
subpopulations?
D. How will the Clean Water Act criterion be affected by this
regulation?
V. EPA's Estimates of Arsenic Occurrence
A. What data did EPA evaluate?
B. What databases did EPA use?
C. How did EPA estimate national occurrence of arsenic in
drinking water?
D. What are the national occurrence estimates of arsenic in
drinking water for community water systems?
E. How do EPA's estimates compare with other recent national
occurrence estimates?
F. What are the national occurrence estimates of arsenic in
drinking water for non-transient, non-community water systems?
G. How do arsenic levels vary from source to source and over
time?
H. How did EPA evaluate co-occurrence?
1. Data
2. Results of the Co-occurrence Analysis (US EPA, 1999f)
VI. Analytical Methods
A. What section of SDWA requires the Agency to specify
analytical methods?
B. What factors does the Agency consider in approving analytical
methods?
C. What analytical methods and method updates are currently
approved for the analysis of arsenic in drinking water?
D. Will any of the approved methods for arsenic analysis be
withdrawn?
E. Will EPA propose any new analytical methods for arsenic
analysis?
F. Other Method-Related Items
1. The Use of Ultrasonic Nebulization with ICP-MS
2. Performance-Based Measurement System
G. What are the estimated costs of analysis?
H. What is the practical quantitation limit?
1. PQL determination
2. PQL for arsenic
I. What are the sample collection, handling and preservation
requirements for arsenic?
J. Laboratory Certification
1. Background
2. What Are the Performance Testing criteria for arsenic?
3. How often is a laboratory required to demonstrate acceptable
PT performance?
4. Externalization of the PT Program (formerly known as the PE
Program)
VII. Monitoring and Reporting Requirements
A. What are the existing monitoring and compliance requirements?
B. How does the Agency plan to revise the monitoring
requirements?
C. Can States grant monitoring waivers?
D. How can I determine if I have an MCL violation?
E. When will systems have to complete initial monitoring?
F. Can I use grandfathered data to satisfy the initial
monitoring requirement?
G. What are the monitoring requirements for new systems and
sources?
H. How does the Consumer Confidence Report change?
I. How will public notification change?
VIII. Treatment Technologies
A. What are the Best Available Technologies (BATs) for arsenic?
What are the issues associated with these technologies?
B. What are the likely treatment trains? How much will they
cost?
C. How are variance and compliance technologies identified for
small systems?
D. When are exemptions available?
E. What are the small systems compliance technologies?
F. How does the Arsenic Regulation overlap with other
regulations?
IX. Costs
A. Why does EPA analyze the regulatory burden?
B. How did EPA prepare the baseline study?
1. Use of baseline data
2. Key data sources used in the baseline analysis for the RIA?
C. How were very large system cost derived?
D. How did EPA develop cost estimates?
E. What are the national treatment costs of different MCL
options?
1. Assumptions affecting the development of the decision tree
2. Assumptions affecting unit cost curves
X. Benefits of Arsenic Reduction
A. Monetized Benefits of Avoiding Bladder Cancer
1. Risk reductions: The Analytic Approach
2. Water Consumption
3. Monte Carlo Analysis
4. Relative Exposure Factors
5. NRC Risk Distributions
[[Page 38891]]
6. Estimated Risk Reductions
B. ``What if?'' scenario for lung cancer risks
C. Evaluation of Benefits
1. Fatal Risks and Value of a Statistical Life (VSL)
2. Nonfatal Risks and Willingness to Pay (WTP)
D. Estimates of Quantifiable Benefits of Arsenic Reduction
F. NDWAC Working Group (NDWAC, 1988) on Benefits
XI. Risk Management Decisions: MCL and NTNCWSs
A. What is the Proposed MCL?
1. Feasible MCL
2. Principal Considerations in Analysis of MCL Options
3. Findings of NRC and Consideration of Risk Levels
4. Non-monetized Health Effects
5. Sources of Uncertainty
6. Comparison of Benefits and Costs
7. Conclusion and Request for Comment
B. Why is EPA proposing a total arsenic MCL?
C. Why is EPA proposing to require only monitoring and
notification for NTNCWSs?
1. Methodology for analyzing NTNCWS risks
2. Results
XII. State Programs
A. How does arsenic affect a State's primacy program?
B. When does a State have to apply?
C. How are Tribes affected?
XIII. HRRCA
A. What are the requirements for the HRRCA?
B. What are the quantifiable and non-quantifiable health risk
reduction benefits?
C. What are the Quantifiable and Non-Quantifiable Costs?
D. What are the Incremental Benefits and Costs?
E. What are the Risks of Arsenic Exposure to the General
Population and Sensitive Subpopulations?
F. What are the Risks Associated with Co-Occurring Contaminants?
G. What are the Uncertainties in the Analysis?
XIV. Administrative Requirements
A. Executive Order 12866: Regulatory Planning and Review
B. Regulatory Flexibility Act (RFA), as amended by the Small
Business Regulatory Enforcement Fairness Act of 1996 (SBREFA), 5
U.S.C. 601 et seq.
1. Overview
2. Use of Alternative Small Entity Definition
3. Initial Regulatory Flexibility Analysis
a. Number of Small Entities Affected
b. Reporting, Recordkeeping and Other Requirements for Small
Systems
4. Small Business Advocacy Review (SBAR) Panel Recommendations
C. Unfunded Mandates Reform Act (UMRA)
1. Summary of UMRA Requirements
a. Authorizing legislation
b. Cost-benefit analysis
c. Financial Assistance
d. Estimates of future compliance costs and disproportionate
budgetary effects
e. Macroeconomic effects
f. Summary of EPA's consultation with State, local, and tribal
governments and their concerns
g. Nature of State, local, and Tribal government concerns and
how EPA addressed these concerns
h. Regulatory Alternatives Considered
2. Impacts on Small Governments
D. Paperwork Reduction Act (PRA)
E. National Technology Transfer and Advancement Act (NTTAA)
F. Executive Order 12898: Environmental Justice
G. Executive Order 13045: Protection of Children from
Environmental Health Risks and Safety Risks
H. Executive Order 13132: Federalism
I. Executive Order 13084: Consultation and Coordination with
Indian Tribal Governments
J. Request for Comments on Use of Plain Language
XV. References
List of Tables
Table V-1. Summary of Arsenic Data Sources
Table V-2. Regional Exceedance Probability Distribution Estimates
Table V-3. Statistical Estimates of Number of Ground Water CWSs with
Average Arsenic Concentrations in Specified Ranges
Table V-4. Statistical Estimates of Number of Surface Water CWSs
with Average Arsenic Concentrations in Specified Ranges
Table V-5. Comparison of CWSs from EPA, NAOS, and USGS Estimates
Exceeding Arsenic Concentrations
Table V-6. Statistical Estimates of Number of Ground Water NTNCWSs
with Average Arsenic Concentrations in Specified Ranges
Table V-7. Statistical Estimates of Number of Surface Water NTNCWSs
with Average Arsenic Concentrations in Specified Ranges
Table V-8. Correlation of Arsenic with Sulfate and Iron (surface and
ground waters)
Table V-9. Correlation of Arsenic with Radon (ground water)
Table VI-1. Approved Analytical Methods (and Method Updates) for
Arsenic (CFR 141.23)
Table VI-2. Estimated Costs for the Analysis of Arsenic in Drinking
Water
Table VI-3. Acceptance Limits and PQLs for Other Metals (in order of
decreasing PQL)
Table VII-1. Comparison of Sampling, Monitoring, and Reporting
Requirements
Table VII-2. Treatment in-place at small water systems (US EPA,
1999e and US EPA, 1999m)
Table VII-3. Table Identifying Regulatory Changes
Table VII-4. Table Listing Deleted Sections
Table VIII-1. Best Available Technologies and Removal Rates
Table VIII-2. Treatment Technology Trains
Table VIII-3. Annual Costs of Treatment Trains (Per household)
Table VIII-4. Affordable Compliance Technology Trains for Small
Systems
Table VIII-5. Affordable Compliance Technology Trains for Small
Systems
Table IX-1. Summary of General Baseline Categories of Affected
Entities
Table IX-2. List of Large Water Systems that Serve More Than 1
Million People
Table IX-3. Total Annual Costs for Large Systems for (serving more
than 1 million people)
Table IX-4. Systems Needing to Add Pre-Oxidation
Table IX-5. Percent of Systems with Coagulation-Filtration and Lime-
Softening in Place
Table IX-6. Waste Disposal Options
Table IX-7. Ground Water: Arsenic and Sulfate
Table IX-8. Surface Water: Arsenic and Sulfate
Table IX-9. Ground Water: Arsenic and Iron
Table IX-10. Surface Water: Arsenic and Iron
Table IX-11. National Annual Treatment Costs (Dollars in Millions)
Table IX-12. Total Annual Costs per Household (Dollars)
Table IX-13. Incremental National Annual Costs (Dollars in Millions)
Table IX-14. Incremental Annual Costs per Household (Dollars)
Table X-1. Source of Water Consumed
Table X-2a. Bladder Cancer Incidence Risks \1\ for High Percentile
U.S. Populations Exposed At or Above MCL Options, After Treatment
\2\ (Community Water Consumption Data \3\)
Table X-2b. Bladder Cancer Incidence Risks1 for High Percentile U.S.
Populations Exposed At or Above MCL Options, After Treatment \2\
(Total Water Consumption Data \3\)
Table X-3a. Percent of Exposed Population At 10\-4\ Risk or Higher
for Bladder Cancer Incidence\1\ After Treatment \2\ (Community Water
Consumption Data \3\)
Table X-3b. Percent of Exposed Population At 10\-4\ Risk or Higher
for Bladder Cancer Incidence\1\ After Treatment \2\ (Total Water
Consumption Data \3\)
Table X-4a. Mean Bladder Cancer Incidence Risks \1\ for U.S.
Populations Exposed At or Above MCL Options, after Treatment \2\
(Community Water Consumption Data \3\)
Table X-4b. Mean Bladder Cancer Incidence Risks \1\ for U.S.
Populations Exposed At or Above MCL Options, after Treatment \2\
(Total Water Consumption Data \3\)
Table X-5. Lifetime Avoided Medical Costs For Survivors (preliminary
estimates, 1996 dollars \1\)
Table X-6. Mean Bladder Cancer Incidence Risks \1\ for U.S.
Populations Exposed At or Above MCL Options, after Treatment \2\
(Composite of Tables X-5a and X-5b)
Table X-7. Estimated Costs and Benefits from Reducing Arsenic in
Drinking Water ($millions, 1999)
Table XI-1. Estimated Costs and Benefits from Reducing Arsenic in
Drinking Water (In 1999 $ millions)
Table XI-2. Exposure Factors Used in the NTNC Risk Assessment
Table XI-3. Composition of Non-Transient, Non-Community Water
Systems (Percentage of Total NTNC Population Served by Sector)
[[Page 38892]]
Table XI-4. Upper Bound School Children Risk Associated with Current
Arsenic Exposure in NTNC Water Systems
Table XI-5. Non-Transient Non-Community Benefit Cost Analysis
Table XI-6. Sensitive Group Evaluation Lifetime Risks
Table XIII-1. Risk Reduction from Reducing Arsenic in Drinking Water
Table XIII-2. Mean Bladder Cancer Risks and Exposed Population
Table XIII-3. Estimated Costs and Benefits from Reducing Arsenic in
Drinking Water (in 1999 $ millions)
Table XIII-4. Estimated Annualized National Costs of Reducing
Arsenic Exposures (in 1999 $ millions)
Table XIII-5. Estimated Annual Costs per Household \1\ (in 1999 $)
Table XIII-6. Summary of the Total Annual National Costs of
Compliance with the Proposed Arsenic Rule Across MCL Options (in
1997 $ millions)
Table XIII-7. Estimates of the Annual Incremental Risk Reduction,
Benefits, and Costs of Reducing Arsenic in Drinking Water
($millions, 1999)
Table XIV-1. Profile of the Universe of Small Water Systems
Regulated Under the Arsenic Rule
Table XIV-2. Average Annual Cost per CWS by Ownership
Table XIV-3. Average Compliance Costs per Household for CWSs
Exceeding MCLs
Table XIV-4. Average Compliance Costs per Household for CWSs
Exceeding MCLs as a Percent of Median Household Income
Table XIV-5. Hour Burden per Activity for Public Water Systems
Table XIV-6. Hour Burden per Activity for States and Tribes
I. Summary of Regulation
EPA is proposing an arsenic regulation for community water systems,
which are systems that provide piped water to at least fifteen service
connections used by year-round residents or regularly serves at least
twenty-five year-round residents. This proposal will require non-
transient, non-community water systems (NTNCWS) to monitor for arsenic
and report exceedances of the MCL. The proposed health-based, non-
enforceable goal, or Maximum Contaminant Level Goal (MCLG), is zero,
based on EPA's revised risk characterization.
EPA evaluated the analytical capability and laboratory capacity,
likelihood of water systems choosing treatment technologies for several
sizes of systems based on source water properties, and the national
occurrence of arsenic in water supplies to determine the proposed
Maximum Contaminant Level (MCL). Furthermore, the Agency analyzed the
quantifiable and nonquantifiable costs and health risk reduction
benefits likely to occur at the treatment levels considered, and the
effects on sensitive subpopulations. Based on the determination that
the costs for the feasible MCL do not justify the benefits, EPA is
proposing an MCL of 0.005 mg/L and requesting comment on 0.003 mg/L,
0.010 mg/L, and 0.020 mg/L. The treatment technologies for large
systems are primarily coagulation/filtration and lime softening, while
EPA expects that small systems (serving less than 10,000 people) will
be able to use ion exchange, activated alumina, reverse osmosis,
nanofiltration, and electrodialysis reversal. The effective date will
be five years after the final rule comes out for community water
systems serving 10,000 people or less, and three years after
promulgation for all other community water systems. EPA is proposing
that States applying to adopt the revised arsenic MCL may use their
most recently approved monitoring and waiver plans or note in their
primacy application any revisions to those plans.
The Agency is clarifying the procedure used for determining
compliance after exceedances for inorganic, volatile organic, and
synthetic organic contaminants in this proposal. Finally, EPA is
proposing in this proposal that States will specify the time frame
which new systems and systems using a new source of water have to
demonstrate compliance with the MCL's including initial sampling
frequencies and compliance periods for new systems and systems that use
a new source of water for inorganic, volatile organic, and synthetic
organic contaminants.
II. Background
A. What Is the Statutory Authority for the Arsenic Drinking Water
Regulation?
Section 1401 of the Safe Drinking Water Act (SDWA) requires a
``primary drinking water regulation'' to specify a maximum contaminant
level (MCL) if it is economically and technically feasible to measure
the contaminant and include testing procedures to insure compliance
with the MCL and proper operation and maintenance. In addition, section
1401(1)(D)(i) requires EPA to establish the minimum quality of
untreated, or raw, water taken into a public water system. A national
primary drinking water regulation (NPDWR) that establishes an MCL also
lists the technologies that are feasible to meet the MCL, but systems
are not required to use the listed technologies (section
1412(b)(3)(E)(i)). As a result of the 1996 amendments to SDWA, when
issuing a NPDWR, EPA will also list affordable technologies for small
systems serving 10,000 to 3301, 3300 to 501, and 500 to 25 that achieve
compliance with the MCL or treatment technique. EPA can list modular
(packaged) and point-of-entry and point-of-use treatment units for the
three small system sizes, as long as the units are maintained by the
public water system or its contractors. Home units must contain
mechanical warnings to notify customers of problems (section
1412(b)(4)(E)(ii)). In section 1412(b)(12)(A) of SDWA, as amended
August 6, 1996, Congress directed EPA to propose a national primary
drinking water regulation for arsenic by January 1, 2000 and issue the
final regulation by January 1, 2001. At the same time, Congress
directed EPA to develop a research plan by February 2, 1997 to reduce
the uncertainty in assessing health risks from low levels of arsenic
and conduct the research in consultation with the National Academy of
Sciences, other Federal agencies, and interested public and private
entities. The amendments allowed EPA to enter into cooperative
agreements for research.
Section 1412(a)(3) requires EPA to propose a maximum contaminant
level goal (MCLG) simultaneously with the national primary drinking
water regulation. The MCLG is defined in section1412(b)(4)(A) as ``the
level at which no known or anticipated adverse effects on the health of
persons occur and which allows an adequate margin of safety.'' Section
1412(b)(4)(B) specifies that each national primary drinking water
regulation will specify a maximum contaminant level (MCL) as close to
the MCLG as is feasible, with two exceptions added in the 1996
amendments. First, the Administrator may establish an MCL at a level
other than the feasible level if the treatment to meet the feasible MCL
would increase the risk from other contaminants or the technology would
interfere with the treatment of other contaminants (section1412(b)(5)).
Second, if benefits at the feasible level would not justify the costs,
EPA may propose and promulgate an MCL ``that maximizes health risk
reduction benefits at a cost that is justified by the benefits (section
1412(b)(6)).''
When proposing an MCL, EPA must publish, and seek public comment
on, the health risk reduction and cost analyses (HRRCA) of each
alternative maximum contaminant level considered (section
1412(b)(3)(C)(i)). This includes the quantifiable and nonquantifiable
benefits from reductions in health risk, including those from removing
co-occurring contaminants (not counting benefits resulting from
compliance with other proposed or final regulations), costs of
compliance (not counting costs resulting from other regulations), any
increased health risks (including those from co-occurring contaminants)
that
[[Page 38893]]
may result from compliance, incremental costs and benefits of each
alternative MCL considered, and the effects on sensitive subpopulations
(e.g., infants, children, pregnant women, elderly, seriously ill, or
other groups at greater risk). EPA must analyze the quality and extent
of the information, the uncertainties in the analysis, and the degree
and nature of the risk.
The 1996 amendments also require EPA to base its action on the best
available, peer-reviewed science and supporting studies and to present
health effects information to the public in an understandable fashion.
To meet the latter obligation, EPA must specify, among other things,
the methodology used to reconcile inconsistencies in the scientific
data for the final regulation (section 1412(b)(3)(B)(v)).
Section 1451(a) allows EPA to delegate primary enforcement
responsibility to federally recognized Indian Tribes, providing grant
and contract assistance, using the procedures applied to States.
Section 1413(a)(1) allows EPA to grant States primary enforcement
responsibility for NPDWRs when EPA has determined that the State has
adopted regulations that are no less stringent than EPA's. States must
adopt comparable regulations within two years of EPA's promulgation of
the final rule, unless a two-year extension is justified. State primacy
also requires, among other things, adequate enforcement (including
monitoring and inspections) and reporting. EPA must approve or deny
State applications within 90 days of submission (section 1413(b)(2)).
In some cases, a State submitting revisions to adopt a national primary
drinking water regulation has enforcement authority for the new
regulation while EPA action on the revision is pending (section
1413(c)).
B. What Is Arsenic?
Arsenic is an element that occurs naturally in rocks, soil, water,
air, plants, and animals. Arsenic is a metalloid, which exhibits both
metallic and nonmetallic chemical and physical properties. The primary
valence states for arsenic are 0, -3, +3 and +5. Although arsenic is
found in nature to a small extent in its elemental form (0 valence), it
occurs most often as inorganic and organic compounds in either the As
(III) (+3) or As (V) (+5) valence states. The trivalent forms of
inorganic arsenic [As (III) (e.g., arsenite,
H3AsO3)] and the pentavalent forms [As (V) (e.g.,
arsenate, H2AsO4-,
HAsO42-)] are inorganic species which tend to be
more prevalent in water than the organic arsenic species (Irgolic,
1994; Clifford and Zhang, 1994). The dominant inorganic species present
in water is largely a function of the pH and the oxidizing/reducing
conditions which affects the need for pretreatment and removal effects.
Arsenates are more likely to occur in aerobic surface waters and
arsenites are more likely to occur in anaerobic ground waters.
C. What Are the Sources of Arsenic Exposure?
1. Natural Sources of Arsenic
There are numerous natural sources as well as human activities that
may introduce arsenic into food and drinking water. The primary natural
sources include geologic formations (e.g., rocks, soil, and sedimentary
deposits), geothermal activity, and volcanic activity. Arsenic and its
compounds comprise 1.5-2% of the earth's crust (Welch, personal
communication). While concentrations of arsenic in the earth's crust
vary, the average concentrations are generally reported to range from
1.5 to 5 mg/kg. Arsenic is a major constituent of many mineral species
in igneous and sedimentary rocks. It is commonly present in the sulfide
ores of metals including copper, lead, silver, and gold. There are over
100 arsenic-containing minerals, including arsenic pyrites (e.g.,
FeAsS), realgar (AsS), lollingite (FeAs2,
Fe2As3, Fe2As5), and
orpiment (As2S3). Geothermal water can be a
source of inorganic arsenic in surface water and ground water. Welch et
al. (1988) identified fourteen areas in the Western United States where
dissolved arsenic concentrations ranged from 80 to 15,000 µg/L.
In addition, natural emissions of arsenic are associated with forest
fires and grass fires. Volcanic activity appears to be the largest
natural source of arsenic emissions to the atmosphere (ATSDR, 1998).
Arsenic compounds, both inorganic and organic, are also found in food.
2. Industrial Sources of Arsenic
Major present and past sources of arsenic include wood
preservatives, agricultural uses, industrial uses, mining and smelting.
The human impact on arsenic levels in water depends on the level of
human activity, the distance from the pollution sources, and the
dispersion and fate of the arsenic that is released. The production of
chromated copper arsenate (CCA), an inorganic arsenic compound and wood
preservative, accounts for approximately 90% of the arsenic used
annually by industry in the United States (USGS, 1998; USGS, 1999). CCA
is used to pressure treat lumber, which is typically used for the
construction of decks, fences, and other outdoor applications. In
addition to wood preservatives, the other EPA-registered use of
inorganic arsenic is for sealed ant bait. In the past, agricultural
uses of arsenic included pesticides, herbicides, insecticides,
defoliants, and soil sterilants. Inorganic arsenic pesticides are no
longer used for agricultural purposes; the last agricultural
application was voluntarily canceled in 1993 (58 FR 64579, US EPA,
1993b).
Organic forms of arsenic are constituents of some agricultural
pesticides that are currently used in the U.S. Monosodium
methanearsonate (MSMA) is the most widely applied organoarsenical
pesticide, which is used to control broadleaf weeds and is applied to
cotton (Jordan et al., 1997). Small amounts of disodium methanearsonate
(DSMA, or cacodylic acid) are also applied to cotton fields as
herbicides. The Food and Drug Administration regulates other organic
arsenicals (e.g., roxarsone and arsanilic acid) used as feed additives
for poultry and swine for increased rate of weight gain, improved feed
efficiencies, improved pigmentation, and disease treatment and
prevention. These additives undergo little or no metabolism before
excretion (NAS, 1977; Moody and Williams, 1964; Aschbacher and Feil,
1991).
Arsenic and arsenic compounds (arsenicals) are used for a variety
of industrial purposes, including: electrophotography, catalysts,
pyrotechnics, antifouling paints, pharmaceutical substances, dye and
soaps, ceramics, alloys (automotive solder and radiators), battery
plates, optoelectronic devices, semiconductors, and light emitting
diodes in digital watches (Azcue and Nriagu, 1994). In addition,
burning of fossil fuels, combustion of wastes, mining and smelting,
pulp and paper production, glass manufacturing, and cement
manufacturing can result in emissions of arsenic to the environment (US
EPA, 1998). Arsenic has been identified as a contaminant of concern at
916 of the 1,467 National Priorities List (Superfund) hazardous waste
sites (ATSDR, 1998).
3. Dietary Sources
Because arsenic is naturally occurring, the entire population is
exposed to low levels of arsenic through food, water, air, and contact
with soil. The National Research Council report (NRC, 1999) described
in sections III.C. and III.E.3. provides Food and Drug Administration
(FDA) ``market basket'' data for total arsenic intake by age
[[Page 38894]]
group. NRC assumed that, for fish and seafood, inorganic arsenic is 10%
of the total arsenic and that other food contains entirely inorganic
arsenic. These assumptions are probably high and conservative for
public health protection to avoid underestimating the contributions
from food. Table 3-5 in the 1999 NRC report characterizes inorganic
arsenic intake from food in the U.S. as being 1.3 µg/day for
infants under one year old, 4.4 µg/day for 2-year olds, almost
10 µg/day for 25-30 year-old males, with a maximum of 12.5
µg/day for 60-65 year-old males (females had lower arsenic
intake in every age group). MacIntosh et al. (1997) estimated that 785
adults had a mean inorganic arsenic consumption of 10.22 µg/
day, with a standard deviation of 6.54 µg/day and a range of
0.36-123.84 µg/day based on semi-quantitative food surveys.
Likewise, the 2 L/day assumption of adult drinking water intake
used to develop the MCLG does not represent intake by the average
person; rather it represents intake of a person in the 90th percentile.
(See Section X.B.1.a. for a description of water consumption for the
general population.)
4. Environmental Sources
Internal exposure after skin contact with water or soil containing
arsenic or inhalation of arsenic from air is believed to be low.
Studies of inorganic arsenic absorption from skin from cadavers
estimated 0.8% uptake from soil and 1.9% uptake from water over a 24-
hour period (Wester et al., 1993). EPA's arsenic health assessment
document for the Clean Air Act (US EPA, 1984) cited respiratory arsenic
as being about 0.12 µg/day from a daily ventilation rate of 20
m\3\ using a 1981 national average arsenic air concentration of 0.006
µg/m\3\. Assuming 30 percent absorption, the daily amount of
arsenic from breathing would be 0.03 µg, so air is a minor
source of arsenic (50 FR 46936 at 46960; US EPA, 1985b). At this time,
EPA is basing health risks on estimates of arsenic exposure from food
and water. The Centers for Disease Control and Prevention (CDC) is
initiating a study of arsenic intake from bathing. EPA requests comment
on whether available data on skin absorption and inhalation indicate
that these are significant exposure routes that should be considered in
the risk assessment.
D. What is the Regulatory History for Arsenic?
Regulation of arsenic has been the subject of scientific debate
that has lasted for decades despite research and scientific review. The
controversy has affected policy and regulatory decisions for arsenic in
drinking water from low, environmental exposure.
1. Earliest U.S. Arsenic Drinking Water Standards
In 1942 the U.S. Public Health Service first established an arsenic
drinking water standard for interstate water carriers at 0.05 mg
arsenic per liter (mg/L, or 50 µg/L), as measured with a
colorimetric method. The report did not cite any reason for choosing
that level, but it defined ``safety of water supplies'' as ``the
danger, if any, is so small that it cannot be discovered by available
means of observation (US Public Health Service 1943).'' In 1946, the
Surgeon General of the U.S. Public Health Service noted that the
American Water Works Association had accepted the 1942 drinking water
standards, including the arsenic standard (U.S. Public Health Service
1946). In 1962 (U.S. Public Health Service 1962) the U.S. Public Health
Service issued more stringent drinking water standards for arsenic of
0.01 mg/L (10 µg/L) for a water supply in 42 CFR 72.205(b)(1)
and 0.05 mg/L in 42 CFR 72.205(b)(2) as grounds for rejection of a
water supply, as measured by the current edition of Standard Methods
for the Examination of Water and Wastewater per 42 CFR 72.207(a).
The Safe Drinking Water Act of 1974 amended the Public Health
Service Act and specified that EPA set primary and secondary drinking
water standards. On December 24, 1975 (40 FR 59566 at 59570; US EPA,
1975), EPA issued a National Interim Primary Drinking Water Regulation
for arsenic in Sec. 141.23(b) of 0.05 mg/L (50 µg/L), effective
18 months later (Sec. 141.6). Commenters recommended an MCL of 100
µg/L, saying there were no observed adverse health effects (40
FR 59566 at 59576; US EPA, 1975). EPA noted long-term chronic effects
at 300-2,750 µg/L, but observed no illnesses in a California
study at 120 µg/L. Drinking 2 liters of water a day containing
arsenic at 50 µg/L would provide approximately 10% of total
ingested arsenic from food and water, estimated to be 900 µg/
day. The section on arsenic noted that arsenic has been believed to be
a carcinogen ``[s]ince the early nineteenth century * *; however
evidence from animal experiments and human experience has accumulated
to strongly suggest that arsenicals do not produce cancer. One
exception is a report from Taiwan * * *. The text goes on to note
occupational skin and lung cancer from arsenic dust and skin cancer in
England from drinking water with 12 mg/L. (US EPA, 1976 Appendix A).
2. EPA's 1980 Guidelines
Scientific data at the time the 1980 Ambient Water Quality
Guidelines were formulated did not support a safe or ``threshold''
concentration for carcinogens, so EPA's public health policy was
``that the recommended concentration for maximum protection of human
health is zero. In addition, the Agency presented a range of
concentrations corresponding to incremental cancer risks of 10-\7\
to 10-\5\ (one additional case of cancer in populations ranging from
ten million to 100,000, respectively) * * * [that did not
necessarily represent] an Agency judgement on an `acceptable' risk
level (45 FR 79318 at 79323, US EPA, 1980).''
In the November 28, 1980 Federal Register document, using its then
current risk assessment approach (assumed toxicity increased as a
natural logarithm linear function across species), EPA set the Clean
Water Act surface water quality criterion for arsenic at 2.2 nanograms
(ng/L) (0.0022 µg/L) at an increased cancer risk of 10-\6\. The
criterion was to prevent skin cancer in humans drinking contaminated
water and eating aquatic organisms from those water bodies (45 FR 79318
at 79326). The 1980 Federal Register notice indicated that drinking
water standards consider a range of factors, including health effects,
technological and economic feasibility of removal, and monitoring
capability. On the other hand the Clean Water Act criteria of section
304(a)(1) ``have no regulatory significance under the SDWA.'' The Clean
Water Act section 304(a)(1) criteria are more similar to the health-
based goals of the recommended maximum contaminant levels (now referred
to as MCLGs), than to MCLs; and differences in mandates ``may result in
differences between the two numbers.'' (45 FR 79318 at 79320; US EPA,
1980). In 1992, the Clean Water Act criterion was recalculated based on
the updated cancer risk assessment in EPA's Integrated Risk Information
System (IRIS) database, to a level of 0.018 µg/L for arsenic at
a 10-\6\ cancer risk (57 FR 60848; US EPA, 1992c).
3. Research and Regulatory Work
The 1980 National Academy of Science (NAS) Volume III of ``Drinking
Water and Health'' report encouraged EPA to research whether arsenic is
essential for humans, as demonstrated in four studies of mammalian
species. The 1983 NAS Volume V report projected that 0.05 mg/kg of
total arsenic may be a desirable level for people, and 25 to 50
µg a day may be required (as cited in 50 FR 46936 at 46960; US
EPA, 1985b).
[[Page 38895]]
In 1983, EPA requested comment on whether the arsenic MCL should
consider carcinogenicity, other health effects, and nutritional
requirements, and whether MCLs are necessary for separate valence
states (e.g., arsenite vs. arsenate) (48 FR 45502 at 45512; US EPA,
1983). On November 13, 1985, EPA proposed (50 FR 46936; US EPA, 1985b)
a recommended maximum contaminant level (RMCL), a non-enforceable
health goal now known as an MCLG, of 50 µg/L based on the 1983
NAS conclusion that 50 µg/L balanced toxicity and possible
essentiality and provided ``a sufficient margin of safety'' (50 FR
46936 at 46960). EPA also requested comment on alternate RMCLs of 100
µg/L based on noncarcinogenic effects (calculated from an
animal study and an uncertainty factor of 1000) and 0 µg/L
based on carcinogenicity (50 FR 46936 at 46961). EPA chose not to base
the proposed RMCL on the animal study because each dose group had only
four Rhesus monkeys. Also, at that time, studies had ``not detected
increased risks via drinking water in the USA'' (50 FR 46936 at 46960).
The 1985 proposed drinking water regulation preamble noted the 1980
excess cancer risk values derived from the ambient water quality
criteria were based on skin cancer using the 1968 Tseng et al. study
(50 FR 46936 at 46961).
The June 19, 1986 amendments to the Safe Drinking Water Act (SDWA;
Public Law 99-339) converted the 1975 interim arsenic standard to a
National Primary Drinking Water Regulation (section 1412(a)(1)),
subject to revision by 1989 (section 1412(b)(1)). Review of the arsenic
risk assessment issues caused the Agency to miss the 1989 deadline for
proposing a revised NPDWR. As a result of a citizen suit to enforce the
deadline, EPA entered into a consent decree providing deadlines for
issuing the arsenic rule.
In 1988, EPA's Risk Assessment Forum issued the Special Report on
Ingested Inorganic Arsenic: Skin Cancer; Nutritional Essentiality (EPA/
625/3-87/013), in part, to evaluate the validity of applying skin
cancer data from Taiwanese studies (published in 1968 and 1977) in
dose-response assessments in the U.S. As described in the report, the
maximum likelihood estimate of risk ranged from 3 x 10-\5\ to 7 x
10-\5\ for a 70-kilogram person consuming 2 liters of water per day
contaminated with 1 µg of arsenic per liter. Calculated at the
50 µg/L standard, the U.S. lifetime risk of skin cancer ranged
from 1 x 10-\3\ to 3 x 10-\3\, which means one to three skin
cancers would occur in a group of one thousand people drinking water
containing arsenic at 50 µg/L. Existing studies could not
determine whether arsenic was an essential nutrient.
After reviewing the scientific evidence for carcinogenicity, EPA's
Science Advisory Board (US EPA, 1989a and b) stated in its August 1989
and September 1989 reports that (1) the animal studies suggesting
arsenic is an essential nutrient are not definitive; (2) the skin
changes seen in hyperkeratosis may not always result in skin cancer;
(3) the 1968 Taiwan data demonstrate that high doses of ingested
arsenic can cause skin cancer; (4) the Taiwan study is inconclusive to
determine cancer risk at levels ingested in the United States (U.S.);
and (5) As (III) levels below 200-250 µg per day may be
detoxified. SAB recommended that EPA set the MCL using a non-linear
dose-response (at some low dose, arsenic would not be toxic). The SAB
report recommended that EPA revise the risk assessment based on dose of
arsenic to target tissues (the concentration of arsenic that damages
tissues, rather than the concentration in water) and consider
detoxification.
The SAB also reviewed EPA's April 12, 1991 Arsenic Research
Recommendations (US EPA, 1991c). The final report provided SAB's
recommendations (US EPA, 1992a) and ``identified research needed to
resolve major uncertainties about inorganic arsenic cancer risk'' to
evaluate if work could be done in three to five years. It noted that
``important work can be done within the time available. Although the
results from this work will not completely resolve any issue, * * * the
results will likely significantly improve the Agency's ability to
evaluate the risk. * * * through improved knowledge of arsenic
metabolism and * * * as a carcinogen.'' The report reflected
uncertainty as to whether or not EPA could obtain enough data to
regulate arsenic using a non-linear model, which needed more
information on how arsenic induces cancer. The group noted that it
would take longer than five years to develop an animal model to help
understand the toxicity of arsenic. SAB recommended four short-term
studies: (a) Investigation of chromosome damage, arsenic metabolites,
and the times cells are most susceptible to arsenic, (b) study of human
liver capacity to add methyl groups to arsenic, (c) identifying the
species in urine in several populations to look for evidence of
saturation of methylation enzymes, and (d) comparing methylated arsenic
excreted in the U.S., Taiwan, Mexico, and Argentina to consider the
effect of nutritional or genetic differences on methylation capacity.
However, if time were not a factor, SAB ranked developing an animal
model of arsenic-induced cancer as the first priority.
In 1993 SAB reviewed EPA's draft ``Drinking Water Criteria Document
on Inorganic Arsenic (US EPA, 1993a).'' In 1995, SAB reviewed the
analytical methods, occurrence estimate, treatment technologies, and
approach for assigning costs in the regulatory impact analysis (US EPA,
1995). Besides highlighting previous SAB reviews of 1989, 1992, and
1994 on health effects, the 1995 report recommended changes to the
practical quantitation limit approach, use of occurrence data, review
of technologies, and support for the decision tree, with some
reservations.
EPA held internal workgroup meetings throughout 1994, addressing
risk assessment, treatment, analytical methods, arsenic occurrence,
exposure, costs, implementation issues, and regulatory options. EPA
decided in early 1995 to defer the arsenic regulation in order to
better characterize health effects and assess cost-effective removal
technologies for small utilities.
The 1996 amendments to SDWA included a new statutory deadline for
the arsenic regulations, as discussed in section II.A.
E. EPA's Arsenic Research Plan
EPA held a workshop in March 1994 entitled ``Workshop on Developing
an Epidemiology Research Strategy for Arsenic in Drinking Water.'' The
cover letter to the final report (US EPA, 1997b), dated April 14, 1997,
notes that EPA has been using the recommendations to direct its
research directions. The report listed ten projects and seventeen
conclusions on exposure, endpoints, study design and statistical power,
population selection, feasibility of conducting a study in the U.S.,
international studies, importance of developing biomarkers to measure
health effects of arsenic, and animal studies.
In 1995, the Water Industry Technical Action Fund (WITAF) ( funded
by the American Water Works Association, National Association of Water
Companies, Association of Metropolitan Water Agencies, National Rural
Water Association, and National Water Resources Association), the AWWA
Research Foundation, and the Association of California Water Agencies
(ACWA) sponsored an Expert Workshop on Arsenic Research Needs in
Ellicott City, MD, May 31-June 2, 1995. The final report (AWWA et al.,
1995) identified research projects in mechanisms, epidemiology,
toxicology, and treatment. It identified ten high
[[Page 38896]]
priority projects which would need over $3 million to fund, eleven
medium priority projects needing over $6 million, and ten low priority
projects costing over $9 million, that totaled over $19 million in
research needs.
Congress recognized the importance of health effects research in
regulating arsenic, as demonstrated by the 1996 statutory requirement
to develop a research plan within 180 days ``in support of drinking
water rulemaking to reduce the uncertainty in assessing health risks
associated with exposure to low levels of arsenic * * * (section
1412(b)(12)(A)(ii)). In the research plan EPA recognized that ``[t]he
research needs are broader than those that EPA can address alone, and
it is anticipated that other entities will be involved in conducting
some of the needed research (US EPA, 1998a).'' (See section III.E.1. on
industry-funded research and the arsenic research plan (at www.epa.gov/
ORD/WebPubs/final/arsenic.pdf) for EPA-funded projects.) In December
1996, EPA submitted its draft research plan for peer review by its
Board of Scientific Counselors' (BOSC) Ad Hoc Committee, and the
committee met in January 1997. The February 1998 Arsenic Research Plan
addressed the June 1997 comments from BOSC.
Major areas covered in the research plan included studies to:
Improve our qualitative and quantitative assessment of the
human toxicity of arsenic;
Understand mechanisms of arsenic toxicity that may aid in
extension of the observed human findings when extrapolation is
required;
Measure exposures of the US population to arsenic from
various sources (particularly diet) to allow better definition of
cumulative exposures to arsenic;
Refine treatment technologies that may better remove
arsenic from water supplies;
Improve methods for analyzing and monitoring arsenic in
drinking water.
EPA also set priorities in the plan and identified projects that
met the short term and long term criteria:
Short Term Criteria
1. Will the research improve the scientific basis for risk
assessments needed for proposing a revised arsenic MCL by January 1,
2000?
2. Will the research improve the scientific basis for risk
management decisons needed for proposinig a revised arsenic MCL by
January 1, 2000?
Long Term Criteria
1. Will the research improve the scientific basis for risk
assessment and risk management decisions needed to review and develop
future MCLs beyond the year 2000?
2. Is the research essential to improving our scientific
understanding of the health risks of arsenic?
The research plan included the following priority topics for
research under the five major areas of investigation supporting
drinking water rulemaking:
Exposure Analysis
Arsenic speciation and preservation: Improvements in
analytical methods to support water treatment decisions.
Measurement of background exposures to arsenic in U.S.
population, particularly inorganic arsenic intake in the U.S. diet.
Development and evaluation of biomarkers (e.g., species of
arsenic in urine) of exposures.
Development of standard reference material for arsenic in
water, food, urine, tissues.
Cancer Effects
Further study of internal cancers associated with arsenic
exposures.
Dose response data on hyperkeratosis as a likely precursor
to skin cancer.
Research on factors influencing human susceptibility
including age, genetic characteristics and dietary patterns.
Metabolic and pharmacokinetic studies that can identify
dose dependent metabolism.
Mechanistic studies for arsenic-induced genotoxicity and
carcinogenicity.
Noncancer Effects
Development of human dose-response data for
hyperkeratosis, cardiovascular disease, neurotoxicity and developmental
effects.
Development of additional health effects and hazard
identification data on other non-cancer endpoints such as diabetes and
hematologic effects.
Risk Management Research
Identification of limitations of treatment technologies
and impacts on water quality.
Development of treatment technologies for small water
systems.
Development of data on cost and performance capabilities
of various treatment options.
Consideration of residuals management issues, including
disposal options and costs.
Risk Assessment/Characterization
Development of risk characterizations to provide interim
support to States and local communities.
Development of predictive tools and statistical models for
assessing bioavailability, interactions and dose-response as better
mass balance data become available.
Comprehensive assessment of exposure levels and
incorporation of data into risk estimates for better characterization
of actual risks associated with arsenic exposure.
Comprehensive assessment of arsenic mode of action provide
a greater understanding of biological mechanisms and factors that may
impact the shape of a dose response curve.
Comprehensive assessment of non-cancer risks and
consideration of appropriate modeling tools for quantitative estimation
of non-cancer risks.
Comprehensive assessment of human dose-response data for
hyperkeratosis, cardiovascular disease, neurotoxicity and developmental
effects.
III. Toxic Forms and Health Effects of Arsenic
A. What Are the toxic Forms of Arsenic?
Arsenic exists in several forms which vary in toxicity and
occurrence. Accordingly, for this proposed regulation, it is important
to consider those forms that can exert toxic effects and to which
people may be exposed. For example, the metallic form of arsenic (0
valence) is not absorbed from the stomach and intestines and does not
exert adverse effects. On the other hand, a volatile compound such as
arsine (AsH3) is toxic, but is not present in water or food.
Moreover, the primary organic forms (arsenobetaine and arsenocholine)
found in fish and shellfish seem to have little or no toxicity
(Sabbioni et al., 1991). Arsenobetaine quickly passes out of the body
in urine without being metabolized to other compounds (Vahter, 1994).
Arsenite (+3) and arsenate (+5) are the most prevalent toxic forms of
inorganic arsenic that are found in drinking water. However, recovery
of identified arsenic species in vegetables, grains and oils has been
limited and difficult, so little is known about types of species in
these foods (NRC, 1999).
In animals and humans, inorganic pentavalent arsenic is converted
to trivalent arsenic that can be methylated (i.e., chemically bonded to
a methyl group, which is a carbon atom linked to
[[Page 38897]]
three hydrogen atoms) to mono-methyl arsenic (MMA) and di-methyl
arsinic acid (DMA), which are organic arsenicals. The primary route of
excretion for arsenic metabolites is in the urine. Studies indicate
that the organic arsenicals MMA and DMA were hundreds of times less
likely to produce genetic changes in animal cells than inorganic
arsenicals. Moreover, many studies reported organic arsenicals to be
less reactive in tissues, to kill less cells, and to be more easily
excreted in urine (NRC, 1999).
B. What Are the Effects of Acute Toxicity?
Inorganic arsenic can exert toxic effects after acute (short-term)
or chronic (long-term) exposure. From human acute poisoning incidents,
the LD50 of arsenic has been estimated to range from 1 to 4
mg/kg (Vallee et al., 1960, Winship, 1984). This dose would correspond
to a lethal dose range of 70 to 280 mg for 50% of adults weighing 70
kg. At nonlethal, but high acute doses, inorganic arsenic can cause
gastroenterological effects, shock, neuritis (continuous pain) and
vascular effects in humans (Buchanan, 1962). Such incidents usually
occur after accidental exposures. However, sometimes high dose acute
exposures may be self-administered. For example, inorganic arsenic is a
component of some herbal medicines and adverse effects have been
reported after use. In one report of 74 cases (Tay and Seah, 1975), the
primary signs were skin lesions (92%), neurological (i.e., nerve)
involvement (51%), and gastroenterological, hematological (i.e., blood)
and renal (i.e., kidney) effects (19 to 23%). Although acute or short-
term exposures to high doses of inorganic arsenic can cause adverse
effects, such exposures do not occur from public water supplies in the
U.S. at the current MCL of 50 µg/L. EPA's proposed drinking
water regulation addresses the long-term, chronic effects of exposure
to low concentrations of inorganic arsenic in drinking water.
C. What Cancers Are Associated With Arsenic?
Inorganic arsenic is a multi-site human carcinogen by the drinking
water route. Asian, Mexican and South American populations with
exposures to arsenic in drinking water generally at or above several
hundred micrograms per liter are reported to have increased risks of
skin, bladder, and lung cancer. The current evidence also suggests that
the risks of liver and kidney cancer may also be increased following
exposures to inorganic forms of arsenic. The weight of evidence for
ingested arsenic as a causal factor of carcinogenicity is much greater
now than a decade ago, and the types of cancer occurring as a result of
ingesting inorganic arsenic have even greater health implications for
U.S. and other populations than the occurrence of skin cancer alone.
(Until the late 1980s skin cancer had been the cancer classically
associated with arsenic in drinking water.) Epidemiologic studies
(e.g., of people) provide direct data on arsenic risks from drinking
water at exposure levels much closer to those of regulatory concern
than environmental risk assessments based on animal toxicity studies.
1. Skin Cancer
Early reports linking inorganic arsenic contamination of drinking
water to skin cancer came from Argentina (Neubauer, 1947, reviewing
studies published as early as 1925) and Poland (Geyer, 1898, as
reported in Tseng et al., 1968). However, the first studies that
observed dose-dependent effects of arsenic associated with skin cancer
came from Taiwan (Tseng et al., 1968; Tseng, 1977). These studies
focused EPA's attention on the health effects of ingested arsenic.
Physicians physically examined over 40,000 residents from 37 villages
and 7500 residents exposed to 0.017 mg/L arsenic ( reference group).
The study population was divided into three groups based on exposure to
inorganic arsenic (0 to 0.29, 0.30 to 0.59 and 0.60 mg of
inorganic As/Liter) measured at the village level. A dose-and age-
related increase of arsenic-induced skin cancer among the villagers was
noted. No skin cancers were observed in the low arsenic reference
areas. The 1999 NRC report noted that the ``primary limitation of this
study * * * was the lack of detail'' reported, such as grouping
individuals into ``broad exposure groups'' (rather than grouping into
37 village exposures). This limits the usefulness of these studies.
However, these Tseng reports and other corroborating studies such as
those by Albores et al. (1979) and Cebrian et al. (1983) on drinking
water exposure and exposures to inorganic arsenic in medicines (Cuzick
et al., 1982) and in pesticides (Roth, 1956) led the EPA, using skin
cancer as the endpoint, to classify inorganic arsenic as a human
carcinogen (Group A) by the oral route (US EPA, 1984).
2. Internal Cancers
Exposure to inorganic arsenic in drinking water has also been
associated with the development of internal cancers. ``No human studies
of sufficient statistical power or scope have examined whether
consumption of arsenic in drinking water at the current MCL results in
an increased incidence of cancer or noncancer effects (NRC, 1999, pg.
7).''
Chen et al. (1985) used standardized mortality ratios (SMRs) to
evaluate the association between ingested arsenic and cancer risk in
Taiwan. (SMRs, ratios of observed to expected deaths from specific
causes, are standardized to adjust for differences in the age
distributions of the exposed and reference populations.) The authors
found statistically significant increased risks of mortality for
bladder, kidney, lung, liver and colon cancers. A subsequent mortality
study in the same area of Taiwan found significant dose-response
relationships for deaths from bladder, kidney, skin, and lung cancers
in both sexes and from liver and prostate cancer for males. They also
found increases in peripheral and cardiovascular diseases but not in
cerebrovascular accidents (Wu et al., 1989). There are several
corroborating reports of the increased risk of cancers of internal
organs from ingested arsenic including two from two South American
countries. In Argentina, significantly increased risks of death from
bladder, lung and kidney cancer were reported (Hopenhayn-Rich et al.,
1996; 1998). In a population of approximately 400,000 in northern
Chile, Smith et al. (1998) found significantly increased risks of
bladder and lung cancer mortality.
There have only been a few studies of inorganic arsenic exposure
via drinking water in the U.S., and most have not considered cancer as
an endpoint. People have written EPA asking that the new MCL be set
considering that these U.S. studies have not seen increases in cancers
at the low levels of arsenic exposure in U.S. drinking water.
Optimally, low-exposure arsenic studies involve long-term residency
(20-40 years with known drinking water arsenic exposure), access to
health records, populations large enough to detect statistically
significant increases in cancers and other health endpoints, and
limited use of multiple sources of water (bottled, filtered, beverages,
food prepared outside the home).
Recently, Lewis et al. (1999) conducted a mortality study of a
population in Utah whose drinking water contained relatively low
concentrations of arsenic (averaged 18-191 µg/L). They reported
no significant increase in bladder or lung mortality. They did report a
statistically significant dose-response for an increased risk of
prostate cancer mortality. Smoking is an established risk factor for
bladder and lung cancer, and inorganic arsenic
[[Page 38898]]
behaves as a comutagen even though it is not mutagenic alone (NRC,
1999, pg. 200). It is possible that inorganic arsenic potentiates other
risk factors for these cancers. This potential role is consistent with
the NRC, 1999 view that arsenic's mode of action may be to interfere
with cell ``housekeeping'' functions that normally repair genetic
damage and ensure that damaged cells die (programmed cell death) rather
than reproduce (see section III.D.2. below).
D. What Non-Cancer Effects Are Associated With Arsenic?
A large number of adverse noncarcinogenic effects have been
reported in humans after exposure to drinking water highly contaminated
with inorganic arsenic. The earliest and most prominent changes are in
the skin, e.g., hyperpigmentation and keratoses (calus-like growths).
Other effects that have been reported include alterations in
gastrointestinal, cardiovascular, hematological (e.g., anemia),
pulmonary, neurological, immunological and reproductive/developmental
function (ATSDR, 1998).
The most common symptoms of inorganic arsenic exposure appear on
the skin and occurr after 5-15 years of exposure equivalent to 700
µg/day for a 70 kg adult, or within 6 months to 3 years at
exposures equivalent to 2,800 µg/day for a 70 kg adult (pg. 131
NRC, 1999). They include alterations in pigmentation and the
development of keratoses which are localized primarily on the palms of
the hands, the soles of the feet and the torso. The presence of
hyperpigmentation and keratoses on parts of the body not exposed to the
sun is characteristic of arsenic exposure (Yeh, 1973, Tseng, 1977). The
same alterations have been reported in patients treated with Fowler's
solution (1% potassium arsenite; Cuzick et al., 1982), used for asthma,
psoriasis, rheumatic fever, leukemia, fever, pain, and as a tonic (WHO
1981 and NRC 1999).
Chronic exposure to inorganic arsenic is often associated with
alterations in gastroenterological (GI) function. For example,
noncirrhotic hypertension is a relatively specific, but not commonly
found manifestation in inorganic arsenic-exposed individuals and may
not become a clinical observation until the patient demonstrates GI
bleeding (Morris et al., 1974; Nevens et al., 1990). Physical
examination may reveal spleen and liver enlargement, and
histopathological examination of tissue specimens may demonstrate
periportal fibrosis (Morris et al., 1974; Nevens et al., 1990; Guha
Mazumder et al., 1997). There have been a few reports of cirrhosis
after inorganic arsenic exposure, but the authors of these studies did
not determine the subjects' alcohol consumption (NRC 1999).
Development of peripheral vascular disease (hardening of the
arteries to the arms and legs, that can cause pain, numbness, tingling,
infection, gangrene, and clots) after inorganic arsenic exposure has
also been reported. In Taiwan, blackfoot disease (BFD, a severe
peripheral vascular insufficiency which may result in gangrene of the
feet and other extremities) has been the most severe manifestation of
this effect. Tseng (1977) reported over 1,000 cases of BFD in the
arsenic study areas of Taiwan. Less severe cases of peripheral vascular
disease have been described in Chile (Zaldivar et al., 1974) and Mexico
(Cebrian, 1987). In a Utah study, increased SMRs for hypertensive heart
disease were noted in both males and females after exposure to
inorganic arsenic-contaminated drinking water (Lewis et al., 1999).
These reports link exposure to inorganic arsenic effects on the
cardiovascular system.
Studies in Taiwan (Lai et al., 1994) and Bangladesh (Rahman et al.,
1998) found an increased risk of diabetes among people consuming
arsenic-contaminated water. Two Swedish studies found an increased risk
of mortality from diabetes among those occupationally exposed to
arsenic (Rahman and Axelson, 1995; Rahman et al., 1998).
Although peripheral neuropathy (numbness, muscle weakness, tremors,
ATSDR 1998) may be present after exposure to short-term, high doses of
inorganic arsenic (Buchanan, 1962; Tay and Seah, 1975), there are no
studies that definitely document this effect after exposure to levels
of less than levels (50 µg/L) of inorganic arsenic in drinking
water. Hindmarsh et al. (1977) and Southwick et al. (1983) have
reported limited evidence of peripheral neuropathy in Canada and the
U.S., respectively, but it was not reported in studies from Taiwan,
Argentina or Chile (Hotta, 1989, as cited by NRC 1999).
There have been a few, scattered reports in the literature that
inorganic arsenic can affect reproduction and development in humans
(Borzysonyi et al., 1992; Desi et al., 1992; Tabacova et al., 1994).
After reviewing the available literature on arsenic and reproductive
effects, the National Research Council panel (NRC 1999) wrote that
``nothing conclusive can be stated from these studies.''
Based on the studies mentioned in this section, it is evident that
inorganic arsenic contamination of drinking water can cause dermal and
internal cancers, affect the GI system, alter cardiovascular function,
and increase risk of diabetes, based on studies of people exposed to
drinking water well above the current arsenic MCL. EPA's MCL is chosen
to be protective of the general population within an acceptable risk
range, not at levels at which adverse health effects are routinely seen
(see section III.F.7. on risk considerations).
E. What Are the Recent Developments in Health Effects Research?
1. Funding of Health Effects Research
As mentioned earlier in section II.A., Congress recognized that we
needed more research to determine the health effects at low levels of
arsenic (below the observed health effects and below 50 µg/L).
On December 6, 1996, EPA issued a Federal Register notice (61 FR 64739;
US EPA, 1996e) asking for public comment on four arsenic health
research topics to fund research projects with $2 million from EPA
appropriations and $1 million in funds raised by water industry groups
(US EPA, 1996d). In addition, the Office of Research and Development's
(ORD's) Board of Scientific Counselors (BOSC) peer reviewed the draft
research topics and the arsenic research plan. In the fall of 1997, EPA
and the industry partners funded their respective choices for arsenic
research, after having the applications peer reviewed. EPA issued three
grants for the following research: Dose Response of Skin Keratoses and
Hyper-Pigmentation, Arsenic Glutathione Interactions and Skin Cancer,
and Cellular Redox Status. The water industry groups awarded two
contracts, studying Contribution of Arsenic From Dietary Sources and
Tumor Studies in Mice.
2. Expert Panel on Arsenic Carcinogenicity
As part of the Integrated Risk Information System (IRIS) update
effort, EPA sponsored an ``Expert Panel on Arsenic Carcinogenicity:
Review and Workshop'' in May 1997 (US EPA, 1997d). The panel evaluated
existing data to comment on arsenic's carcinogenic mode of action and
the effect on dose-response extrapolations. The panel noted that
arsenic compounds have not formed DNA adducts (i.e., bound to DNA) nor
caused point mutations. Trivalent inorganic forms inhibit enzymes, but
arsenite and arsenate do not affect DNA replication. The panel
discussed several modes of action, concluding that arsenic indirectly
affects DNA, inducing chromosomal changes. The panel thought that
arsenic-induced
[[Page 38899]]
chromosomal abnormalities could possibly come from errors in DNA repair
and replication that affect gene expression; that arsenic may increase
DNA hypermethylation and oxidative stress; that arsenic may affect cell
proliferation (cell death appears to be nonlinear); and that arsenic
may act as a co-carcinogen. Arsenite causes cell transformation but not
mutation of cells in culture. It also induces gene amplification
(multiple copies of DNA sequences) in a way which suggests interference
with DNA repair or cell control instead of direct DNA damage. The panel
noted that all identified modes of action support a nonlinear dose-
response curve, that few data supports any one mode as most important,
and that more than one mode of action may be operating. At low doses
the slope of the dose response would decrease, and at very low doses
``might effectively be linear but with a very shallow slope, probably
indistinguishable from a threshold.''
In terms of implications for the risk assessment, the panel noted
that risk per unit dose estimates from human studies can be biased
either way. For the Taiwanese study, the ``* * * biases associated with
the use of average doses and with the attribution of all increased risk
to arsenic would both lead to an overestimation of risk (US EPA, 1997d,
page 31).'' While health effects are most likely observed in people
getting high doses, the effects are assigned to the average dose of the
exposure group. Thus, risk per unit dose estimated from the average
doses would lead to an overestimation of risk (US EPA, 1997d, page 31).
3. NAS Review of EPA's Risk Assessment
In 1997, at EPA's request, the National Academy of Sciences' (NAS)
Subcommittee on Arsenic of the Committee on Toxicology of the National
Research Council (NRC) met. Their charge was to review EPA's
assessments of arsenic. The NAS/NRC Subcommittee finished their work in
March 1999 (The report can be viewed from the National Academy Press
website: www.nap.edu/books/0309063337/html/index.html). The detailed
discussion of their work is in section III.F. In general, the NRC
report confirms and extends concerns about human carcinogenicity of
drinking water containing arsenic and offers perspective on dose-
response issues and needed research. For the decisions in this
regulation, the EPA has relied upon the NRC report as presenting the
best available, peer reviewed science as of its completion and has
augmented it with more recently published, peer reviewed information.
Further work on the risk assessment will also be done before the final
rule is issued to analyze the risks of internal cancers. The NRC
provided risk numbers for bladder cancer using the Agency's approach.
The NRC report noted that ``some studies have shown that excess lung
cancer deaths attributed to arsenic are 2-5 fold greater than the
excess bladder cancer deaths. * * * (NRC, 1999, pg. 8).'' The NRC
recommended that EPA analyze risks of internal cancers both separately
and combined. Peer-reviewed quantitative analysis of lung tumor risk is
expected to be available for consideration in the final rulemaking.
Meanwhile, this proposal, in a ``what if'' analysis (discussed in
section X.B), estimates the potential monetary benefits that would
result if the lung cancer and bladder cancer risks were the same, which
would be the case if the excess lung cancer deaths actually were 2- to
5-fold greater than the excess bladder cancer deaths.
4. May 1999 Utah Mortality Study
EPA scientists conducted an epidemiological study of 4,058 Mormons
exposed to arsenic in drinking water in seven communities in Millard
County, Utah (Lewis et al., 1999). The 151 samples from their public
and private drinking water sources had arsenic concentrations ranging
from 4 to 620 µg/L with seven mean (arithmetic average)
community exposure concentrations of 18 to 191 µg/L and all
seven community exposure medians (mid-point of arsenic values) 200
µg/L. Observed causes of death in the study group (numbering
2,203) were compared to those expected from the same causes based upon
death rates for the general white male and female population of Utah.
Several factors suggest that the study population may not be
representative of the rest of the United States. The Mormon church, the
predominant religion in Utah, prohibits smoking and consumption of
alcohol and caffeine. Utah had the lowest statewide smoking rates in
the U.S. from 1984 to 1996, ranging from 13 to 17%. Mormon men had
about half the cancers related to smoking (mouth, larynx, lung,
esophagus, and bladder cancers) as the U.S. male population from 1971
to 1985 (Lyon et al., 1994). The Utah study population was relatively
small (4,000 persons) and primarily English, Scottish, and
Scandinavian in ethnic background.
While the study population males had a significantly higher risk of
prostate cancer mortality, females had no significantexcess risk of
cancer mortality at any site. Millard County subjects had higher
mortality from kidney cancer, but this was not statistically
significant. Both males and females in the study group had less risk of
bladder, digestive system and lung cancer mortality than the general
Utah population. The Mormon females had lower death rates from breast
and female genital cancers than the State rate. These decreased death
rates were not statistically significant.
Although deaths due to hypertensive heart disease were roughly
twice as high as expected in both sexes, increases in death did not
relate to increases in dose, calculated as the years of exposure times
the median arsenic concentration. The Utah data indicate that heart
disease should be considered in the evaluation of potential benefits of
U.S. regulation. Vascular effects have also been reported as an effect
of arsenic exposure in studies in the U.S. (Engel et al. 1994), Taiwan
(Wu et al., 1989) and Chile (Borgono et al., 1977). The overall
evidence indicating an association of various vascular diseases with
arsenic exposure supports consideration of this endpoint in evaluation
of potential noncancer health benefits of arsenic exposure reduction.
5. 1999 Review of Health Effects
Tsai et al. (1999) estimated standardized mortality ratios (SMR's)
for 23 cancer and non-cancer causes of death in women and 27 causes of
death in men in an area of Taiwan with elevated arsenic exposures
(Tsai, et al., 1999). The SMRs in this study are an expression of the
ratio between deaths that were observed in an area with elevated
arsenic levels and those that were expected to occur, compared to both
the mortality of populations in nearby areas without elevated arsenic
levels and to the national population. Drinking water (250-1,140
µg/L) and soil (5.3-11.2 mg/kg) in the Tsai (1999) population
study had high arsenic content. There are, of course, possible
differences between the population and health care in Taiwan and the
United States; and arsenic levels in the U.S. are not generally as high
as they were in the study area of Taiwan. However, the study gives an
indication of the types of health effects that may be associated with
arsenic exposure via drinking water. The study reports a high mortality
rate (SMR > 3) for both sexes from bladder, kidney, skin, lung, and
nasal cavity cancers and for vascular disease. Females also had high
mortalities for laryngeal cancer.
The SMRs calculated by Tsai (1999) used the single cause of death
noted on the death certificates. Many chronic
[[Page 38900]]
diseases, including some cancers, are not generally fatal.
Consequently, the impact indicated by the SMR in this study may
underestimate the total impact of these diseases. The causes of death
reported in this study are consistent with what is known about the
adverse effects of arsenic. Tsai et al. (1999) identified ``bronchitis,
liver cirrhosis, nephropathy, intestinal cancer, rectal cancer,
laryngeal cancer, and cerebrovascular disease'' as possibly ``related
to chronic arsenic exposure via drinking water,'' which had not been
reported before. In addition, people in the study area were observed to
have nasal cavity and larynx cancers not caused by occupational
exposure to inhaled arsenic.
6. Study of Bladder and Kidney Cancer in Finland
Kurttio et al. (1999) conducted a case-cohort design study of 61
bladder and 49 kidney cancer cases and 275 controls to evaluate the
risk of these diseases with respect to arsenic drinking water
concentrations. In this study the median exposure was 0.1 µg/L,
the maximum reported was 64 µg/L, and 1% of the exposure was
greater than 10 µg/L. The authors reported that very low
concentrations of arsenic in drinking water were significantly
associated with being a case of bladder cancer when exposure occurred
2-9 years prior to diagnosis. Arsenic exposure occurring greater than
10 years prior to diagnosis was not associated with bladder cancer
risk. Arsenic was not associated with kidney cancer risk even after
consideration of a latency period.
F. What Did the National Academy of Sciences/National Research Council
Report?
1. The National Research Council and Its Charge
Due to controversy surrounding the risk assessment of inorganic
arsenic, EPA asked the National Research Council (NRC) to do the
following: (1) Review EPA's characterization of potential human health
risks from ingestion of inorganic arsenic in drinking water; (2) review
the available data on the carcinogenic and noncarcinogenic effects of
inorganic arsenic; (3) review the data on the metabolism, kinetics and
mechanism(s)/mode(s) of action of inorganic arsenic; and (4) identify
research needs to fill data gaps. To accomplish this task, NRC convened
a panel of scientific experts with backgrounds in chemistry,
toxicology, genetics, epidemiology, nutrition, medicine, statistics and
risk assessment. In addition to the general expertise of the panel
members, many had conducted research on inorganic arsenic. NRC
identified the thirteen scientists with ``diverse perspectives and
technical expertise'' that peer reviewed the draft report. The report
noted that ``EPA did not request, nor did the subcommittee endeavor to
provide, a formal risk assessment for arsenic in drinking water (NRC,
1999).''
2. Exposure
Arsenic is naturally occurring and ubiquitously distributed in the
earth's surface. Because of this, the general population is exposed to
low levels of arsenic through the food supply. The NRC report provides
FDA market basket data for inorganic arsenic intake by age group which,
along with similar data for water intake, will permit communication of
total exposure estimates of the general population by age group. The
assumption is made in the FDA data that, for fish and seafood,
inorganic arsenic is 10% of total arsenic. This 10% assumption is
acknowledged to be conservative and has been adopted for public health
protection so as not to underestimate the contribution from fish and
seafood. Likewise, the 2 L/day assumption of adult drinking water
intake does not represent intake by the average person; rather it
represents intake of a person in the 90th percentile.
3. Essentiality
The NRC report examined the question of essentiality of arsenic in
the human diet. It found no information on essentiality in humans and
only data in experimental animals suggesting growth promotion
(arsenicals are fed to livestock for this reason). Inorganic arsenic
has not been found to be essential for human well-being or involved in
any required biochemical pathway. Given this and the fact that arsenic
occurs naturally in food, consideration of essentiality is not
necessary for public health decisions about water.
4. Metabolism and Disposition
Data from humans show that inorganic arsenic is readily absorbed
and transported through the body. It has a half-life in the body of
approximately four days and is primarily excreted in the urine. If a
human is exposed to the inorganic arsenate form (+5 valence), the
arsenite will be reduced to arsenite (+3). Some of the arsenite will be
sequentially methylated to form monomethylarsonic acid (MMA) and
dimethylarsinic acid (DMA). This methylation process decreases acute
toxicity and facilitates excretion from the body. Individuals and
populations vary in their metabolism of arsenic. Such variations may be
due to genetic differences, species and dose of inorganic arsenic
ingested, nutrition, disease and possibly other factors. Whether these
methylated products (MMA and DMA) play a role in the development of
cancer and noncancer endpoints is unknown at the present time (NRC,
1999). The NRC report recommended that experiments be conducted on the
factors affecting interspecies differences in inorganic arsenic
toxicity including use of human tissue when available.
5. Human Health Effects and Variations in Sensitivity
The NRC panel concluded that there is sufficient evidence that
chronic ingestion of inorganic arsenic causes bladder, lung and skin
cancers and adverse noncancer effects on the cardiovascular systems,
mainly from studies exposed to ``several hundred micrograms per liter.
Few data address the degree of cancer risk at lower concentrations of
ingested arsenic (NRC, 1999, pg. 130).'' The Utah study (Lewis et al.,
1999), published after the NRC report, indicates that cardiovascular
effects can occur at lower exposures than those seen in the studies
available for the NRC report. At the present time, the NRC report
indicates that there is insufficient evidence to judge whether
inorganic arsenic can affect reproduction or development in humans.
However, inorganic arsenic can pass through the placenta (Concha et
al., 1998), and developmental toxicity needs investigation. In animal
studies, intraperitoneal (injection into the abdominal cavity)
administration of inorganic arsenic can cause malformations, and oral
dosing has been reported to alter fetal growth and viability. The NRC
report recommended additional studies to characterize the dose-response
curve for inorganic arsenic-induced cancer and noncancer health
endpoints. They also stated that the reported beneficial effects of
inorganic arsenic in animals should be carefully monitored. In
addition, the potential effects of inorganic arsenic on human
reproduction should be investigated.
There are many factors (genetics, diet, metabolism, health and sex)
that may affect a human's response to inorganic arsenic exposure. For
example, reduction in methylation of inorganic arsenic methylation can
cause humans to retain more arsenic in their tissues. The retention of
a greater arsenic load could place a person at a greater risk. The NRC
report (1999) recommended that various factors that have the ability
[[Page 38901]]
to alter a human's response to inorganic arsenic exposure be carefully
examined. Specifically, these studies should focus on the extent of
human variability with respect to metabolism, tissue deposition and
excretion under different environmental conditions.
Humans are variable in their metabolic processing of inorganic
arsenic, and internal dose will vary from person to person because of
this as well as because of diet, nutritional status, lifestyle, and
health status. Human variability also exists in response
characteristics (susceptibility). The full quantitative extent of this
variability is not known. For instance, men are more susceptible than
women to bladder cancer throughout the world even though bladder cancer
rates vary from region to region. We do not know whether arsenic may
have a greater effect at different ages (e.g., infants v.s. adults).
6. Modes of Action
Knowledge of a ``mode of action'' means that data are available to
describe the key events at the cellular and/or subcellular level that
lead to the development of the cancer or noncancer endpoint. A number
of potential modes of carcinogenic action have been proposed for
arsenic, with varying degrees of supporting data. The key events in the
cancer process caused by arsenic exposure are not known. Nevertheless,
the data are sufficient to support the conclusion of the NRC report and
the EPA 1997 expert panel workshop report that: ``Arsenic exposure
induces chromosomal abnormalities without direct reaction with DNA (US
EPA, 1997d).''
There is strong evidence against a mode of action for inorganic
arsenic involving direct reaction with DNA. One of the hallmarks of
direct DNA reactivity is multi-species carcinogenic activity. For
arsenic, long-term bioassays for carcinogenic activity in rats, mice,
dogs, and monkeys have been uniformly negative (Furst, 1983). The kinds
of genetic alterations seen in both in vivo and in vitro studies of
arsenic effects are at the level of loss and rearrangement of
chromosomes; these are results of errors of ``cellular housekeeping''
either in DNA repair or in chromosome replication. The NRC and EPA
expert panel (US EPA, 1997d) reports examined several lines of evidence
for various modes of action that might be operative. These included
changes in DNA methylation patterns that could change gene expression
and repair, oxidative stress, potentiation of effects of mutations
caused by other agents, cell proliferative effects, and interference
with normal DNA repair processes. Further examination in both of these
reports of dose-response shapes associated with these effects led to
the conclusion that they involve processes that have either thresholds
of dose at which there would be no response or sublinearity of the dose
response relationship (response decreasing disproportionately as dose
decreases).
The NRC report concluded: ``For arsenic carcinogenicity, the mode
of action has not been established, but the several modes of action
that are considered plausible (namely, indirect mechanisms of
mutagenicity) would lead to a sublinear dose-response curve at some
point below the point at which a significant increase in tumors is
observed. * * * However, because a specific mode (or modes) of action
has not yet been identified, it is prudent not to rule out the
possibility of a linear response.''
The NRC report noted that in certain in vitro studies of human and
animal cells, genotoxic effects have been shown to occur at
submicromolar concentrations of arsenite that are similar to
concentrations found in urine of humans ingesting water at the current
MCL. This emphasizes the potentially low margin of exposure (health
effects observed at concentrations eight times above the MCL) for
arsenic in water at the current MCL.
For noncancer effects, inhibition of cellular respiration in
mitochondria by arsenic may be the focal point of its toxicity. In
addition, inorganic arsenic causes oxidative stress that could play a
role in the development of adverse health effects. The NRC report
(1999) recommended that biomarkers of inorganic arsenic exposure and
cancer appearance be thoroughly studied. Such data might better
characterize the dose-response effects of inorganic arsenic at lower
exposure levels. For noncancer effects, a greater understanding of
arsenic's effects on cellular respiration and subsequent effects of
methylation and oxidative stress are needed (NRC, 1999).
NRC recommended several mode of action studies, using biomarkers,
to help predict the shape of the dose-response curve for cancer and
non-cancer endpoints. NRC concluded that `` * * *Additional
epidemiological evaluations are needed to characterize the dose-
response relationship for arsenic-associated cancer and non-cancer
endpoints, especially at low doses.''
7. Risk Considerations
The NRC study used the results of epidemiological, (i.e., human)
studies; research on the mode of action, and information about factors
affecting sensitivity to arsenic to project to risks to the U.S.
population. The numerical estimation of risk in the NRC report has
several features to consider. The range of drinking water levels
associated with health endpoints in the available studies is generally
hundreds of ppb which is, however, within a factor of 10 of the
existing standard of 50 ppb. Because of uncertainty about the shape of
the dose-response relationship below this range of observed responses,
the NRC report used the approach of the 1996 EPA proposed carcinogen
risk assessment guidelines (US EPA, 1996b). For the male bladder cancer
deaths which were emphasized in the report, NRC used a lower limit on
the dose associated with a 1% (1 in 100) cancer response, and the
LED01 is estimated to be 400 ppb. This is a
point of departure for extrapolating to exposure levels outside the
range of observed data based on inference. Consistent with the proposed
revisions to the Guidelines for Cancer Risk Assessment, the report
shows both a linear extrapolation and a margin of exposure
extrapolation (difference between the point of departure and selected
exposure). Because current data on potential modes of action are
supportive of sub-linear extrapolations, the linear approach could
overestimate risk at low doses. However, EPA believes that within the
several-fold range (10x) just below the point of departure, this should
make little difference. EPA's scientists note that it makes an
increasing difference as dose decreases, and the difference results in
an overestimate of risk at lower exposures. With a straight-line
extrapolation from the point of departure, the report estimated risk to
be 1.0 to 1.5 x 10-\3\ at the current MCL of 50 ppb and the margin of
exposure to be less than 8.
As described further in section X.A., EPA used parts of NRC's risk
analysis and applied U.S. water consumption, weights, and estimate of
population exposed to arsenic to model the U.S. population risk. In
selecting the proposed MCL, EPA considered the uncertainties of the
quantitative dose-response assessment for inorganic arsenic's health
effects, particularly the possible nonlinearity of the dose-response
and multiple cancer risks. Given the current outstanding questions
about human risk at low levels of exposure, decisions about safe levels
are public health policy judgments.
8. Risk Characterization
In 1983 the National Academy of Sciences (NAS, 1983) defined risk
[[Page 38902]]
assessment as containing four steps: hazard identification, dose-
response assessment, exposure assessment, and risk characterization.
Risk characterization is the process of estimating the health effects
based on evaluating the available research, extrapolating to estimate
health effects at exposure levels, and characterizing uncertainties. In
risk management, regulatory agencies such as EPA evaluate alternatives
and select the regulatory action. Risk management considers
``political, social, economic, and engineering information'' using
value judgments to consider ``the acceptability of risk and the
reasonableness of the costs of control (NAS, 1983).''
Unlike most chemicals, there is a large data base on the effects of
arsenic on humans. Inorganic arsenic is a human poison, and oral or
inhalation exposure to the chemical can induce many adverse health
conditions in humans. Specifically oral exposure to inorganic arsenic
in drinking water has been reported to cause many different human
illnesses, including cancer and noncancer effects, as described in
Section III. The NRC panel (1999) reviewed the inorganic arsenic health
effects data base. The panel members concluded that the studies from
Taiwan provided the current best available data for the risk assessment
of inorganic arsenic-induced cancer. (There are corroborating studies
from Argentina and Chile.) They obtained more detailed Taiwanese
internal cancer data and modeled the data using the multistage Weibull
model and a Poisson regression model. Three Poisson data analyses
showed a 1% response level of male bladder cancer at approximately 400
µg of inorganic arsenic/L. The 1% level was used as a Point of
Departure (POD) for extrapolating to exposure levels outside the range
of observed data.
For an agent that is either acting by reacting directly with DNA or
whose mode of action has not been sufficiently characterized, EPA's
public health policy is to assume that dose and response will be
proportionate as dose decreases (linearity of the extrapolated dose-
response curve). This is a science policy approach to provide a public
health conservative assessment of risk. The dose-response relationship
is extrapolated by taking a straight line from the POD rather than by
attempting to extend the model used for the observed range. This
approach was adopted by the NRC report which additionally noted that
using this approach for arsenic data provides results with alternative
models that are consistent at doses below the observed range whereas
extending the alternative models below the observed range gives
inconsistent results. Drawing a straight line from the POD to zero
gives a risk of 1 to 1.5 per 1,000 at the current MCL of 50 µg/
L. Since some studies show that lung cancer deaths may be 2- to 5-fold
higher than bladder cancer deaths, the combined cancer risk could be
even greater. The NRC panel also noted that the MCL of 50 µg/L
is less than 10-fold lower than the 1% response level for male bladder
cancer. Based on its review, the consensus opinion of the NRC panel was
that the current MCL of 50 µg/L does not meet the EPA's goal of
public-health protection. Their report recommended that EPA lower the
MCL as soon as possible.
IV. Setting the MCLG
A. How Did EPA Approach It?
For the decisions in this regulation, the EPA has relied upon the
NRC report as presenting the best available, peer reviewed science as
of its completion and has augmented it with more recently published,
peer reviewed information. EPA used the 1999 NRC report and other
published scientific papers to characterize the potential health
hazards of ingested inorganic arsenic. As NRC (1999) noted, DMA may
enhance the carcinogenicity of other chemicals, but more data are
needed. Based on current knowledge, the organic forms of arsenic in
fish and shellfish do not appear to present a significant risk to
humans. The overall weight of evidence indicates that the inorganic
arsenate and arsenite forms found in drinking water are responsible for
the adverse health effects of ingested arsenic. EPA focused its risk
assessment on the carcinogenic effects of inorganic arsenic (the forms
found in drinking water sources).
A factor that could modify the degree of individual response to
inorganic arsenic is its metabolism. There is ample evidence (NRC,
1999) that the quantitative patterns of inorganic arsenic methylation
vary considerably and that the extent of this variation is unknown. It
is certainly possible that the metabolic patterns of people affect
their response to inorganic arsenic.
There are studies underway in humans and experimental animals under
the EPA research plan and other sponsorships. Over the next several
years these will provide better understanding of the mode(s) of
carcinogenic action of arsenic, metabolic processes that are important
to its toxicity, human variability in metabolic processes, and the
specific contributions of various food and other sources to arsenic
exposure in the U.S. These are important issues in projecting risk from
the observed data range in the epidemiologic studies to lower
environmental exposures experienced from U.S. drinking water.
Until further research is completed, questions will remain
regarding the dose-response relationship at low environmental levels.
The several Taiwan studies have strengths in their long-term
observation of exposed persons and coverage of very large populations
(>40,000 persons). Additionally, the collection of pathology data was
unusually thorough. Moreover, the populations were quite homogeneous in
terms of lifestyle. Limitations in exposure information exist that are
not unusual in such studies. In ecological epidemiology studies of this
kind, the exposure of individuals is difficult to measure because their
exposure from water and food is not known. This results in
uncertainties in defining a dose-response relationship. The studies in
Chile and Argentina are more limited in extent, (e.g., years of
coverage, number of persons, or number of arsenic exposure categories
analyzed), but provide important findings which corroborate one another
and those of the Taiwan studies.
These epidemiological studies provide the basis for assessing
potential risk from lower concentrations of inorganic arsenic in
drinking water, without having to adjust for cross-species toxicity
interpretation. Ordinarily, the characteristics of human carcinogens
can be explored and experimentally defined in test animals. Dose-
response can be measured, and animal studies may identify internal
transport, metabolism, elimination, and subcellular events that explain
the carcinogenic process. Arsenic presents unique problems for
quantitative risk assessment because there is no test animal species in
which to study its carcinogenicity. While such studies have been
undertaken, it appears that test animals, unlike humans, do not respond
to inorganic arsenic exposure by developing cancer. Their metabolism of
inorganic arsenic is also quantitatively different than humans.
Inorganic arsenic does not react directly with DNA. If it did, it would
be expected to cause similar effects across species and to cause
response in a proportionate relationship to dose. Moreover, its
metabolism, internal disposition, and excretion are different and vary
across animal and plant species and humans--in test studies and in
nature.
[[Page 38903]]
Until more is known, EPA will take a traditional, public health
conservative approach to considering the potential risks of drinking
water containing inorganic arsenic. EPA recognizes that the traditional
approach may overestimate risk, as explained in the next section.
B. What Is the MCLG?
EPA concludes that exposure to inorganic arsenic induces cancer in
humans. It also is associated with adverse noncancer effects such as
hypertension (NRC, 1999). The NRC report stated that ``Data on the
modes of action for carcinogenicity can help to predict the shape of
cancer dose-response curves below the level of direct observation of
tumors. * * * For arsenic carcinogenicity * * * modes of action that
are considered most plausible (namely, indirect mechanisms of
mutagenicity) lead to a sublinear dose-response at some point below the
level at which a significant increase in tumors is observed. However,
because a specific mode (or modes) of action has not been identified at
this time, it is prudent not to rule out the possibility of a linear
response (NRC 1999, pgs. 213-214).'' The expert panel report (US EPA,
1997d, pg. 31) stated: ``* * * for each of the modes of action regarded
as plausible, the dose-response would either show a threshold or would
be nonlinear. * * * [H]owever, ``the dose response for arsenic at low
doses would likely be truly nonlinear--i.e., with a decreasing slope as
the dose decreased. However, at very low doses such a curve might
effectively be linear but with a very shallow slope, probably
indistinguishable from a threshold.'' In the absence of a known mode of
action(s), EPA has no basis for determining the shape of a sublinear
dose-response curve for inorganic arsenic. As a result, consistent with
EPA public health policy, EPA will continue to use a linear dose-
response curve for inorganic arsenic effects. Using a linear type of a
dose-response curve, EPA is proposing an MCLG of zero. The Agency
welcomes comments on setting a nonzero MCLG and submission of data
supporting a nonzero MCLG.
C. How Will a Health Advisory Protect Potentially Sensitive
Subpopulations?
The NRC report was inconclusive about the health risks to pregnant
woman, developing fetus, infants, lactating women, and children. When
the Agency completes this rulemaking, it intends to issue a health
advisory on arsenic in drinking water, in order to decrease risk to
sensitive subpopulations prior to the implementation of the new MCL.
The effective date of a revised MCL will be three to five years after
the final rule is issued (2004-2006).
A health advisory is a non-regulatory document that supports water
providers in their independent decisions on actions to take regarding
water contaminants and their communication with the general public. In
the health advisory on arsenic the Agency intends to address a
precautionary step to protect infants. This step would be to avoid
using water containing high levels of arsenic to make up infant
formula. The reason for this precaution is that epidemiologic studies
indicate that arsenic in drinking water (Lewis et al., 1999) affects
the cardiovascular system. While there are no studies of effects of
arsenic on human infants, both the cardiovascular system and brain (and
its vascular system) continue to develop after birth (Thompson, P.M et
al. 2000); thus, the effects discussed in this notice on the
cardiovascular system raise a concern about potential effects of
arsenic on infant development. In large part, causes of cerebrovascular
incidents (stroke) in children are not understood except for certain,
known associations with organic diseases and genetic diseases.
Congenital and acquired heart disease are the most common cause of
stroke in children. The current toxicity data on arsenic do not
contradict this precautionary view.
D. How Will the Clean Water Act Criterion Be Affected by This
Regulation?
EPA is also working to harmonize the human health arsenic criteria
for the Clean Water Act (CWA) and the SDWA. The major reason for the
present difference (discussed in section II.D.) between the MCL and the
Ambient Water Quality Criterion (AWQC) was the result of using separate
bases for determining the two standards. The AWQC for arsenic was
derived from the risk assessment for arsenic-induced skin cancer, while
the current SDWA MCL, adopted in 1975 as a National Interim Primary
Drinking Water Regulation, evolved from the U.S. Public Health Service
standard dating back to the 1940s. The Agency will use the conclusions
of the NRC (1999) report to form the human health basis for both the
AWQC and the MCL. However, the CWA and SDWA statutes require that the
Agency consider different factors during the derivation of a standard.
For example, SDWA requires that the Agency consider: (1) Cost/benefit
analyses, including sizes of the public water systems, (2) the level of
arsenic that can be analyzed by laboratories on a routine basis, [i.e.,
the practical quantitation limit (PQL)] and (3) treatment techniques
for removing the chemical from the water. On the other hand, the CWA
requires the EPA to consider water and fish consumption (including
amount of fish eaten, percent lipid in the fish and the bioaccumulation
factor for the chemical in the fish), but not cost/benefits, analytical
or treatment techniques. Accordingly, developing a AWQC under the CWA
may produce a standard that differs from the MCL derived under the SDWA
even though both standards are based on the same health endpoint. The
Agency will begin work on a new AWQC for arsenic after promulgating the
MCL for arsenic.
V. EPA's Estimates of Arsenic Occurrence
One of the key components in the development of the proposed
arsenic rule is the analysis of arsenic occurrence in public water
supplies, both community water systems (CWS) and non-transient, non-
community, water systems (NTNCWS). EPA's national occurrence assessment
of arsenic provides a basis for estimating:
(1) The number of systems expected to exceed various arsenic
levels;
(2) the number of people exposed to the different levels of
arsenic; and
(3) the variability in arsenic levels in water systems among the
wells and/or entry points to the distribution system.
EPA uses the estimate of the total number of systems and populations
affected in the United States in its cost-benefit analysis. EPA is
seeking comment on its analysis of arsenic occurrence in the U.S., as
well as requesting additional data.
A. What Data Did EPA Evaluate?
For previous occurrence analyses EPA used four older national
arsenic databases: (1) The National Inorganic and Radionuclide Survey
(NIRS), conducted from 1984 to 1986, for ground water CWSs; (2) a 1976-
1977 National Organic Monitoring Survey (NOMS); (3) a 1978-1980 Rural
Water Survey (RWS); and (4) the 1978 Community Water System Survey
(CWSS) for surface water CWSs. However, these older databases have
several limitations. First, the surveys of surface water systems will
not reflect changes in raw water sources which occurred in the last
twenty years. Second, filtration treatment added to comply with the
Surface Water Treatment Rule (110 54 FR 27486, June 29, 1989) would
tend to decrease arsenic exposure, through incidental arsenic removal.
Finally, most of the
[[Page 38904]]
data were censored (reported as less than the analytical test method
detection level or reporting limit, e.g., ``not detected'' or ``5
µg/L''). NIRS, CWSS, and RWS, respectively, had 93%, 97%, and
90% censored data. This limits the estimation of low level occurrence
of arsenic and makes it statistically difficult to extrapolate
occurrence with the limited amount of non-censored data. The EPA
Science Advisory Board recommended that EPA abandon the older data when
sufficient new data become available because of the high percentage of
censored data in the older surveys and the difficulty of using highly
censored data sets to estimate occurrence (US EPA, 1995). Therefore,
with improved analytical techniques for detecting arsenic at lower
levels, as low as 0.5 µg/L, and the lower reporting limits in
the new data received by EPA, the Agency focused the data evaluation on
post-1980 data sources for estimating national occurrence.
Since 1992, EPA OGWDW has received arsenic databases from other EPA
offices, States, public water utilities, and associations. EPA combined
the compliance monitoring data obtained from States into the ``25
States'' database. The Agency evaluated the databases listed in Table
V-1. (Note that EPA's database, the Safe Drinking Water Information
System (SDWIS), only records violations of the current arsenic MCL, so
it is censored at 50 µg/L.) A more detailed description of the
databases and evaluations are presented in the EPA document titled
``Arsenic Occurrence in Public Drinking Water Supplies,'' (US EPA,
2000b).
Table V-1.--Summary of Arsenic Data Sources
----------------------------------------------------------------------------------------------------------------
Reporting level
Data source (µg/L) Number of CWSs Source water Water type
----------------------------------------------------------------------------------------------------------------
25 States\1\.................. 1 to 10......... >19,000......... Surface, Ground...... finished.
Metro \2\..................... 1............... 140............. Surface, Ground...... raw & finished.
NAOS \3\...................... 0.5............. 517............. Surface, Ground...... raw & predicted
finished.
USGS \4\...................... 1............... not available Ground............... raw.
(20,000 sites).
ACWA \5\...................... 0.1 to 1........ 180 (1,500 Surface, Ground...... finished.
samples).
WESTCAS \6\................... not available... not available... Ground............... finished.
----------------------------------------------------------------------------------------------------------------
\1\ Arsenic compliance monitoring data from community water systems (CWSs) from Alabama, Alaska, Arizona,
Arkansas, California, Illinois, Indiana, Kentucky, Kansas, Maine, Michigan, Minnesota, Missouri, Montana,
Nevada, New Hampshire, New Jersey, New Mexico, North Carolina, North Dakota, Ohio, Oklahoma, Oregon, Texas,
and Utah.
\2\ Metropolitan Water District of Southern California (MWDSC, or Metro) 1992-1993 national survey of 140 CWSs
serving more than 10,000 people.
\3\ 1996 National Arsenic Occurrence Survey (NAOS) funded by the Water Industry Technical Action Fund (WITAF),
which includes the following organizations: American Water Works Association, National Association of Water
Companies, Association of Metropolitan Water Agencies, National Rural Water Association, and National Water
Resources Association.
\4\ U.S. Geological Survey (USGS) ambient (raw water) ground water from approximately 20,000 wells throughout
the U.S. used for various purposes, including public supply, research, agriculture, industry and domestic
supply.
\5\ 1993 survey from 180 water agencies, utilities, and cities in southern California, conducted by the
Association of California Water Agencies (ACWA).
\6\ 1997 Western Coalition of Arid States (WESTCAS) Research Committee Arsenic Occurrence Study which aggregated
arsenic data (e.g., median arsenic value for county, city, or provider) from Arizona, New Mexico, and Nevada.
B. What Databases Did EPA Use?
EPA evaluated the databases for representativeness, accuracy and
coverage of community water systems in the U.S. EPA determined that the
compliance monitoring data from the 25 States (``25-States database'')
would establish the most accurate and scientifically defensible
national occurrence and exposure distributions of arsenic in public
ground water and surface water supplies. Figure V.1 shows the coverage
of these States in the U.S. The 25-States database provides more
finished water arsenic data, from over 19,000 ground and surface water
CWSs, than the other national databases. EPA is interested in finished
water data, rather than raw water data, because it indicates the
current arsenic levels in water systems after treatment and reflects
their customers' level of exposure to arsenic. The 25-States database
provides system and individual arsenic data for a significant number of
CWSs in each State. The arsenic data can be linked directly to specific
water systems by their identification code to obtain additional
information in SDWIS, such as population served, system type (e.g.,
CWS, NTNCWS), source type (e.g., ground water, surface water, purchased
water, ground water under the influence), and location. For this
reason, EPA chose to use the compliance monitoring data from the States
of California, Nevada, New Mexico, and Arizona, rather than the data
about these States from ACWA and WESTCAS.
Most of the 25-States data had reporting limits of less than 2
µg/L. In addition, the database includes multiple samples from
the water systems over time and from multiple sources within the
systems. The multiple samples provide for a more accurate estimate of
the arsenic levels in the systems, than a survey with one sample per
system. The arsenic compliance monitoring data provides point-of-entry
or well data within systems from eight States, which is used for
intrasystem variability analysis (discussed in Section V.G).
Intrasystem variability analysis provides an understanding of the
variation of arsenic levels within a system, from well to well or ![[logo] US EPA](http://www.epa.gov/epafiles/images/logo_epaseal.gif){kind=logo}