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National Primary Drinking Water Regulations:
Disinfectants and Disinfection Byproducts
[Federal Register: December 16, 1998 (Volume 63, Number 241)]
[Rules and Regulations]
[Page 69389-69476]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr16de98-17]
[[Page 69389]]
_______________________________________________________________________
Part IV
Environmental Protection Agency
_______________________________________________________________________
40 CFR Parts 9, 141, and 142
National Primary Drinking Water Regulations: Disinfectants and
Disinfection Byproducts; Final Rule
[[Page 69390]]
ENVIRONMENTAL PROTECTION AGENCY
40 CFR Parts 9, 141, and 142
[WH-FRL-6199-8]
RIN 2040-AB82
National Primary Drinking Water Regulations: Disinfectants and
Disinfection Byproducts
AGENCY: Environmental Protection Agency (EPA).
ACTION: Final rule.
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SUMMARY: In this document, EPA is finalizing maximum residual
disinfectant level goals (MRDLGs) for chlorine, chloramines, and
chlorine dioxide; maximum contaminant level goals (MCLGs) for four
trihalomethanes (chloroform, bromodichloromethane,
dibromochloromethane, and bromoform), two haloacetic acids
(dichloroacetic acid and trichloroacetic acid), bromate, and chlorite;
and National Primary Drinking Water Regulations (NPDWRs) for three
disinfectants (chlorine, chloramines, and chlorine dioxide), two groups
of organic disinfection byproducts (total trihalomethanes (TTHMs)--a
sum of the four listed above, and haloacetic acids (HAA5)--a sum of the
two listed above plus monochloroacetic acid and mono-and dibromoacetic
acids), and two inorganic disinfection byproducts (chlorite and
bromate). The NPDWRs consist of maximum residual disinfectant levels
(MRDLs) or maximum contaminant levels (MCLs) or treatment techniques
for these disinfectants and their byproducts. The NPDWRs also include
monitoring, reporting, and public notification requirements for these
compounds. This document includes the best available technologies
(BATs) upon which the MRDLs and MCLs are based. The set of regulations
promulgated today is also know as the Stage 1 Disinfection Byproducts
Rule (DBPR). EPA believes the implementation of the Stage 1 DBPR will
reduce the levels of disinfectants and disinfection byproducts in
drinking water supplies. The Agency believes the rule will provide
public health protection for an additional 20 million households that
were not previously covered by drinking water rules for disinfection
byproducts. In addition, the rule will for the first time provide
public health protection from exposure to haloacetic acids, chlorite (a
major chlorine dioxide byproduct) and bromate (a major ozone
byproduct).
The Stage 1 DBPR applies to public water systems that are community
water systems (CWSs) and nontransient noncommunity water systems
(NTNCWs) that treat their water with a chemical disinfectant for either
primary or residual treatment. In addition, certain requirements for
chlorine dioxide apply to transient noncommunity water systems
(TNCWSs).
EFFECTIVE DATE: This regulation is effective February 16, 1999.
Compliance dates for specific components of the rule are discussed in
the Supplementary Information Section. The incorporation by reference
of certain publications listed in today's rule is approved by the
Director of the Federal Register as of February 16, 1999.
ADDRESSES: Public comments, the comment/response document, applicable
Federal Register documents, other major supporting documents, and a
copy of the index to the public docket for this rulemaking are
available for review at EPA's Drinking Water Docket: 401 M Street, SW.,
Washington, DC 20460 from 9 a.m. to 4 p.m., Eastern Standard Time,
Monday through Friday, excluding legal holidays. For access to docket
materials, please call 202/260-3027 to schedule an appointment and
obtain the room number.
FOR FURTHER INFORMATION CONTACT: For general information contact, the
Safe Drinking Water Hotline, Telephone (800) 426-4791. The Safe
Drinking Water Hotline is open Monday through Friday, excluding Federal
holidays, from 9:00 am to 5:30 pm Eastern Time. For technical
inquiries, contact Tom Grubbs, Office of Ground Water and Drinking
Water (MC 4607), U.S. Environmental Protection Agency, 401 M Street SW,
Washington, DC 20460; telephone (202) 260-7270. For Regional contacts
see Supplementary Information.
SUPPLEMENTARY INFORMATION: This regulation is effective 60 days after
publication of Federal Register document for purposes of the
Administrative Procedures Act and the Congressional Review Act.
Compliance dates for specific components of the rule are discussed
below. Solely for judicial review purposes, this final rule is
promulgated as of 1 p.m. Eastern Time December 30, 1998, as provided in
40 CFR 23.7.
Regulated entities. Entities regulated by the Stage 1 DBPR are
community and nontransient noncommunity water systems that add a
disinfectant during any part of the treatment process including a
residual disinfectant. In addition, certain provisions apply to
transient noncommunity systems that use chlorine dioxide. Regulated
categories and entities include:
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Category Examples of regulated entities
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Industry............................... Community and nontransient noncommunity water systems that treat their
water with a chemical disinfectant for either primary of residual
treatment. In addition, certain requirements for chlorine dioxide
apply to transient noncommunity water systems.
State, Local, Tribal, or Federal Same as above.
Governments.
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This 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 Sec. 141.130 of this rule. If you have
questions regarding the applicability of this action to a particular
entity, contact one of the persons listed in the preceding FOR FURTHER
INFORMATION CONTACT section or the Regional contacts below.
Regional Contacts
I. Kevin Reilly, Water Supply Section, JFK Federal Bldg., Room 203,
Boston, MA 02203, (617) 565-3616
II. Michael Lowy, Water Supply Section, 290 Broadway 24th Floor, New
York, NY 10007-1866, (212) 637-3830
III. Jason Gambatese, Drinking Water Section (3WM41), 1650 Arch Street,
Philadelphia, PA 19103-2029, (215) 814-5759
[[Page 69391]]
IV. David Parker, Water Supply Section, 345 Courtland Street, Atlanta,
GA 30365, (404) 562-9460
V. Miguel Del Toral, Water Supply Section, 77 W. Jackson Blvd.,
Chicago, IL 60604, (312) 886-5253
VI. Blake L. Atkins, Drinking Water Section, 1445 Ross Avenue, Dallas,
TX 75202, (214) 665-2297
VII. Ralph Flournoy, Drinking Water/Ground Water Management Branch, 726
Minnesota Ave., Kansas City, KS 66101, (913) 551-7374
VIII. Bob Clement, Public Water Supply Section (8P2-W-MS), 999 18th
Street, Suite 500, Denver, CO 80202-2466, (303) 312-6653
IX. Bruce Macler, Water Supply Section, 75 Hawthorne Street, San
Francisco, CA 94105, (415) 744-1884
X. Wendy Marshall, Drinking Water Unit, 1200 Sixth Avenue (OW-136),
Seattle, WA 98101, (206) 553-1890
Abbreviations Used in This Document
AWWA: American Water Works Association
AWWSCo: American Water Works Service Company
BAT: Best available technology
BDCM: Bromodichloromethane
CDC: Centers for Disease Control and Prevention
C.I.: Confidence Intervals
CMA: Chemicals Manufacturers Association
CPE: Comprehensive performance evaluation
CWS: Community water system
DBCM: Dibromochloromethane
DBP: Disinfection byproducts
D/DBP: Disinfectants and disinfection byproducts
DBPR: Disinfection Byproducts Rule
DBPRAM: Disinfection byproducts regulatory analysis model
DCA: Dichloroacetic acid
DOC: Dissolved organic carbon
DWSRF: Drinking Water State Revolving Fund
EC: Enhanced coagulation
EJ: Environmental justice
EPA: United States Environmental Protection Agency
ESWTR: Enhanced Surface Water Treatment Rule
FACA: Federal Advisory Committee Act
GAC10: Granular activated carbon with ten minute empty bed contact time
and 180 day reactivation frequency
GAC20: Granular activated carbon with twenty minute empty bed contact
time and 180 day reactivation frequency
GDP: Gross Domestic Product
GWR: Groundwater rule
HAA5: Haloacetic acids (five)(chloroacetic acid, dichloroacetic acid,
trichloroacetic acid, bromoacetic acid, and dibromoacetic acid)
HAN: Haloacetonitriles
ICR: Information collection rule (issued under section 1412(b) of the
SDWA)
ILSI: International Life Sciences Institute
IESTWR: Interim Enhanced Surface Water Treatment Rule
LOAEL: Lowest Observed Adverse Effect Level
LT1ESTWR: Long-Term 1Enhanced Surface Water Treatment Rule
MCL: Maximum contaminant level
MCLG: Maximum contaminant level goal
M-DBP: Microbial and Disinfectants/Disinfection Byproducts
mg/L: Milligrams per liter
MRDL: Maximum residual disinfectant level
MRDLG: Maximum residual disinfectant level goal
NDWAC: National Drinking Water Advisory Council
NIST: National Institute of Science and Technology
NOAEL: No Observed Adverse Effect Level
NODA: Notice of Data Availability
NOM: Natural organic matter
NPDWR: National Primary Drinking Water Regulation
NTNCWS: Nontransient noncommunity water system
NTP: National Toxicology Program
NTTAA: National Technology Transfer and Advancement Act
NTU: Nephelometric turbidity unit
OMB: Office of Management and Budget
PAR: Population attributable risk
PBMS: Performance based measurement system
PE: Performance evaluation
PODR: Point of diminishing return
PQL: Practical quantitation limit
PWS: Public water system
QC: Quality control
Reg. Neg.: Regulatory Negotiation
RFA: Regulatory Flexibility Act
RfD: Reference dose
RIA: Regulatory impact analysis
RSC: Relative source contribution
SAB: Science Advisory Board
SBREFA: Small Business Regulatory Enforcement Fairness Act
SDWIS: Safe Drinking Water Information System
SUVA: Specific ultraviolet absorbance
SDWA: Safe Drinking Water Act, or the ``Act,'' as amended 1996
SWTR: Surface Water Treatment Rule
TC: Total coliforms
TCA: Trichloroacetic acid
TCR: Total Coliform Rule
TOC: Total organic carbon
TOX: Total organic halides
TTHM: Total trihalomethanes (chloroform, bromdichloromethane,
dibromochloromethane, and bromoform)
TNCWS: Transient noncommunity water systems
TWG: Technical work group
UMRA: Unfunded mandates reform act
URTH: Unreasonable risk to health
WIDB: Water Industry Data Base
Table of Contents
I. Background
A. Statutory Requirements and Legal Authority
B. Regulatory History
1. Existing Regulations
2. Public Health Concerns To Be Addressed
3. Regulatory Negotiation Process
4. Federal Advisory Committee Process
5. 1997 and 1998 Notices of Data Availability (NODA)
II. Summary of Final Stage 1 Disinfection Byproduct Rule
A. Applicability
B. MRDLGs and MRDLs for Disinfectants
C. MCLGs and MCLs for TTHMs, HAA5, Chlorite, and Bromate
D. Treatment Technique for Disinfection Byproducts Precursors
E. BAT for Disinfectants, TTHMs, HAA5, Chlorite, and Bromate
F. Compliance Monitoring Requirements
G. Analytical Methods
H. Laboratory Certification Criteria
I. Variances and Exemptions
J. State Recordkeeping, Primacy, Reporting Requirements
K. System Reporting Requirements
L. Guidance Manuals
M. Regulation Review
III. Explanation of Final Rule
A. MCLGs/MRDLGs
1. MCLG for Chloroform
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
2. MCLG for Bromodichloromethane (BDCM)
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
3. MCLG for Dibromochloromethane (DBCM)
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
4. MCLG for Bromoform
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
5. MCLG for Dichloroacetic Acid (DCA)
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
6. MCLG for Trichloroacetic Acid (TCA)
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
7. MCLG for Chlorite and MRDLG for Chlorine Dioxide
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
8. MCLG for Bromate
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
[[Page 69392]]
9. MCLG for Chloral Hydrate
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
10. MRDLG for Chlorine
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
11. MRDLG for Chloramine
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
B. Epidemiology
1. Cancer Epidemiology
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
2. Reproductive and Developmental Epidemiology
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
C. MCLs and BAT for TTHM, HAA5, Chlorite, and Bromate; MRDLs and
BAT for Chlorine, Chloramines, and Chlorine Dioxide
1. MCLs for TTHMs and HAA5
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
2. MCL for Bromate
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
3. MCL for Chlorite
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
4. MRDL for Chlorine
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
5. MRDL for Chloramines
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
6. MRDL for Chlorine Dioxide
a. Today's Rule
b. Background Analysis
c. Summary of Comments
D. Treatment Technique Requirement
1. Today's Rule
2. Background and Analysis
3. Summary of Comments
E. Predisinfection Disinfection Credit
1. Today's Rule
2. Background and Analysis
3. Summary of Comments
F. Requirements for Systems to Use Qualified Operators
G. Analytical Methods
1. Today's Rule
2. Background and Analysis
3. Summary of Comments
4. Performance Based Measurement Systems
H. Monitoring Requirements
1. Today's Rule
2. Background and Analysis
3. Summary of Comments
I. Compliance Schedules
1. Today's Rule
2. Background and Analysis
3. Summary of Comments
J. Public Notice Requirements
1. Today's Rule
2. Background and Analysis
3. Summary of Comments
K. System Reporting and Record Keeping Requirements
1. Today's Rule
2. Summary of Comments
L. State Recordkeeping, Primacy, and Reporting Requirements
1. State Recordkeeping Requirements
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
2. Special Primacy Requirements
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
3. State Reporting Requirements
a. Today's Rule
b. Background and Analysis
c. Summary of Comments
M. Variances and Exemptions
1. Today's Rule
2. Background and Analysis
3. Summary of Comments
N. Laboratory Certification and Approval
1. Today's Rule
2. Background and Analysis
3. Summary of Comments
IV. Economic Analysis
A. Today's Rule
B. Background
1. Overview of RIA for the Proposed Rule
2. Factors Affecting Changes to the 1994 RIA
a. Changes in Rule Criteria
b. New Information Affecting DBP Occurrence and Compliance
Forecast
c. New Epidemiology Information
C. Cost Analysis
1. Revised Compliance Forecast
2. System Level Unit Costs
3. National Costs
D. Benefits Analysis
1. Exposure Assessment
2. Baseline Risk Assessment Based on TTHM Toxicological Data
3. Baseline Analysis Based on Epidemiology Data
4. Exposure Reduction Analysis
5. Monetization of Health Endpoints
E. Net Benefits Analysis
F. Summary of Comments
V. Other Requirements
A. Regulatory Flexibility Analysis
1. Today's Rule
2. Background and Analysis
3. Summary of Comments
B. Paperwork Reduction Act
C. Unfunded Mandates Reform Act
1. Summary of UMRA Requirements
2. Written Statement for Rules with Federal Mandates of $100
million or More
a. Authorizing Legislation
b. Cost Benefit Analysis
c. Estimates of Future Compliance Costs and Disproportionate
Budgetary Effects
d. Macro-economic Effects
e. Summary of State, Local, and Tribal Government and
TheirConcerns
f. Regulatory Alternative Considered
3. Impacts on Small Governments
D. National Technology Transfer and Advancement Act
E. Executive Order 12866: Regulatory Planning and Review
F. Executive Order 12898: Environmental Justice
G. Executive Order 13045: Protection of Children from
Environmental Health Risks and Safety Risks
H. Consultation with the Science Advisory Board, National
Drinking Water Advisory Council, and the Secretary of Health and
Human Services
I. Executive Order 12875: Enhancing the Intergovernmental
Partnership
J. Executive Order 13084: Consultation and Coordination with
Indian Tribal Governments
K. Submission to Congress and the General Accounting Office
L. Likely Effect of Compliance with the Stage 1 DBPR on the
Technical, Financial, and Managerial Capacity of Public Water
Systems
VI. References
I. Background
A. Statutory Requirements and Legal Authority
The Safe Drinking Water Act (SDWA or the Act), as amended in 1986,
requires USEPA to publish a ``maximum contaminant level goal'' (MCLG)
for each contaminant which, in the judgement of the USEPA
Administrator, ``may have any adverse effect on the health of persons
and which is known or anticipated to occur in public water systems''
(Section 1412(b)(3)(A)). MCLGs are to be set at a level at which ``no
known or anticipated adverse effect on the health of persons occur and
which allows an adequate margin of safety'' (Section 1412(b)(4)).
The Act was amended in August 1996. As a result of these
Amendments, several of these provisions were renumbered and augmented
with additional language. Other sections were added establishing new
drinking water requirements. These modifications are outlined below.
The Act also requires that at the same time USEPA publishes an
MCLG, which is a non-enforceable health goal, it also must publish a
National Primary Drinking Water Regulation (NPDWR) that specifies
either a maximum contaminant level (MCL) or treatment technique
(Sections 1401(1) and 1412(a)(3)). USEPA is authorized to promulgate a
NPDWR ``that requires the use of a treatment technique in lieu of
establishing a MCL,'' if the Agency finds that ``it is not economically
or technologically feasible to ascertain the level of the
contaminant''.
As amended, EPA's general authority to set a maximum contaminant
level goal (MCLG) and National Primary Drinking Water Regulation
(NPDWR) applies to contaminants that may ``have an adverse effect on
the health of persons,'' that are ``known to occur or there is a
substantial likelihood that the contaminant will occur in public water
[[Page 69393]]
systems with a frequency and at levels of public health concern,'' and
for which ``in the sole judgement of the Administrator, regulation of
such contaminant presents a meaningful opportunity for health risk
reduction for persons served by public water systems'' (SDWA Section
1412(b)(1)(A)).
The amendments, also require EPA, when proposing a NPDWR that
includes an MCL or treatment technique, to publish and seek public
comment on an analysis of health risk reduction and cost impacts. In
addition, EPA is required to take into consideration the effects of
contaminants upon sensitive subpopulations (i.e. infants, children,
pregnant women, the elderly, and individuals with a history of serious
illness), and other relevant factors. (Section 1412 (b)(3)(C)).
The amendments established a number of regulatory deadlines,
including schedules for a Stage 1 Disinfection Byproduct Rule (DBPR),
an Interim Enhanced Surface Water Treatment Rule (IESWTR), a Long-Term
Final Enhanced Surface Water Treatment Rule (LTESWTR) affecting Public
Water Systems (PWSs) that serve under 10,000 people, and a Stage 2 DBPR
(Section 1412(b)(2)(C)). The Act as amended also requires EPA to
promulgate regulations to address filter backwash (Section
1412(b)(14)). Finally, the Act requires EPA to promulgate regulations
specifying criteria for requiring disinfection ``as necessary'' for
ground water systems (Section 1412 (b)(8)).
Finally, as part of the 1996 SDWA Amendments, recordkeeping
requirements were modified to apply to ``every person who is subject to
a requirement of this title or who is a grantee'' (Section 1445
(a)(1)(A)). Such persons are required to ``establish and maintain such
records, make such reports, conduct such monitoring, and provide such
information as the Administrator may reasonably require by regulation *
* * ''.
B. Regulatory History
1. Existing Regulations
Surface Water Treatment Rule. Under the Surface Water Treatment
Rule (SWTR) (54 FR 27486, June 29, 1989) (EPA,1989a), EPA set maximum
contaminant level goals of zero for Giardia lamblia, viruses, and
Legionella; and promulgated NPDWR for all PWSs using surface water
sources or ground water sources under the direct influence of surface
water. The SWTR includes treatment technique requirements for filtered
and unfiltered systems that are intended to protect against the adverse
health effects of exposure to Giardia lamblia, viruses, and Legionella,
as well as many other pathogenic organisms. Briefly, those requirements
include: (1) requirements for a maintenance of a disinfectant residual
in the distribution system; (2) removal and/or inactivation of 3 logs
(99.9%) for Giardia and 4 logs (99.99%) for viruses; (3) combined
filter effluent performance of 5 nephelometric turbidity unit (NTU) as
a maximum and 0.5 NTU at 95th percentile monthly, based on 4-hour
monitoring for treatment plants using conventional treatment or direct
filtration (with separate standards for other filtration technologies);
and (4) watershed protection and other requirements for unfiltered
systems.
Total Coliform Rule. The Total Coliform Rule (TCR) (54 FR 27544;
June 29, 1989) applies to all public water systems (EPA, 1989b). This
regulation sets compliance with the MCL for total coliforms (TC) as
follows. For systems that collect 40 or more samples per month, no more
than 5.0% of the samples may be TC-positive; for those that collect
fewer than 40 samples, no more than one sample may be TC-positive. In
addition, if two consecutive samples in the system are TC-positive, and
one is also fecal coliform or E. coli-positive, then this is defined as
an acute violation of the MCL. If a system exceeds the MCL, it must
notify the public using mandatory language developed by the EPA. The
required monitoring frequency for a system depends on the number of
people served and, ranges from 480 samples per month for the largest
systems to once annually for certain of the smallest systems. All
systems must have a written plan identifying where samples are to be
collected.
If a system has a TC-positive sample, it must test that sample for
the presence of fecal coliforms or E. coli. The system must also
collect a set of repeat samples, and analyze for TC (and fecal coliform
or E. coli) within 24 hours of the first TC-positive sample.
The TCR also requires an on-site inspection every 5 years (10 years
for non-community systems using only protected and disinfected ground
water) for each system that collects fewer than five samples per month.
This on-site inspection (referred to as a sanitary survey) must be
performed by the State or by an agent approved by the State.
Total Trihalomethane Rule. In November 1979 (44 FR 68624) (EPA,
1979) EPA set an interim MCL for total trihalomethanes (TTHM) of 0.10
milligrams per liter (mg/L) as an annual average. Compliance is defined
on the basis of a running annual average of quarterly averages of all
samples. The value for each sample is the sum of the measured
concentrations of chloroform, bromodichloromethane (BDCM),
dibromochloromethane (DBCM) and bromoform.
The interim TTHM standard only applies to community water systems
using surface water and/or ground water serving at least 10,000 people
that add a disinfectant to the drinking water during any part of the
treatment process. At their discretion, States may extend coverage to
smaller PWSs; however, most States have not exercised this option.
Information Collection Rule. The Information Collection Rule (ICR)
is a monitoring and data reporting rule that was promulgated on May 14,
1996 (61 FR 24354) (EPA, 1996a). The purpose of the ICR is to collect
occurrence and treatment information to help evaluate the need for
possible changes to the current SWTR and existing microbial treatment
practices, and to help evaluate the need for future regulation for
disinfectants and disinfection byproducts (D/DBPs). The ICR will
provide EPA with additional information on the national occurrence in
drinking water of (1) chemical byproducts that form when disinfectants
used for microbial control react with naturally occurring compounds
already present in source water and (2) disease-causing microorganisms,
including Cryptosporidium, Giardia, and viruses. The ICR will also
provide engineering data on how PWSs currently control for such
contaminants. This information is being collected because the 1992
Regulatory Negotiating Committee (henceforth referred to as the Reg.
Neg. Committee) on microbial pathogens and disinfectants and DBPs
concluded that additional information was needed to assess the
potential health problem created by the presence of DBPs and pathogens
in drinking water and to assess the extent and severity of risk in
order to make sound regulatory and public health decisions. The ICR
will also provide information to support regulatory impact analyses for
various regulatory options, and to help develop monitoring strategies
for cost-effectively implementing regulations.
The ICR pertains to large public water systems serving populations
at least 100,000; a more limited set of ICR requirements pertain to
ground water systems serving between 50,000 and 100,000 people. About
300 PWSs operating 500 treatment plants are involved with the extensive
ICR data collection. Under the ICR, these PWSs monitor for water
quality factors affecting DBP formation and DBPs
[[Page 69394]]
within the treatment plant and in the distribution system monthly for
18 months. In addition, PWSs must provide operating data and a
description of their treatment plan design and surface water systems
must monitor for bacteria, viruses, and protozoa. Finally, a subset of
PWSs must perform treatment studies, using either granular activated
carbon (GAC) or membrane processes, to evaluate DBP precursor removal
and control of DBPs. Monitoring for treatment study applicability began
in September 1996. The remaining occurrence monitoring began in July
1997.
One initial intent of the ICR was to collect pathogen occurrence
data and other information for use in developing the IESWTR and to
estimate national costs for various treatment options. However, because
of delays in promulgating the ICR and technical difficulties associated
with laboratory approval and review of facility sampling plans, ICR
monitoring did not begin until July 1, 1997, which was later than
originally anticipated. As a result of this delay and the new statutory
deadlines for promulgating the Stage 1 DBPR and IESWTR in November of
1998 (resulting from the 1996 SDWA amendments), ICR data were not
available in time to support these rules. In place of the ICR data, the
Agency worked with stakeholders to identify other sources of data
developed since 1994 that could be used to support the development of
the Stage 1 DBPR and IESWTR. EPA will continue to work with
stakeholders in analyzing and using the comprehensive ICR data and
research for developing future Enhanced Surface Water Treatment
requirements and the Stage 2 DBPR.
2. Public Health Concerns to be Addressed
EPA's main mission is the protection of human health and the
environment. When carrying out this mission, EPA must often make
regulatory decisions with less than complete information and with
uncertainties in the available information. EPA believes it is
appropriate and prudent to err on the side of public health protection
when there are indications that exposure to a contaminant may present
risks to public health, rather than take no action until risks are
unequivocally proven.
In regard to the Stage 1 DBPR, EPA recognizes that the assessment
of public health risks from disinfection of drinking water currently
relies on inherently difficult and preliminary empirical analysis. On
one hand, epidemiologic studies of the populations in various
geographic areas are hampered by difficulties of study design, scope,
and sensitivity. On the other hand, uncertainty is involved in the
interpretation of results using high dose animal toxicological studies
of a few of the numerous byproducts that occur in disinfected drinking
water to estimate the risk to humans from chronic exposure to low doses
of these and other byproducts. Such studies of individual DBPs is
insufficient to characterize risks from exposure to the entire mixture
of DBPs in disinfected drinking water. While recognizing these
uncertainties, EPA continues to believe that the Stage 1 DBPR is
necessary for the protection of public health from exposure to
potentially harmful DBPs.
A fundamental component in assessing the risk for a contaminant is
the number of people that may be exposed to the parameter of concern.
In this case, there is a very large population potentially exposed to
DBPs through drinking water in the U.S. Over 200 million people are
served by PWSs that apply a disinfectant (e.g., chlorine) to water in
order to provide protection against microbial contaminants. While these
disinfectants are effective in controlling many microorganisms, they
react with natural organic and inorganic matter in the water to form
DBPs, some of which may pose health risks. One of the most complex
questions facing water supply professionals is how to minimize the
risks from DBPs and still maintain adequate control over microbial
contaminants. Because of the large number of people exposed to DBPs,
there is a substantial concern for any risks associated with DBPs that
may impact public health.
Since the discovery of chlorination byproducts in drinking water in
1974, numerous toxicological studies have been conducted. Results from
these studies have shown several DBPs (e.g., bromodichloromethane,
bromoform, chloroform, dichloroacetic acid, and bromate) to be
carcinogenic in laboratory animals . Some DBPs (e.g., chlorite, BDCM,
and certain haloacetic acids) have also been shown to cause adverse
reproductive or developmental effects in laboratory animals. Although
many of these studies have been conducted at high doses, EPA believes
the studies provide evidence that DBPs present a potential public
health risk that needs to be addressed.
In the area of epidemiology, a number of epidemiology studies have
been conducted to investigate the relationship between exposure to
chlorinated surface water and cancer. While EPA cannot conclude there
is a causal link between exposure to chlorinated surface water and
cancer, these studies have suggested an association, albeit small,
between bladder, rectal, and colon cancer and exposure to chlorinated
surface water. While there are fewer published epidemiology studies
that have been conducted to evaluate the possible relationship between
exposure to chlorinated surface water and reproductive and
developmental effects, a recent study has suggested an association
between early term miscarriage and exposure to drinking water with
elevated trihalomethane levels. In addition to this study, another new
study reported a small increased risk of neural tube defects associated
with consumption of drinking water containing high levels of TTHMs.
However, no significant associations were observed with individual
THMs, HAAs, and haloacetonitriles (HANs) and adverse outcomes in this
study. As with cancer, EPA cannot conclude at this time there is a
causal link between exposure to DBPs and reproductive and developmental
effects.
While EPA recognizes there are data deficiencies in the information
on the health effects from the DBPs and the levels at which they occur,
the Agency believes the weight-of-evidence presented by the available
epidemiological studies on chlorinated drinking water and toxicological
studies on individual DBPs support a potential hazard concern and
warrant regulatory action at this time to reduce DBP levels in drinking
water. Recognizing the deficiencies in the existing data, EPA believes
the incremental two-stage approach for regulating DBPs, agreed upon by
the regulatory negotiation process, is prudent and necessary to protect
public health and meet the requirements of the SDWA.
In conclusion, because of the large number of people exposed to
DBPs and the different potential health risks (e.g., cancer and adverse
reproductive and developmental effects) that may result from exposure
to DBPs, EPA believes the Stage 1 DBPR is needed to further prevent
potential health effects from DBPs, beyond that controlled for by the
1979 total trihalomethane rule. Both the Reg. Neg. Committee for the
1994 proposed rule and the Microbial and Disinfectants/Disinfection
Byproducts Advisory Committee (henceforth cited as the M-DBP Advisory
Committee) formed in March 1997 under the Federal Advisory Committee
Act (FACA), agreed with the need for the Stage 1 DBPR to reduce
potential risks from DBPs in the near term, while acknowledging
additional information is still needed for the Stage 2 DBPR (especially
on health effects),
[[Page 69395]]
3. Regulatory Negotiation Process
In 1992 EPA initiated a negotiated rulemaking to address public
health concerns associated with disinfectants, DBPs, and microbial
pathogens. The negotiators included representatives of State and local
health and regulatory agencies, public water systems, elected
officials, consumer groups and environmental groups. The Reg. Neg.
Committee met from November 1992 through June 1993.
Early in the process, the negotiators agreed that large amounts of
information necessary to understand how to optimize the use of
disinfectants to concurrently minimize microbial and DBP risk on a
plant-specific basis were unavailable. Nevertheless, the Reg. Neg.
Committee agreed that EPA propose a Stage 1 DBPR to extend coverage to
all community and nontransient noncommunity water systems that use
disinfectants, reduce the current TTHM MCL, regulate additional DBPs,
set limits for the use of disinfectants, and reduce the level of
organic precursor compounds in the source water that may react with
disinfectants to form DBPs.
EPA's most significant concern in developing regulations for
disinfectants and DBPs was the need to ensure that adequate treatment
be maintained for controlling risks from microbial pathogens. One of
the major goals addressed by the Reg. Neg. Committee was to develop an
approach that would reduce the level of exposure from disinfectants and
DBPs without undermining the control of microbial pathogens. The
intention was to ensure that drinking water is microbiologically safe
at the limits set for disinfectants and DBPs and that these chemicals
do not pose an unacceptable health risk at these limits. Thus, the Reg.
Neg. Committee also considered a range of microbial issues and agreed
that EPA should also propose a companion microbial rule (IESWTR).
Following months of intensive discussions and technical analysis,
the Reg. Neg. Committee recommended the development of three sets of
rules: a two-staged approach for the DBPs (proposal: 59 FR 38668, July
29, 1994) (EPA, 1994a), an ``interim'' ESWTR (proposal: 59 FR 38832,
July 29, 1994) (EPA, 1994b), and an information collection rule
(proposal: 59 FR 6332, February 10, 1994) (EPA, 1994c) (promulgation:
61FR24354, May 14, 1996) (EPA, 1996a). The approach used in developing
these proposals considered the constraints of simultaneously treating
water to control for both microbial contaminants and D/DBPs.
The Reg. Neg. Committee agreed that the schedules for IESWTR and
LTESWTR should be ``linked'' to the schedule for the Stage 1 DBPR to
assure simultaneous compliance and a balanced risk-risk based
implementation. The Reg. Neg. Committee agreed that additional
information on health risk, occurrence, treatment technologies, and
analytical methods needed to be developed in order to better understand
the risk-risk tradeoff, and how to accomplish an overall reduction in
health risks to both pathogens and D/DBPs.
Finally the Reg. Neg. Committee agreed that to develop a reasonable
set of rules and to understand more fully the limitations of the
current SWTR, additional field data were critical. Thus, a key
component of the regulation negotiation agreement was the promulgation
of the ICR previously described.
4. Federal Advisory Committee Process
In May 1996, the Agency initiated a series of public informational
meetings to provide an update on the status of the 1994 proposal and to
review new data related to microbial and DBP regulations that had been
developed since July 1994. In August 1996, Congress enacted the 1996
SDWA Amendments which contained a number of new requirements, as
discussed above, as well as specifying deadlines for final promulgation
of the IESWTR and Stage 1 DBPR. To meet these deadlines and to maximize
stakeholder participation, the Agency established the M-DBP Advisory
Committee under FACA in March 1997, to collect, share, and analyze new
information and data, as well as to build consensus on the regulatory
implications of this new information. The Committee consisted of 17
members representing EPA, State and local public health and regulatory
agencies, local elected officials, drinking water suppliers, chemical
and equipment manufacturers, and public interest groups.
The M-DBP Advisory Committee met five times in March through July
1997 to discuss issues related to the IESWTR and Stage 1 DBPR.
Technical support for these discussions was provided by a Technical
Work Group (TWG) established by the Committee at its first meeting in
March 1997. The Committee's activities resulted in the collection,
development, evaluation, and presentation of substantial new data and
information related to key elements of both proposed rules. The
Committee reached agreement on a number of major issues that were
discussed in Notices of Data Availability (NODA) for the IESWTR (62 FR
59486, November 3, 1997) (EPA, 1997a) and the Stage 1 DBPR (62 FR
59388, November 3, 1997) (EPA, 1997b). The major recommendations
addressed by the Committee and in the NODAs were to: (1) Maintain the
proposed MCLs for TTHM, HAA5, and bromate; (2) modify the enhanced
coagulation requirements as part of DBP control; (3) include a
microbial benchmarking/profiling to provide a methodology and process
by which a PWS and the State, working together, assure that there will
be no significant reduction in microbial protection as the result of
modifying disinfection practices in order to meet MCLs for TTHM and
HAA5; (4) continue credit for compliance with applicable disinfection
requirements for disinfection applied at any point prior to the first
customer, consistent with the existing SWTR; (5) modify the turbidity
performance requirements and add requirements for individual filters;
(6) establish an MCLG for Cryptosporidium; (7) add requirements for
removal of Cryptosporidium; (8) provide for mandatory sanitary surveys;
and (9) make a commitment to additional analysis of the role of
Cryptosporidium inactivation as part of a multiple barrier concept in
the context of a subsequent Federal Register microbial proposal. The
new data and analysis supporting the technical areas of agreement were
summarized and explained at length in EPA's 1997 NODAs (EPA, 1997a and
EPA, 1997b).
5. 1997 and 1998 Notices of Data Availability
In November 1997 EPA published a NODA (USEPA, 1997b) that
summarized the 1994 proposal; described new data and information that
the Agency has obtained and analyses that have been developed since the
proposal; provided information concerning the July 1997 recommendations
of the M-DBP Advisory Committee on key issues related to the proposal
(described above); and requested comment on these recommendations, as
well as on other regulatory implications that flow from the new data
and information. The Agency solicited additional data and information
that were relevant to the issues discussed in the DBP NODA. EPA also
requested that any information the Agency should consider as part of
the final rule development process regarding data or views submitted to
the Agency since the close of the comment period on the 1994 proposal,
be formally resubmitted during the 90-day
[[Page 69396]]
comment period unless already in the underlying record in the docket
for the NODA.
In March 1998, EPA issued a second DBP NODA (EPA, 1998a) that
summarized new health effects information received and analyzed since
the November 1997 NODA and requested comments on several issues related
to the simultaneous compliance with the Stage 1 DBPR and the Lead and
Copper Rule. The 1998 NODA indicated EPA was considering increasing the
MCLG for chloroform from zero to 0.3 mg/L and the proposed MCLG for
chlorite from 0.08 mg/L to 0.8 mg/L. EPA also requested comment on
increasing the Maximum Residual Disinfection Level Goal (MRDLG) for
chlorine dioxide from 0.3 mg/L to 0.8 mg/L. Today's final rule was
developed based on the outcome of the 1992 Reg. Neg., the 1994 proposed
rule, the 1997 FACA process, and both the 1997 and 1998 DBP NODAs, as
well as a wide range of technical comments from stakeholders and
members of the public. A summary of today's rule follows.
II. Summary of Final Stage 1 Disinfection Byproduct Rule
A. Applicability
The final Stage 1 DBPR applies to community water systems (CWSs)
and nontransient noncommunity water systems (NTNCWs) that treat their
water with a chemical disinfectant for either primary or residual
treatment. In addition, certain requirements for chlorine dioxide apply
to transient noncommunity water systems (TNCWSs).
B. MRDLGs and MRDLs for Disinfectants
EPA is finalizing the following MRDLGs and maximum residual
disinfectant levels (MRDLs) for chlorine, chloramines, and chlorine
dioxide in Table II-1.
Table II-1.--MRDLGs and MRDLs for Disinfectants
----------------------------------------------------------------------------------------------------------------
Disinfectant residual MRDLG (mg/L) MRDL (mg/L)
----------------------------------------------------------------------------------------------------------------
Chlorine................................ 4 (as Cl<INF>2) 4.0 (as Cl<INF>2)
Chloramine.............................. 4 (as Cl<INF>2) 4.0 (as Cl<INF>2)
Chlorine Dioxide........................ 0.8 (as ClO<INF>2) 0.8 (as ClO<INF>2)
----------------------------------------------------------------------------------------------------------------
C. MCLGs and MCLs for TTHMs, HAA5, Chlorite, and Bromate
EPA is finalizing the MCLGs and MCLs in Table II-2.
Table II-2.--MCLGs and MCLs for Disinfection Byproducts
------------------------------------------------------------------------
Disinfection byproducts MCLG (mg/L) MCL (mg/L)
------------------------------------------------------------------------
Total trihalomethanes (TTHM) \1\............ N/A 0.080
--Chloroform............................ 0 ............
--Bromodichloromethane.................. 0 ............
--Dibromochloromethane.................. 0.06 ............
--Bromoform............................. 0 ............
Haloacetic acids (five) (HAA5) \2\.......... N/A 0.060
--Dichloroacetic acid................... 0 ............
--Trichloroacetic acid.................. 0.3 ............
Chlorite.................................... 0.8 1.0
Bromate..................................... 0 0.010
------------------------------------------------------------------------
N/A--Not applicable because there are no individual MCLGs for TTHMs or
HAAs.
\1\ Total trihalomethanes is the sum of the concentrations of
chloroform, bromodichloromethane, dibromochloromethane, and bromoform.
\2\ Haloacetic acids (five) is the sum of the concentrations of mono-,
di-, and trichloroacetic acids and mono- and dibromoacetic acids.
D. Treatment Technique for Disinfection Byproduct Precursors
Water systems that use surface water or ground water under the
direct influence of surface water and use conventional filtration
treatment are required to remove specified percentages of organic
materials (measured as total organic carbon) that may react with
disinfectants to form DBPs as indicated in Table II-3. Removal will be
achieved through a treatment technique (enhanced coagulation or
enhanced softening) unless a system meets alternative criteria
discussed in Section III.D.
Table II-3.--Required Removal of Total Organic Carbon by Enhanced
Coagulation and Enhanced Softening for Subpart H Systems Using
Conventional Treatment <SUP>a,\<SUP>b,\<SUP>c
------------------------------------------------------------------------
Source Water Alkalinity (mg/L as
CaCO<INF>3) (percent)
Source Water TOC (mg/L) --------------------------------------
0-60 >60-120 >120
------------------------------------------------------------------------
>2.0-4.0......................... 35.0 25.0 15.0
>4.0-8.0......................... 45.0 35.0 25.0
[[Page 69397]]
>8.0............................. 50.0 40.0 30.0
------------------------------------------------------------------------
<SUP>a Systems meeting at least one of the conditions in Section
141.135(a)(2) (i)-(vi) of the rule are not required to operate the
removals in this table.
<SUP>b Softening systems meeting one of the two alternative compliance
criteria in Section 141.135(a)(3) of the rule are not required to meet
the removals in this table.
<SUP>c Systems practicing softening must meet the TOC removal requirements in
the last column to the right.
E. BAT for Disinfectants, TTHMs, HAA5, Chlorite, and Bromate
Under the SDWA, EPA must specify the BAT for each MCL (or MRDL)
that is set. PWS that are unable to achieve an MCL or MRDL may be
granted a variance if they use the BAT and meet other requirements (see
section III.M for a discussion of variances and exemptions). Table II.4
includes the BATs for each of the MCLs or MRDLs that EPA is
promulgating in today's Stage 1 DBPR.
Table II-4.--BAT for Disinfectants and Disinfection Byproducts
------------------------------------------------------------------------
Disinfectant/DBP Best available technology
------------------------------------------------------------------------
Disinfectants
------------------------------------------------------------------------
Chlorine residual............ Control of treatment processes to reduce
disinfectant demand and control of
disinfection treatment processes to
reduce disinfectant levels.
Chloramine residual.......... Control of treatment processes to reduce
disinfectant demand and control of
disinfection treatment processes to
reduce disinfectant levels.
Chlorine dioxide residual.... Control of treatment processes to reduce
disinfectant demand and control of
disinfection treatment processes to
reduce disinfectant levels.
------------------------------------------------------------------------
Disinfection Byproducts
------------------------------------------------------------------------
Total trihalomethanes........ Enhanced coagulation or enhanced
softening or GAC10*, with chlorine as
the primary and residual disinfectant.
Total haloacetic acids....... Enhanced coagulation or enhanced
softening or GAC10*, with chlorine as
the primary and residual disinfectant.
Chlorite..................... Control of treatment processes to reduce
disinfectant demand and control of
disinfection treatment processes to
reduce disinfectant levels.
Bromate...................... Control of ozone treatment process to
reduce production of bromate.
------------------------------------------------------------------------
* GAC10 means granular activated carbon with an empty bed contact time
of 10 minutes and reactivation frequency for GAC of no more than six
months.
F. Compliance Monitoring Requirements
Compliance monitoring requirements are explained in Section III.H
of today's rule. EPA has developed routine and reduced compliance
monitoring schemes for disinfectants and DBPs to be protective from
different types of health concerns, including acute and long-term
effects.
G. Analytical Methods
EPA has approved five methods for measurement of free chlorine,
four methods for combined chlorine, and six for total chlorine. EPA has
also approved two methods for the measurement of chlorine dioxide
residuals; three methods for the measurement of HAA5; three methods for
the measurement of TTHMs; three methods for the measurement of TOC/
Dissolved Organic Carbon (DOC); two methods for the monthly measurement
of chlorite and one method for the daily monitoring of chlorite; two
methods for bromide; one method for the measurement of bromate; and one
method for the measurement of UV<INF>254</INF>. Finally, EPA approved
all methods allowed in Sec. 141.89(a) for measuring alkalinity. These
issues are discussed in more detail in section III.G.
H. Laboratory Certification Criteria
Consistent with other drinking water regulations, determinations of
compliance with the MCLs may only be conducted by certified
laboratories. EPA is requiring that analyses can be conducted by a
party acceptable to EPA or the State in those situations where the
parameter can adequately be measured by someone other than a certified
laboratory and for which there is a good reason to allow analysis at
other locations (e.g., for samples which normally deteriorate before
reaching a certified laboratory, especially when taken at remote
locations). For a detailed discussion of the lab certification
requirements, see section III.N.
I. Variances and Exemptions
Variances and exemptions will be permitted in accordance with
existing statutory and regulatory authority. For a detailed discussion
see section III.M.
J. State Recordkeeping, Primacy, and Reporting Requirements
The Stage 1 DBPR requires States to adopt several regulatory
requirements, including public notification requirements, MCLs for
DBPs, MRDLs for disinfectants, and the requirements in Subpart L. In
addition, States are required to adopt several special primacy
requirements for the Stage 1 DPBR. States are also required to keep
specific records in accordance with existing regulations and additional
records specific to the Stage 1 DBPR. Finally, the rule does not
require any
[[Page 69398]]
State additional reporting requirements beyond those required under
existing regulations. These requirements are discussed in more detail
in Section III.L.
K. System Reporting Requirements
System are required to report monitoring data to the State as
discussed in Section III.K.
L. Guidance Manuals
EPA is developing guidance for both systems and States for the
implementation of the Stage 1 DBPR and the IESWTR. The guidance manuals
include: Guidance Manual for Enhanced Coagulation and Precipitative
Softening; Disinfection Benchmark Guidance Manual; Turbidity Guidance
Manual; Alternative Disinfectants and Oxidants Guidance Manual; M/DBP
Simultaneous Compliance Manual; Sanitary Survey Guidance Manual;
Unfiltered Systems Guidance Manual; and Uncovered Finished Water
Reservoirs. Guidance manuals will be available after the publication of
the Stage 1 DBPR.
M. Regulation Review
Under the provisions of the SDWA (Section 1412(b)(9)), the Agency
is required to review NPDWRs at least once every six years. As
mentioned previously, today's final rule revises, updates, and
supersedes the regulations for total trihalomethanes, initially
published in 1979. Since that time, there have been significant changes
in technology, treatment techniques, and other regulatory controls that
provide for greater protection of human health. As such, for today's
rule, EPA has analyzed innovations and changes in technology and
treatment techniques that have occurred since promulgation of the
interim TTHM regulations. That analysis, contained primarily in the
cost and technology document supporting this rule, supports the changes
in the Stage 1 DBPR from the 1979 TTHM rule. EPA believes that the
innovations and changes in technology and treatment techniques that
result in changes to the 1979 TTHM regulations are feasible within the
meaning of SDWA Section 1412(b).
III. Explanation of Final Rule
A. MCLGs/MRDLGs
MCLGs are set at levels at which no known or anticipated adverse
health effects occur, allowing for an adequate margin of safety.
Establishment of an MCLG for each specific contaminant is based on the
available evidence of carcinogenicity or noncancer adverse health
effects from drinking water exposure using EPA's guidelines for risk
assessment (see the proposed rule at 59 FR 38677 for a detailed
discussion of the process for establishing MCLGs).
The final Stage 1 DBPR contains MCLGs for: four THMs (chloroform,
bromodichloromethane, dibromochloromethane, and bromoform); two
haloacetic acids (dichloroacetic acid and trichloroacetic acid);
bromate; and chlorite (see table II-2 for final MCLG levels). These
MCLGs are the same as those proposed in 1994 with the exception of
chlorite, which increased from 0.08 mg/L to 0.8 mg/L. The MCLG for
chloral hydrate has been dropped since EPA has concluded that it will
be controlled by the MCLs for TTHM and HAA5 and the enhanced
coagulation treatment technique.
The final Stage 1 DBPR contains MRDLGs for chlorine, chloramines
and chlorine dioxide (see table II-1 for final MRDLG levels). The
MRDLGs are as the same as those proposed in 1994, with the exception of
chlorine dioxide, which increased from 0.3 mg/L to 0.8 mg/L.
The MRDLG concept was introduced in the proposed rule for
disinfectants to reflect the fact that these substances have beneficial
disinfection properties. As with MCLGs, MRDLGs are established at the
level at which no known or anticipated adverse effects on the health of
persons occur and which allows an adequate margin of safety. MRDLGs are
nonenforceable health goals based only on health effects and exposure
information and do not reflect the benefit of the addition of the
chemical for control for waterborne microbial contaminants. By using
the term ``residual disinfectant'' in lieu of ``contaminant'', EPA
intends to avoid situations in which treatment plant operators are
reluctant to apply disinfectant dosages above the MRDLG during short
periods of time to control for microbial risk.
EPA received numerous comments on the use of the term MRDLG. The
majority of commenters agreed that the term MRDLG was appropriate to
use in place of MCLG for disinfectants. Other commenters agreed, but
felt that the language should more strongly reflect that disinfectants
are necessary and that short-term exposure to elevated levels of the
disinfectants is not a health concern. Some commenters suggested that
MRDLGs be extended to ozone, potassium permanganate and iodine.
In response, EPA agrees with the majority of commenters that the
use of the term MRDLG is appropriate and therefore the final rule
retains this term. EPA believes the language on the importance of
disinfectants is adequate in the rule and thus has not changed this
language. EPA does not agree that the potential health effects from
short-term exposure to elevated levels of disinfectants can be
dismissed. Ozone does not require an MRDLG because it reacts so
completely that it does not occur in water delivered to consumers.
Finally, EPA believes the use of the MRDLGs for other disinfectants or
oxidants would not be appropriate since MRDLGs are developed for
regulated compounds controlled by MRDLs or treatment techniques and EPA
does not allow these compounds to be used to demonstrate compliance
with disinfection requirements.
The information EPA relied on to establish the MCLGs and MRDLGs was
described in the 1994 proposal (EPA, 1994a), the 1997 DBP NODA (EPA,
1997b), and the 1998 NODA (EPA, 1998a). Criteria and assessment
documents to support the MCLGs and MRDLGs are included in the docket
(EPA, 1993a; EPA, 1994 d-h; EPA, 1997c; EPA, 1998 b-f; and EPA, 1998p).
A summary of the occurrence and exposure information for this rule are
detailed in ``Occurrence Assessment for Disinfectants and Disinfection
Byproducts in Public Drinking Water Supplies' (EPA, 1998u). The
discussion of the data used to establish the MCLGs and MRDLGs and a
summary of the major public comments for these chemicals are included
below. A more detailed discussion is included below for chloroform,
DCA, chlorite, chloride dioxide, and bromate than the other
disinfectants and DBPs. This is the case because significant new data
has become available since the 1994 proposal for these four DBPs and
one disinfectant.
1. MCLG for Chloroform
a. Today's Rule. After careful consideration of all public
comments, EPA has concluded at this time to promulgate an MCLG for
chloroform of zero as proposed. This conclusion reflects an interim
risk-management decision on the part of the Agency. The Agency
recognizes the strength of the science in support of a non-linear
approach for estimating carcinogenicity of chloroform. EPA received
public comments that questioned the underlying basis and approach used
to reach the science judgment that the mode of chloroform's
carcinogenic action supports a nonlinear approach. Equally important
are the policy and regulatory issues raised by stakeholders that touch
on this issue. EPA believes that it is essential to pursue a further
dialogue with stakeholders on the issues raised in the public comments
before applying the substantial new data and science on the mode of
carcinogenic
[[Page 69399]]
action discussed in the 1998 NODA to the important decision of moving
to a non-linear cancer extrapolation approach for drinking water
contaminants under the SDWA. Moreover, EPA will complete additional
deliberations with the Agency's Science Advisory Board (SAB) (open to
stakeholder presentations to the SAB) on the analytical approach used
to evaluate and reach conclusions on mode of action data, and the
science basis for the mode of carcinogenic action for chloroform.
In evaluating how to proceed in the development of an MCLG for
chloroform, the Agency believes two additional factors must be taken
into consideration. First, as part of the 1996 SDWA amendments,
Congress mandated that the Stage 1 DBPR rule be promulgated by November
1998. EPA has concluded that it would be impossible to complete the
additional deliberations noted above in time to meet this statutory
deadline. Second, as explained below, the Agency has also completed
analysis indicating that regardless of whether the MCLG is based on a
low-dose linear or non-linear extrapolation approach, the MCL
enforceable standard for TTHMs of 0.08 mg/L will not be affected. In
light of these issues, EPA believes it is appropriate and consistent
with the public health goals of the SDWA to establish a zero MCLG for
chloroform based on a linear default extrapolation approach until the
Agency is able to complete additional deliberations with the Agency's
SAB on the analytical approach used to evaluate and reach conclusions
on mode of action data and the science basis for the mode of
carcinogenic action for chloroform, and complete the process of further
public dialogue on the important question of moving to a non-linear
cancer extrapolation approach. EPA also notes that its approach is
consistent with legislative history of the SDWA (see 56 FR 3533--EPA,
1991) and the 1996 SDWA Amendments.
b. Background and Analysis. As part of its 1994 Stage 1 DBP
proposal (EPA, 1994a), EPA requested comment on a zero MCLG for
chloroform. This was consistent with information provided to the 1992
Reg. Neg. Committee and was based on data from a drinking water study
by Jorgensen et al. (1985) indicating an increase of kidney tumors in
male rats in a dose-related manner. However, at the time of the
proposal there was insufficient data to determine the mode of
carcinogenic action for chloroform. Therefore, EPA based its 1994
proposal on a risk management decision that a presumptive or low-dose
linear default (i.e, MCLG of zero) was appropriate until more research
became available and there was an adequate opportunity to work with
stakeholders and the scientific community to evaluate and assess the
technical as well as policy and regulatory implications of such new
information. The 1994 proposal also reflected the Agency's 1986
Guidelines for Carcinogen Risk Assessment (EPA, 1986) which recommended
reliance on the default assumption of low-dose linearity in the absence
of substantial information on the mechanism of carcinogenicity.
Since the 1994 proposal, over 30 toxicological studies have been
published on chloroform. These studies were discussed in the November
1997 Stage 1 DBP NODA (EPA, 1997b). In addition, EPA published a second
DBP NODA in March 1998 (EPA, 1998a) which discussed recommendations and
findings from a 1997 International Life Sciences Institute project
(ILSI, 1997), co-sponsored by EPA, on the cancer assessment for
chloroform. The ILSI project included the analysis and conclusions from
an expert panel which was convened and charged with reviewing the
available database relevant to the carcinogenicity of chloroform, and
considering how end points related to mode of action can be applied in
hazard and dose-response assessment by using guidance provided by the
EPA's 1996 Proposed Guidelines for Carcinogen Assessment (EPA, 1996b).
The panel was made up of 10 internationally recognized scientists from
academia, industry, government, and the private sector. Based on a
consideration of the ILSI panel findings and an assessment of new data
on chloroform since 1994, EPA requested comment in the 1998 NODA on the
Agency's science conclusion that chloroform is a likely human
carcinogen and that available scientific analysis supports a non-linear
mode of action for estimating the carcinogenic risk associated with
lifetime exposure from ingesting drinking water.
As part of the 1998 NODA, EPA also requested comment on a revised
chloroform MCLG of 0.30 mg/L. The revised MCLG was premised on the
substantial new science noted above that supports a non-linear mode of
action. In calculating the specific MCLG, EPA relied upon data relating
to hepatoxicity in dogs (EPA, 1994a). This hepatoxicity endpoint was
deemed appropriate given that hepatic injury is the primary effect
following chloroform exposure; and that an MCLG based on protection
against liver toxicity should be protective against carcinogenicity
given that the putative mode of action understanding for chloroform
involves cytotoxicity as a key event preceding tumor development. The
MCLG of 0.3 mg/L was calculated using a relative source contribution
(RSC) of 80 percent. The RSC of 80 percent was based on the assumption
that most exposure to chloroform is likely to come from ingestion of
drinking water. The 80 percent assumption for the RSC was consistent
with the calculations used to derive the MCLGs for D/DBPs in the 1994
proposal. Based on information received during the public comment
period for the 1998 NODA, EPA is considering revising its estimate of
the RSC for chloroform as discussed below.
Since the 1998 NODA, EPA has reevaluated elements of the analysis
underlying a revised MCLG of 0.30 mg/L. Considering recent information
not fully analyzed as part of the 1998 NODA, the Agency is considering
revising the assumption of an 80% RSC from ingestion of drinking water
in view of data which indicates that exposure to chloroform via
inhalation and dermal exposure may potentially contribute a substantial
percentage of the overall exposure to chloroform depending on the
activity patterns of individuals. Also, EPA is in the process of
developing a policy for incorporating inhalation and dermal exposure
into the derivation of the RSC. Furthermore, there is considerable
uncertainty regarding the potential exposure to chloroform via the
dietary route and there is information which indicates individuals who
are frequent swimmers may receive a large amount of chloroform during
swimming. There are additional uncertainties regarding other possible
highly exposed sub-populations, e.g., from use of humidifiers, hot-
tubs, and outdoor misters. In conclusion, because there may be a
potential for exposure to chloroform from other routes of exposure than
ingestion of drinking water, EPA is considering using the 20 percent
default floor to ensure adequate public health protection. The 20
percent has been used historically for drinking water contaminants
other than D/DBPs when there is uncertainty in the available exposure
data. The use of the 20 percent RSC for chloroform would produce a MCLG
of 0.07 mg/L:
[[Page 69400]]
[GRAPHIC] [TIFF OMITTED] TR16DE98.000
In addition to its reassessment of technical assumptions underlying
the revised MCLG, the Agency has also reviewed and carefully considered
in detail a number of significant comments on the 1998 NODA. These
comments reflect both substantial scientific support as well as
significant concerns with a possible MCLG of 0.30 mg/L. As outlined in
more detail below, a number of nationally recognized scientific experts
strongly affirmed the data and technical rationale for relying upon a
non-linear mode of action for chloroform. Other commenters, however,
highlighted several scientific issues they felt were not adequately
considered. These commenters also emphasized their concern that the
policy, regulatory, and enforcement implications related to a revised
MCLG were not raised by EPA in either the 1992 or the 1997 regulatory
negotiation processes leading up to today's final rule. Thus, these
commenters felt that a number of stakeholders who recommended support
for components of the Stage 1 DBPR rule did so under one set of
conditions and assumptions that the Agency subsequently changed without
providing a sufficient opportunity for further debate and discussion.
EPA believes that an adequate opportunity for notice and comment
was provided as a result of the 1997 and 1998 DBP NODAs on the
underlying scientific data and technical issue of moving to a non-
linear extrapolation approach based on an understanding of the mode of
carcinogenic action for chloroform and recalculating the chloroform
MCLG to a nonzero number. However, the Agency recognizes that reliance
on a non-linear mode of action under the SDWA does represent a
significant and precedential, albeit sound, application of new science
to the policy development and risk management decision making process
of establishing appropriately protective MCLGs. The Agency also
recognizes that although, as discussed below, a revised MCLG for
chloroform would not affect the TTHM MCL under today's rule, the
precedential decision to utilize a non-linear cancer extrapolation
approach clearly has important implications for the development of
future MCLGs where there is also adequate scientific research and data
to support such a non-linear analysis.
In reviewing the range of scientific, policy, and regulatory
analyses and strongly held views associated with development of the
chloroform MCLG, EPA notes that the one question not fundamentally at
issue is the establishment of the 0.080 mg/L TTHM MCL. The majority of
commenters who addressed the proposed TTHM MCL continue to support it.
This is particularly important to EPA in light of congressional action
with regard to the M-DBP process in the 1996 SDWA Amendments. In
enacting the Amendments and particularly in expressing congressional
intent in the conference Report, Congress was careful to emphasize
``that the new provisions of this conference agreement not conflict
with the parties' agreement nor disrupt the implementation of the
regulatory actions,'' (such as the current agreement on an TTHM MCL of
0.080 mg/L). Both of these important elements of the Congressional
intent were reflected in the statutory text. Section 1412(b)(2)(C)
requires EPA to maintain the M-DBP rule staggered promulgation strategy
agreed to by the negotiated rulemaking; and Section 1412(b)(6)(C)
exempted the future M-DBP rules from the new cost-benefit standard-
setting provision (1412(b)(6)(A)) but not from the new risk-risk
provision (1412(b)(5)), because the latter was a part of the negotiated
rulemaking agreement but the former was not.
The Agency, itself, also believes that the underlying logic, data,
and rationale supporting establishment of a TTHM of 0.080 mg/L MCL is
compelling, and this is a critical factor in the Agency's chloroform
MCLG decision under today's rule. Under either a low-dose linear or
non-linear extrapolation to derive the MCLG, the final TTHM MCL remains
unaffected.
After thorough review of the data and comments, EPA believes the
nonlinear cancer extrapolation approach is the most appropriate means
to establish an MCLG for chloroform based on carcinogenic risk.
However, in light of its own reconsideration of the appropriate RSC for
chloroform under such an approach, considering the range of policy,
regulatory, and enforcement issues raised as part of the public comment
period, recognizing the importance of deliberations with SAB before
proceeding further and, yet, recognizing that this cannot be
accomplished within the constraints of meeting the statutory deadline
for Stage 1 DBPR rule of November 1998, EPA has determined that on
balance the more appropriate and prudent risk management decision at
this time is to establish an MCLG for chloroform at the proposed
presumptive default level of zero. As part of this decision, the Agency
will complete additional deliberations with the Agency's SAB on the
analytical approach used to evaluate and reach conclusions on mode of
action data, and the science basis for the mode of carcinogenic action
for chloroform. The SAB's review will be factored into the Agency's
Stage 2 DBP rulemaking process. EPA will also include consideration of
the regulatory, policy, and precedential issues involving chloroform in
the Agency's Round 2 M-BP stakeholder process. EPA wishes to make clear
that its interim decision in today's rule to set an MCLG of zero
pending SAB review and further stakeholder involvement is not intended
to prejudge the question of what the appropriate MCLG should be for
purposes of regulatory decisions under the Stage 2 DBPR. EPA may decide
to retain the zero MCLG for that rule, or to revise it, depending on
the outcome of the SAB review, as well as any new scientific evidence
that may become available. In regard to the appropriate RSC factor, in
case a non-linear approach should ultimately be adopted, the Agency
requests that stakeholders provide any data they man have bearing on
this determination.
The fundamental objective of the SDWA is to establish protective
public health goals (MCLGs) together with enforceable standards (MCLs
or treatment techniques) to move the water treatment systems as close
to the public health goal as is technologically and economically
feasible. In the case of the chloroform and TTHMs, this objective is
met with whichever extrapolation approach (low dose linear versus
nonlinear) is relied upon.
c. Summary of Comments. EPA received numerous comments on both the
1994 proposed rule regarding the MCLG of zero for chloroform and the
MCLG of 0.3 mg/L contained in the 1998 NODA. Some commenters were
supportive of the MCLG of zero, while others were supportive of the 0.3
mg/L MCLG. The major reason raised by commenters for establishing a
nonzero MCLG (e.g., 0.3 mg/L) was that there was convincing scientific
evidence to conclude that a nonlinear margin of exposure approach for
evaluating the carcinogenic risk from chloroform is warranted.
Commenters who were
[[Page 69401]]
against establishing a nonzero MCLG for chloroform presented policy and
scientific concerns. Scientific concerns raised by commenters opposed
to the nonzero MCLG included their perceptions that: there is
insufficient scientific evidence of a threshold for chloroform; the
threshold assumption is also invalid because chloroform co-occurs with
other mutagenic carcinogens; EPA ignored human data in establishing the
MCLG for chloroform; the linkage between cytotoxicity and regenerative
proliferation and kidney tumors is not supported by the data; and the
evidence for genotoxicity is mixed and it would be difficult if not
impossible to conclude that the evidence demonstrate chloroform has no
direct effect on DNA. As detailed at greater length in the docket, EPA
does not agree with these comments as a technical matter. The Agency
does agree with the commenters view that further discussion of these
issues with both the SAB and as part of additional public dialogue is
appropriate.
The policy issues raised by commenters included their belief that:
a zero MCLG is required to comply with provisions of the SDWA; EPA is
required to use the 1986 Cancer Guidelines (EPA, 1986) until the 1996
Cancer Guidelines (EPA, 1996b) are formally finalized, and under the
1986 guidelines the MCLG for chloroform must be set at zero; EPA did
not provide sufficient opportunity for the members of the FACA,
established to assist in the development of the Stage 1 DBP rule, to
properly consider the potential implications of a nonzero MCLG; and
setting a MCLG for chloroform (0.3 mg/L) above the MCL for the TTHMs
(0.08 mg/L) is illogical.
In response, EPA believes that the underlying science for using a
nonlinear extrapolation approach to evaluate the carcinogenic risk from
chloroform is well founded. As explained above, because of the issues
raised during the public comment period, EPA believes additional review
and dialogue with stakeholders is needed prior to departing from a
long-held EPA policy of establishing zero MCLGs for known or probable
carcinogens. EPA will also complete additional deliberations with the
Agency's SAB on the analytical approach used to evaluate and reach
conclusions on mode of action data, and the science basis for the mode
of carcinogenic action for chloroform.
In response to the policy issues raised by commenters, EPA,
historically, has established MCLGs of zero for known or probable human
carcinogens based on the principle that any exposure to carcinogens
might represent some finite level of risk and therefore an MCLG above
zero did not meet the statutory requirement that the goal be set where
no known anticipated adverse effects occur, allowing for an adequate
margin of safety (56 FR 3533; EPA, 1991). However, if there is
scientific evidence that indicates there is a ``safe threshold'' then a
non-zero MCLG could be established with an adequate margin of safety
(56 FR 3533; EPA, 1991)). Even though EPA, as an interim matter, is
establishing an MCLG of zero for chloroform in today's rule, it
believes it has the authority to establish nonzero MCLGs for
carcinogens if the scientific evidence supports this finding.
In response to commenter's concerns with EPA using the proposed
1996 Guidelines for Carcinogen Risk Assessment (EPA, 1996b) instead of
the Agency's 1986 guidelines, EPA believes it is important to point out
that the 1986 guidelines provide for departures from default
assumptions such as low dose linear assessment. For example, the 1986
EPA guidelines reflect the position of the OSTP (1985; Principle 26)
``No single mathematical procedure is recognized as the most
appropriate for low-dose extrapolation in carcinogenesis. When relevant
biological evidence on mechanisms of action exists (e.g,
pharmacokinetics, target organ dose), the models or procedure employed
should be consistent with the evidence.'' The 1986 guideline goes on to
further state ``The Agency will review each assessment as to the
evidence on carcinogenesis mechanisms and other biological or
statistical evidence that indicates the suitability of a particular
extrapolation model.'' The EPA's 1996 Proposed Guidelines for
Carcinogen Risk Assessment allow EPA to use other default approaches to
estimate cancer risk than the historic, linearized multistage default
when there is an understanding of an agent's mode of carcinogenic
action. EPA believes that reliance on the 1986 guidance allows EPA to
reach the same conclusion on the carcinogenic risk from chloroform as
if the 1996 guidelines were used. The use of the best available science
is a core EPA principle and is statutorily mandated by the SDWA
amendments of 1996. The 1996 Proposed Guidelines for Carcinogen Risk
Assessment reflect new science and are consistent with the existing
1986 Guidelines for Carcinogen Risk Assessment. EPA considered the 1996
proposed guidelines in assessing the health effects data for chloroform
and the other contaminants discussed in the 1998 March NODA.
EPA agrees with commenters that additional review by the FACA of
the regulatory implications of a nonlinear approach is appropriate for
policy reasons, and will initiate these discussions in the context of
the Stage 2 DBPR FACA deliberations. In light of the November 1998
statutory deadline to promulgate the Stage 1 DBP rule and the steps
necessary to complete a final rule, EPA has concluded that there is not
enough time to meet with the SAB and FACA, provide ample opportunity
for debate, resolve differing points of views, and complete additional
analysis to meet stakeholders policy concerns in the context of the
Stage 1 DBP rule. EPA notes, however, that regardless of the MCLG for
chloroform, the MCL for the THMs remains at 0.08 mg/L. Since the MCL is
the enforceable standard that water systems will be required to meet, a
nonlinear or low dose linear extrapolation to derive the MCLG will not
have a direct impact on the compliance obligations of public water
systems or on the levels of chloroform allowed in public water systems,
although it may be relevant to development of enforceable regulatory
limits established under future rules.
2. MCLG for Bromodichloromethane (BDCM)
a. Today's Rule. The final MCLG for BDCM is zero. The zero MCLG is
based on the classification of BDCM as a probable human carcinogen. The
MCLG was determined in a weight-of-evidence evaluation which considered
all relevant health data including carcinogenicity and reproductive and
developmental toxicity animal data. EPA believes the data are
insufficient at this time to determine the mode of carcinogenic action
for BDCM, and therefore a low dose linear extrapolation approach is
used to estimate lifetime cancer risk as a default.
b. Background and Analysis. In the 1994 Stage 1 DBPR proposal, the
MCLG of zero for BDCM was based on large intestine and kidney tumor
data from a National Toxicology Program (NTP) chronic animal study
(NTP, 1987). Since the proposal, several new studies have been
published on BDCM metabolism (EPA, 1997c). In addition, several new
genotoxicity studies and short-term toxicity studies including
reproductive evaluations were found for BDCM (EPA, 1997c). These new
studies contribute to the weight-of-evidence conclusions reached in the
1994 proposal. Based on this evidence, the final MCLG for BDCM is zero
based on sufficient evidence of carcinogenicity in animals.
c. Summary of Comments. Several commenters disagreed with the use
of a
[[Page 69402]]
corn oil gavage animal cancer study to determine the MCLG for BDCM.
Some commenters agreed with the EPA decision to use large intestine and
kidney tumor data from the corn oil gavage study, but not liver tumor
data in the quantitative estimation of carcinogenic risk. One commenter
agreed that a low-dose linear extrapolation approach to dose-response
assessment was appropriate at this time and consistent with EPA policy.
However, this commenter suggested that EPA undertake chronic studies
that include a drinking water study of BDCM and toxicokinetics. One
commenter disagreed with the EPA conclusion that the evidence on the
mutagenicity of BDCM is adequate.
In response, EPA agrees with commenters that a drinking water study
is preferable to a corn oil gavage study to assess risk from DBPs in
drinking water. However, the NTP corn oil gavage study is the best data
available on BDCM for a quantitative risk estimation at this time. BDCM
is currently being tested for toxicokinetics and cancer in a chronic
BDCM drinking water rodent study by the NTP. When these data are
available, EPA will reassess the cancer risk of BDCM. EPA believes that
the animal data currently available on BDCM are consistent with EPA
cancer guidelines on classifying BDCM as a probable human carcinogen
given the evidence on mutagenicity and given there was an increased
incidence of tumors at several sites in the animals. Additionally,
tumors were found in both sexes of two rodent species. Finally, there
have been several new studies on the genotoxicity of BDCM that have
supported a mutagenic potential for BDCM (EPA, 1997c)
3. MCLG for Dibromochloromethane (DBCM)
a. Today's Rule. The final MCLG for DBCM is 0.06 mg/L. This MCLG is
based on a weight of evidence evaluation of the cancer and noncancer
data which resulted in the classification of DBCM as a possible human
carcinogen.
b. Background and Analysis. In the 1994 proposal, the MCLG of 0.06
mg/L for DBCM was based on observed liver toxicity from a subchronic
study and possible carcinogenicity (NTP, 1985). EPA is not aware of any
new information that would change its evaluation of DBCM since the
proposal. The final MCLG is therefore 0.06 mg/L.
c. Summary of Comments. Several commenters disagreed with the
additional safety factor of 10 to account for possible carcinogenicity
that was used in the MCLG calculation. One commenter agreed with EPA's
decision to base the MCLG on noncarcinogenic endpoints. Several
commenters disagreed with the use of a corn oil gavage study to
determine the MCLG for DBCM.
In response, because the evidence of carcinogenicity was limited on
DBCM (i.e., increased tumor response in only one of the two species
tested), EPA classified DBCM as a possible human carcinogen. The
additional factor of 10 to account for possible carcinogenicity follows
EPA's science policy for establishing MCLGs (EPA, 1994a). EPA used
liver effects from the NTP subchronic corn oil gavage study as the
basis for the Reference Dose (RfD). EPA agrees with the comment that
this is an appropriate basis for deriving the RfD for DBCM. EPA agrees
with commenters that a drinking water study is preferable to a corn oil
gavage study to assess risk from DBPs in drinking water. However, the
NTP corn oil gavage study is the best data available on DBCM for
derivation of the MCLG at this time. EPA does not plan to conduct
additional chronic studies for DBCM but is conducting additional
toxicokinetics and short term drinking water studies on DBCM to better
understand the potential risk associated with exposure through drinking
water.
4. MCLG for Bromoform
a. Today's Rule. The final MCLG for bromoform is zero. The zero
MCLG is based on a weight-of-evidence classification that bromoform is
a probable human carcinogen based on a consideration of all relevant
health data including cancer and noncancer effects. EPA believes the
data are insufficient at this time to determine the mode of
carcinogenic action for bromoform, and therefore a low dose linear
extrapolation approach is used to estimate lifetime cancer risk as a
default.
b. Background and Analysis. The proposed MCLG for bromoform was
zero. This MCLG was based on an NTP chronic animal carcinogenicity
study (NTP, 1989). Since the proposal, new studies on the genotoxicity
of bromoform were found. However, these new studies do not support
changing the proposed MCLG of zero for bromoform. The final MCLG for
bromoform is therefore zero.
c. Summary of Comments. Several commenters agreed with EPA's
classification for bromoform as a probable carcinogen. Other commenters
disagreed with this classification stating that there was insufficient
evidence available because tumors were found in only one species and
the increased number of tumors was small. These commenters generally
felt that EPA should use an RfD approach in quantifying the risk for
bromoform. Some commenters encouraged EPA to conduct more experiments
on bromoform toxicity. Some commenters were concerned with the use of a
corn oil gavage study to determine carcinogenic risk.
In response, although the increase in tumors was small, the
increase was considered significant because large intestine tumors in
both male and female rats are rare and thus provides sufficient
evidence to classify bromoform as a probable human carcinogen. EPA does
not plan on conducting additional chronic testing for bromoform at this
time, but is conducting toxicokinetic studies and shorter term drinking
water studies to better understand the potential risk associated with
exposure to bromoform in drinking water. EPA agrees with commenters
that drinking water studies are preferable to a corn oil gavage study
to assess risk from DBPs in drinking water. However, the NTP corn oil
gavage study is the best data available on bromoform for derivation of
the MCLG.
5. MCLG for Dichloroacetic Acid (DCA)
a. Today's Rule. The final MCLG for DCA is zero. EPA has developed
a weight-of-evidence characterization for DCA in which it evaluated all
relevant health data (both cancer and noncancer effects). The MCLG of
zero is based on sufficient evidence of carcinogenicity in animals
which indicates that DCA is a probable human carcinogen (likely under
proposed cancer guidelines). EPA believes the data are insufficient at
this time to determine the mode of carcinogenic action for DCA and that
the data is insufficient to quantify the potential cancer risk from
DCA.
b. Background and Analysis. EPA proposed an MCLG of zero for DCA.
This was based on classifying DCA as a probable human carcinogen in
accordance with the 1986 EPA Guidelines for Carcinogen Risk Assessment
(EPA, 1986). The DCA categorization was based primarily on findings of
liver tumors in rats and mice, which was regarded as ``sufficient''
evidence in animals. No lifetime risk calculation was conducted at the
time of the proposal because there was insufficient data to quantify
the risk (EPA, 1994a).
As pointed out in the 1997 and 1998 DBP NODAs, several
toxicological studies have been identified for DCA since the 1994
proposal (EPA, 1997c). In addition, EPA co-sponsored an ILSI project in
which an expert panel was
[[Page 69403]]
convened to explore the application of the EPA's 1996 Proposed
Guidelines for Carcinogen Risk Assessment (EPA, 1996b) to the available
data on the potential carcinogenicity of chloroform and DCA. The panel
considered data on DCA which included chronic rodent bioassay data and
information on mutagenicity, tissue toxicity, toxicokinetics, and other
mode of action information. The panel concluded that the potential
human carcinogenicity of DCA ``cannot be determined'' primarily because
of the lack of adequate rodent bioassay data (ILSI, 1997).
EPA prepared a new hazard characterization regarding the potential
carcinogenicity of DCA in humans (EPA, 1998b). One objective of this
report was to develop a weight-of-evidence characterization using the
principles of the EPA's 1996 Proposed Guidelines for Carcinogen Risk
Assessment (EPA, 1996b) which are consistent with the 1986 Guidelines.
Another objective of the report was to consider new data since the 1994
proposal and to address the issues raised by the 1997 ILSI panel
report.
EPA agreed with the ILSI panel report that the mode of action
through which DCA induces liver tumors in both rats and mice cannot be
reasonably determined at this time. EPA disagrees with the ILSI panel
that the potential human carcinogenicity cannot be determined. Based on
the hepatocarcinogenic effects of DCA in both rats and mice in multiple
studies, as well as other date, for example, showing that DCA alters
cell replication and gene expression, EPA concludes that DCA should be
considered as a ``likely'' (probable) cancer hazard to humans (EPA,
1998b). Therefore, as in the 1994 proposed rule, EPA believes that the
MCLG for DCA should remain zero to assure public health protection.
c. Summary of Comments. Some commenters agreed with the zero MCLG
for DCA based on positive carcinogenic findings in two animal species.
Several commenters stated that a zero MCLG was inappropriate due to
evidence which indicates a nongenotoxic mode of action for DCA. The
comment was raised that the animal evidence was insufficient to
consider DCA a likely (probable) human carcinogen, and that DCA should
be considered at most suggestive of carcinogenicity.
In response, EPA concludes that DCA should be considered as a
probable (likely under the 1996 proposed guidelines) cancer hazard to
humans (EPA, 1998b) based on the hepatocarcinogenic effects of DCA in
both rats and mice in multiple studies, and mode of action related
effects (e.g., mutational spectra in oncogenes, elevated serum
glucocorticoid levels, alterations in cell replication and death). EPA
considers the mode of action through which DCA induces liver tumors in
both rats and mice to be unclear, and thus the likelihood of human
hazard associated with low levels of DCA usually encountered in the
environment or in drinking water is not sufficiently understood. EPA
acknowledges that a mutagenic mechanism (i.e., direct DNA reactivity)
may not be an important influence on the carcinogenic process at low
doses. EPA believes that the lack of mutagenicity is not a sufficient
basis to depart from a low dose linear default extrapolation approach
for the cancer assessment. There must be other convincing evidence to
explain how the tumors are caused by the chemical. The commenters have
not presented such evidence. Although DCA tumor effects are associated
with high doses used in the rodent bioassays, there is uncertainty
regarding whether the mode of tumorgenesis is solely through mechanisms
that are operative only at high doses. Therefore, as in the 1994
proposed rule, EPA believes that the MCLG for DCA should remain as zero
to assure public health protection. NTP is implementing a new two year
rodent bioassay that will include full histopathology at lower doses
than those previously studied. Additionally, studies on the mode of
carcinogenic action are being done by various investigators including
the EPA health research laboratory.
6. MCLG for Trichloroacetic Acid (TCA)
a. Today's Rule. The final MCLG for TCA is 0.3 mg/L, as was
proposed in 1994. This MCLG is based on developmental toxicity and
limited evidence of carcinogenicity in animals.
b. Background and Analysis. The 1994 proposed rule included a MCLG
of 0.3 mg/L for TCA based on developmental toxicity and possible
carcinogenicity based on limited evidence in animal studies (i.e.,
hepatocarcinogenicity in mice). Since the proposal, a 2-year
carcinogenicity study on TCA (DeAngelo et al., 1997) found that TCA was
not carcinogenic in male rats. As was discussed in the 1997 DBP NODA
(EPA, 1997b), there have also been several recent studies examining the
mode of carcinogenic action for TCA. These new studies suggest that TCA
does not operate via mutagenic mechanisms. For a more in depth
discussion of this new data refer to the 1997 DBP NODA (EPA, 1997b) and
related support documents (EPA, 1997c). This new information does not
alter the original assessment of the health effects of TCA based on
developmental toxicity and limited evidence of carcinogenicity.
Therefore, the MCLG will remain 0.3 mg/L.
c. Summary of Comments. Several commenters agreed with the
classification of TCA as a possible human carcinogen. One commenter
felt that toxicity data on TCA indicated a threshold. Some commenters
disagreed with the study selected for estimating the RfD (Smith et al.
1989). Some commenters stated the uncertainty factors used to establish
the RfD were too high.
In response, EPA acknowledges that a DNA reactive mutagenic
mechanism may not be involved in TCA's mode of carcinogenicity. Because
an RfD was used in lieu of a quantitative cancer assessment for
establishing the MCLG, however, there was no need to evaluate the mode
of carcinogenic action for TCA at this time. EPA believes that the
Smith et al. (1989) study is appropriate to use in quantifying risk
from TCA since developmental toxicity was the most critical effect. EPA
believes that an uncertainty factor of 3,000 is appropriate to account
for inter and intraspecies differences (100), a lowest observed adverse
effects level (LOAEL) (10), and lack of a two-generation reproductive
study (3) (EPA, 1994a). These uncertainty factors are consistent with
current Agency science policy on using uncertainty factors (EPA,
1994a).
7. MCLG for Chlorite and MRDLG for Chlorine Dioxide
a. Today's Rule. The final MCLG for chlorite is 0.8 mg/L and the
final MRDLG for chlorine dioxide is 0.8 mg/L. The MCLG for chlorite was
increased from the proposed value of 0.08 mg/L to 0.8 mg/L based on a
weight-of-evidence evaluation of all health data on chlorite including
a recent two-generation reproductive rat study sponsored by the
Chemical Manufactures Association (CMA, 1996). The MRDLG for chlorine
dioxide was increased from the proposed value of 0.3 mg/L to 0.8 mg/L
based on a weight-of-evidence evaluation using all the health data on
chlorine dioxide including the information on chlorite from the CMA
study. EPA believes that data on chlorite are relevant to assessing the
risks of chlorine dioxide because chlorine dioxide is rapidly reduced
to chlorite. Therefore, the findings from the CMA study and previously
described studies in the 1994 proposal were used to assess the risk for
both chlorite and chlorine dioxide.
b. Background and Analysis. The 1994 proposal included an MCLG of
[[Page 69404]]
0.08 mg/L for chlorite. The proposed MCLG was based on an RfD of 3 mg/
kg/d estimated from a lowest-observed-adverse-effect-level (LOAEL) for
neurodevelopmental effects identified in a rat study by Mobley et al.
(1990). This determination was based on a weight of evidence evaluation
of all the available data at that time (EPA, 1994d). An uncertainty
factor of 1000 was used to account for inter-and intra-species
differences in response to toxicity (a factor of 100) and to account
for use of a LOAEL (a factor of 10).
The 1994 proposal included an MRDLG of 0.3 mg/L for chlorine
dioxide. The proposed MRDLG was based on a RfD of 3 mg/kg/d estimated
from a no-observed-adverse-effect-level (NOAEL) for developmental
neurotoxicity identified from a rat study (Orme et al., 1985; EPA,
1994d). This determination was based on a weight of evidence evaluation
of all available health data at that time (EPA, 1994a). An uncertainty
factor of 300 was applied that was composed of a factor of 100 to
account for inter-and intra-species differences in response to toxicity
and a factor of 3 for lack of a two-generation reproductive study
necessary to evaluate potential toxicity associated with lifetime
exposure. To fill this important data gap, the CMA sponsored a two-
generation reproductive study in rats (CMA, 1996).
As described in more detail in the 1998 NODA (EPA, 1998a), EPA
reviewed the CMA study and completed an external peer review of the
study (EPA, 1997d). In addition, EPA reassessed the noncancer health
risk for chlorite and chlorine dioxide considering the new CMA study
(EPA, 1998d). This reassessment was also peer reviewed (EPA, 1998d).
Based on this reassessment, EPA requested comment in the 1998 NODA
(EPA, 1998a) on changing the proposed MCLG for chlorite from 0.08 mg/L
to 0.8 mg/L based on the NOAEL identified from the new CMA study which
reinforced the concern for neurodevelopmental effects associated with
short-term exposures.
EPA determined that the NOAEL for chlorite should be 35 ppm (3 mg/
kg/d chlorite ion, rounded) based on a weight-of-evidence approach. The
data considered to support the NOAEL are summarized in EPA (1998d) and
included the CMA study as well as previous reports on developmental
neurotoxicity and other adverse health effects (EPA, 1998d). EPA
continues to believe, as stated in the 1998 NODA (EPA, 1998a), that the
RfD for chlorite should be 0.03 mg/kg/d (NOAEL of 3 mg/kg/d with an
uncertainty factor of 100) and that a MCLG of 0.8 mg/L is appropriate.
EPA has concluded that the RfD for chlorine dioxide should be 0.03 mg/L
(NOAEL of 3 mg/kg/d with an uncertainty factor of 100) and that a MRDLG
of 0.8 mg/L is appropriate.
c. Summary of Comments. EPA received numerous comments on the 1994
proposal (EPA, 1994a) and 1998 NODA (EPA, 1998a). The major comment
from the 1994 proposal was that reliance on the Mobley et al. (1990)
study for the MCLG for chlorite and the Orme et al. (1985) study for
chlorine dioxide were inappropriate and that the results from the CMA
study must be evaluated before any conclusions on the MCLG for chlorite
or chlorine dioxide could be drawn. In relation to the 1998 NODA,
several commenters supported changing the MCLG for chlorite and MRDLG
for chlorine dioxide while others were concerned that the science did
not warrant a change in these values. The major comments submitted
against raising the MCLG and MRDLG focused on several issues. First,
one commenter argued that the 1000-fold uncertainty factor used for
chlorite in the proposal should remain in place because the CMA study
used to reduce the uncertainty factor was flawed. Second, several
commenters indicated that the LOAEL should be set at the lowest dose
level (35 ppm) because certain effects at the lowest dose tested may
have been missed. Finally, some commenters argued that an additional
safety factor should be included to protect children and drinking water
consumption relative to the body weight of children should be used
instead of the default assumption of 2 L per day and 70 kg adult body
weight.
EPA agrees with commenters on the 1994 proposal that the results
from the CMA should be factored into any final decision on the MCLG for
chlorite and chlorine dioxide. As explained in more detail in the 1998
DBP NODA (EPA, 1998a), EPA considered the findings from the CMA study
along with other available data to reach its conclusions regarding the
MCLG and MRDLG for chlorite and chlorine dioxide.
EPA disagrees with the commenter who suggested that the 1000-fold
uncertainty factor for chlorite should remain because the CMA study was
flawed. The study design for the neurodevelopmental component of the
CMA study was in accordance with EPA's testing guidelines at the time
the study was initiated. EPA had previously reviewed the study protocol
for the CMA neurotoxicity component and had approved the approach.
While EPA initially had some questions regarding the design of the
neurodevelopmental component of the study (Moser, 1997), subsequent
information submitted by the CMA provided clarification on certain
aspects of the study design (CMA, 1998). EPA agrees that even with the
clarifications that there are some limitations with the
neurodevelopmental component of the CMA study. EPA believes that the
neuropathology components of the CMA study were adequate. The
functional operation battery had some shortcomings in that forelimb and
hindlimb grip strength and foot splay were not evaluated. EPA believes
the results from the motor activity component of the CMA study were
difficult to interpret because of the high variability in controls.
However, in its evaluation of the MCLG for chlorite and chlorine
dioxide, EPA did not rely solely on the CMA study, but used a weight-
of-evidence approach that included consideration of several studies.
Thus, the shortcomings of one study are offset by the weight from other
studies. EPA believes that the CMA study contributes to the weight-of
the-evidence. The studies by Orme et al. (1985), Mobley et al. (1990),
and CMA (1996) support a NOAEL of 3 mg/kg/d based on neurodevelopmental
effects (e.g., decreased exploratory, locomotor behavior, decreased
brain weight). Furthermore, the CMA study was reviewed by outside
scientists as well as by EPA scientists. EPA's re-assessment for
chlorite and chlorine dioxide presented in the 1998 March NODA was
reviewed internally and externally in accordance with EPA peer-review
policy. The three outside experts who reviewed the Agency's assessment
agreed with the NOAEL of 3 mg/kg/day and the derived RfD.
Finally, EPA disagrees that an additional safety factor should be
applied to provide additional protection for children or that drinking
water consumption relative to the body weight of children should be
used in developing the MCLG. The MCLG and MRDLG presented for chlorite
and chlorine dioxide are considered to be protective of susceptible
groups, including children, given that the RfD is based on a NOAEL
derived from developmental testing, which includes a two-generation
reproductive study. A two-generation reproductive study evaluates the
effects of chemicals on the entire developmental and reproductive life
of the organism. Additionally, current methods for developing RfDs are
designed to be protective for sensitive populations. In the case of
chlorite and chlorine dioxide a factor of 10 was used to account for
variability between the average human response and the
[[Page 69405]]
response of more sensitive individuals. In addition, the important
exposure is that of the pregnant and lactating female and the nursing
pup. The 2 liter per day water consumption and the 70 kg body weight
assumptions are viewed as adequately protective of all groups.
Based on a review of all the data and public comments, EPA believes
that the MCLG for chlorite should be 0.8 mg/L and the MRDLG for
chlorine dioxide should be 0.8 mg/L. EPA believes the MCLG and MRDLG
are consistent with the discussions during the regulatory negotiations
which recognized the need for an acceptable two-generation reproductive
study prior to reducing the uncertainty factors for chlorite and
chlorine dioxide. EPA believes the CMA provided an acceptable two-
generation study with which to reduce the uncertainty factors. In
addition, EPA believes potential health concerns in the proposal with
having a MCLG for chlorite significantly below the MCL are no longer
relevant because the MCL for chlorite in today's rule will remain at
1.0 mg/L while the MCLG has been revised to 0.8 mg/L. Given the margin
of safety that is factored into the estimation of the MCLG of 0.8 mg/L,
EPA believes that the MCL of 1.0 mg/L will be protective of public
health of all groups, including fetuses and children.
The MCLG for chlorite is based on an RfD of 0.03 mg/kg/d using a
NOAEL of 3 mg/kg/d and an uncertainty factor of 100 to account for
inter- and intra-species differences. The MCLG for chlorite is
calculated to be 0.8 mg/L by assuming an adult tap water consumption of
2 L per day for a 70 kg adult and using a relative source contribution
of 80% (because most exposure to chlorite is likely to come from
ingestion of drinking water--EPA,1998u). A more detailed discussion of
this assessment is included in the public docket for this rule (EPA,
1998d).
[GRAPHIC] [TIFF OMITTED] TR16DE98.001
For chlorine dioxide the MCLG is based on a NOAEL of 3 mg/kg/d and
applying an uncertainty factor of 100 to account for inter-and intra-
species differences in response to toxicity, the revised MRDLG for
chlorine dioxide is calculated to be 0.8 mg/L. This MRDLG takes into
account an adult tap water consumption of 2 L per day for a 70 kg adult
and applies a relative source contribution of 80% (because most
exposure to chlorine dioxide is likely to come from ingestion of
drinking water--EPA, 1998u). A more detailed discussion of this
assessment is included in the public docket for this rule (EPA, 1998d).
[GRAPHIC] [TIFF OMITTED] TR16DE98.002
8. MCLG for Bromate
a. Today's Rule. The final MCLG for bromate is zero. The zero MCLG
is based on a weight-of-evidence evaluation of both the cancer and
noncancer effects which indicates there is sufficient laboratory animal
data to conclude that bromate is a probable (likely under the 1996
proposed cancer guidelines) human carcinogen. EPA believes the data are
insufficient at this time to determine the mode of carcinogenic action
for bromate, and therefore a low dose linear extrapolation approach is
used to estimate lifetime cancer risk as a default.
b. Background and Analysis. The 1994 proposed rule included a MCLG
of zero for bromate based on a determination that bromate was a
probable human carcinogen. This determination was based on results from
a two species rodent bioassay by Kurokawa et al. (1986a and 1986b) that
found kidney tumors in rats. Since the 1994 proposed rule, EPA has
completed and analyzed a new chronic cancer study in male rats and mice
for potassium bromate (DeAngelo et al., 1998). EPA reassessed the
cancer risk associated with bromate exposure (EPA, 1998e), had this
reassessment peer reviewed (EPA, 1998e), and presented its findings in
the March 1998 NODA (EPA, 1998a). The new rodent cancer study by
DeAngelo et al. (1998) contributes to the weight of the evidence for
the potential human carcinogenicity of potassium bromate and confirms
the study by Kurokawa et al. (1986 a,b).
c. Summary of Comments. Several commenters supported the zero MCLG
for bromate. Others believed the MCLG of zero was not justified because
there is evidence of a carcinogenic threshold. This evidence indicates
that bromate causes DNA damage indirectly via lipid peroxidation, which
generates oxygen radicals which in turn induce DNA damage. Other
commenters argued that even if there is no carcinogenic threshold, EPA
has overstated the potency of bromate by using the linearized
multistage model and should instead use the Gaylor-Kodell model.
In response, EPA disagrees with commenters who believed that the
zero MCLG was inappropriate. At this time, under the principles of both
the 1986 EPA Guidelines for Carcinogen Risk Assessment (EPA, 1986) and
the draft 1996 EPA Proposed Guidelines for Carcinogen Risk Assessment
(EPA, 1996b) weight-of-evidence approach, bromate is considered to be a
probable or likely human carcinogen. This weight of evidence conclusion
of potential human carcinogenicity is based on sufficient experimental
findings that include the following: tumors at multiple sites in rats;
tumor responses in both sexes; and evidence for mutagenicity including
point mutations and chromosomal aberrations in in vitro genotoxicity
assays. Furthermore, EPA believes there is insufficient evidence at
this time to draw conclusions regarding the mode of carcinogenic action
for bromate. EPA acknowledges there are studies available showing that
bromate may generate oxygen radicals which increase lipid peroxidation
and damage DNA. However, no data are available that link this proposed
mechanism to tumor induction. Thus, EPA believes that while there are
studies which provide some evidence to support the commenters' claims,
these studies are insufficient at this time to establish
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lipid peroxidation and free radical production as key events
responsible for the induction of the multiple tumor responses seen in
the bromate rodent bioassays (EPA, 1998e). Given the uncertainty about
the mode of carcinogenic action for bromate, EPA believes it is
appropriate to use the default assumption of low dose linearity to
estimate the cancer risk and establish the MCLG of zero for bromate.
EPA is conducting additional studies investigating the mode of action
for bromate.
EPA also disagrees with commenters who suggested that the Gaylor-
Kodell model should be used for low-dose extrapolation of the bromate
data. In the 1998 NODA, a low dose linear extrapolation of the DeAngelo
et al. (1998) data was conducted using a one-stage Weibull time-to-
tumor model. The Weibull model was considered to be the preferred
approach to account for the reduction in animals at risk that may be
due to the decreased survival observed in the high dose group toward
the end of the study. The estimate of cancer risk from the DeAngelo et
al. (1998) study is similar with the risk estimate derived from the
Kurokawa et al. (1986a) study presented in the 1994 proposed rule.
Based on an evaluation of all the data and after review and
consideration of the public comments, EPA believes the MCLG for bromate
should be zero.
9. MCLG for Chloral Hydrate
a. Today's Rule. EPA has decided to not include an MCLG for chloral
hydrate in the Stage 1 DBPR. This decision is based on an analysis of
the technical comments and on the fact that chloral hydrate will be
controlled by the MCLs for TTHM and HAAs and by the treatment technique
of enhanced coagulation.
b. Background and Analysis. The 1994 proposed rule included an MCLG
for chloral hydrate of 0.04 mg/L. This was based on a 90-day mice study
by Sanders et al. (1982) which reported liver toxicity. A RfD of 0.0016
mg/kg/d was used (LOAEL of 16 mg/kg/d with an uncertainty factor of
10,000). In the 1997 DBP NODA (EPA,1997b) and supporting documents
(EPA, 1997c), additional studies on chloral hydrate were discussed,
however, these new studies did not indicate a change in the MCLG for
chloral hydrate.
c. Summary of Comments. The majority of commenters disagreed with
the MCLG of 0.04 mg/L for chloral hydrate. Several commenters
questioned the need for an MCLG for chloral hydrate. These commenters
mentioned its low toxic potential and the fact that safe concentrations
of chloral hydrate are substantially greater than those present in
drinking water. Commenters also questioned the need for an MCLG for
chloral hydrate because the MCLs for THMs and HAAs and the treatment
technique of enhanced coagulation will adequately control for chloral
hydrate and because there were no monitoring provisions proposed. Other
commenters argued that the use of a 10,000 uncertainty factor and the
selection of the Sanders et al. (1982) study as a basis for setting the
MCLG were inappropriate.
In response, EPA agrees with commenters that an MCLG for chloral
hydrate is not needed. This is based on the fact that the TTHM and HAA
MCLs and the treatment technique (i.e., enhanced coagulation/softening)
will control for chloral hydrate, as well as other chlorination
byproducts. In addition, chloral hydrate does not serve as an important
indicator for other chlorination byproducts. The final rule, therefore,
does not contain an MCLG for chloral hydrate. In light of this
decision, EPA is not responding to comments on the uncertainty factor
used as the basis for setting the MCLG.
10. MRDLG for Chlorine
a. Today's Rule. EPA is promulgating an MRDLG of 4 mg/L for
chlorine based on a NOAEL from a chronic study in animals.
b. Background and Analysis. EPA proposed an MRDLG of 4 mg/L for
chlorine. The MRDLG was based on a two-year rodent drinking water study
in which chlorine was given to rats at doses |
