National Primary Drinking Water Regulations: Stage 2 Disinfectants and Disinfection Byproducts Rule; National Primary and Secondary Drinking Water Regulations: Approval of Analytical Methods for Chemical Contaminants

Note: EPA no longer updates this information, but it may be useful as a reference or resource.

[Federal Register: August 18, 2003 (Volume 68, Number 159)]
[Proposed Rules]
[Page 49547-49596]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr18au03-44]

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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Parts 141, 142 and 143
[FRL-7530-3]
RIN 2040-AD38

National Primary Drinking Water Regulations: Stage 2
Disinfectants and Disinfection Byproducts Rule; National Primary and
Secondary Drinking Water Regulations: Approval of Analytical Methods
for Chemical Contaminants

AGENCY: Environmental Protection Agency.
ACTION: Proposed rule.

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SUMMARY: In this document, the Environmental Protection Agency (EPA) is
proposing maximum contaminant level goals (MCLGs) for chloroform,
monochloroacetic acid (MCAA) and trichloroacetic acid (TCAA); National
Primary Drinking Water Regulations (NPDWRs) which consist of maximum
contaminant levels (MCLs) and monitoring, reporting, and public
notification requirements for total trihalomethanes (TTHM--a sum of
chloroform, bromodichloromethane, dibromochloromethane, and bromoform)
and haloacetic acids (HAA5--a sum of mono-, di-, and trichloroacetic
acids and mono- and dibromoacetic acids); and revisions to the reduced
monitoring requirements for bromate. This document also specifies the
best available technologies (BATs) for the proposed MCLs. EPA is also
proposing additional analytical methods for the determination of
disinfectants and disinfection byproducts (DBPs) in drinking water and
proposing to extend approval of DBP methods for the determination of
additional chemical contaminants. This set of regulations proposed
today is known as the Stage 2 Disinfectants and Disinfection Byproducts
Rule (Stage 2 DBPR). EPA's objective for the Stage 2 DBPR is to reduce
the potential risks of reproductive and developmental health effects
and cancer associated with disinfection byproducts (DBPs) by reducing
peak and average levels of DBPs in drinking water supplies.
The Stage 2 DBPR applies to public water systems (PWS) that are
community water systems (CWSs) or nontransient noncommunity water
systems (NTNCWs) that add a primary or residual disinfectant other than
ultraviolet light or deliver water that has been treated with a primary
or residual disinfectant other than ultraviolet light.

DATES: The Agency requests comments on today's proposal. Comments must
be received or post-marked by midnight November 17, 2003.

ADDRESSES: Comments may be submitted by mail to: Water Docket,
Environmental Protection Agency, Mail Code 4101T, 1200 Pennsylvania
Ave., NW., Washington, DC 20460, Attention Docket ID No. OW-2002-0043.
Comments may also be submitted electronically or through hand delivery/
courier by following the detailed instructions as provided in section
I.C. of the SUPPLEMENTARY INFORMATION section.

FOR FURTHER INFORMATION CONTACT: For technical inquiries, contact Tom
Grubbs, Office of Ground Water and Drinking Water (MC 4607M), U.S.
Environmental Protection Agency, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460; telephone (202) 564-5262. For regulatory
inquiries, contact Jennifer McLain at the same address; telephone (202)
564-5248. For general information contact the Safe Drinking Water
Hotline, Telephone (800) 426-4791. The Safe Drinking Water Hotline is
open Monday through Friday, excluding legal holidays, from 9 a.m. to
5:30 p.m. Eastern Time.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Who Is Regulated by This Action?

Entities potentially regulated by the Stage 2 DBPR are community
and nontransient noncommunity water systems that add a primary or
residual disinfectant other than ultraviolet light or deliver water
that has been treated with a primary or residual disinfectant other
than ultraviolet light. Regulated categories and entities are
identified in the following chart.

------------------------------------------------------------------------
Category Examples of regulated entities
------------------------------------------------------------------------
Industry..................... Community and nontransient noncommunity
water systems that add a primary or
residual disinfectant other than
ultraviolet light or deliver water that
has been treated with a primary or
residual disinfectant other than
ultraviolet light.
State, Local, Tribal, or Community and nontransient noncommunity
Federal Governments. water systems that add a primary or
residual disinfectant other than
ultraviolet light or deliver water that
has been treated with a primary or
residual disinfectant other than
ultraviolet light.
------------------------------------------------------------------------

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 of which EPA is now
aware that 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 definition of ``public water system'' in Sec.
141.2 and the section entitled ``coverage'' (Sec. 141.3) in Title 40
of the Code of Federal Regulations and applicability criteria in Sec.
141.600 and 141.620 of today's proposal. If you have questions
regarding the applicability of the Stage 2 DBPR to a particular entity,
contact one of the persons listed in the preceding section entitled FOR
FURTHER INFORMATION CONTACT.

B. How Can I Get Copies of This Document and Other Related Information?

1. Docket. EPA has established an official public docket for this
action under Docket ID No. OW-2002-0043. The official public docket
consists of the documents specifically referenced in this action, any
public comments received, and other information related to this action.
Although a part of the official docket, the public docket does not
include Confidential Business Information (CBI) or other information
whose disclosure is restricted by statute. The official public docket
is the collection of materials that is available for public viewing at
the Water Docket in the EPA Docket Center, (EPA/DC) EPA West, Room
B102, 1301 Constitution Ave., NW., Washington, DC. The EPA Docket
Center Public Reading Room is open from 8:30 a.m. to 4:30 p.m., Monday
through Friday, excluding legal holidays. The telephone number for the
Public Reading Room is (202) 566-1744, and the telephone number for the
Water Docket is (202) 566-2426. For access to docket material, please
call (202) 566-2426 to schedule an appointment.
2. Electronic Access. You may access this Federal Register document
electronically through the EPA Internet under the ``Federal Register''
listings at http://www.epa.gov/fedrgstr/.

[[Page 49549]]

An electronic version of the public docket is available through
EPA's electronic public docket and comment system, EPA Dockets. You may
use EPA Dockets at http://www.epa.gov/edocket/ to submit or view public
comments, access the index listing of the contents of the official
public docket, and to access those documents in the public docket that
are available electronically. Once in the system, select ``search,''
then key in the appropriate docket identification number.
Certain types of information will not be placed in the EPA Dockets.
Information claimed as CBI and other information whose disclosure is
restricted by statute, which is not included in the official public
docket, will not be available for public viewing in EPA's electronic
public docket. EPA's policy is that copyrighted material will not be
placed in EPA's electronic public docket but will be available only in
printed, paper form in the official public docket. Although not all
docket materials may be available electronically, you may still access
any of the publicly available docket materials through the docket
facility identified in section I.B.1.
For public commenters, it is important to note that EPA's policy is
that public comments, whether submitted electronically or in paper,
will be made available for public viewing in EPA's electronic public
docket as EPA receives them and without change, unless the comment
contains copyrighted material, CBI, or other information whose
disclosure is restricted by statute. When EPA identifies a comment
containing copyrighted material, EPA will provide a reference to that
material in the version of the comment that is placed in EPA's
electronic public docket. The entire printed comment, including the
copyrighted material, will be available in the public docket.
Public comments submitted on computer disks that are mailed or
delivered to the docket will be transferred to EPA's electronic public
docket. Public comments that are mailed or delivered to the Docket will
be scanned and placed in EPA's electronic public docket. Where
practical, physical objects will be photographed, and the photograph
will be placed in EPA's electronic public docket along with a brief
description written by the docket staff.

C. How and to Whom Do I Submit Comments?

You may submit comments electronically, by mail, or through hand
delivery/courier. To ensure proper receipt by EPA, identify the
appropriate docket identification number in the subject line on the
first page of your comment. Please ensure that your comments are
submitted within the specified comment period. Comments received after
the close of the comment period will be marked ``late.'' EPA is not
required to consider these late comments.
1. Electronically. If you submit an electronic comment as
prescribed below, EPA recommends that you include your name, mailing
address, and an e-mail address or other contact information in the body
of your comment. Also include this contact information on the outside
of any disk or CD ROM you submit, and in any cover letter accompanying
the disk or CD ROM. This ensures that you can be identified as the
submitter of the comment and allows EPA to contact you in case EPA
cannot read your comment due to technical difficulties or needs further
information on the substance of your comment. EPA's policy is that EPA
will not edit your comment, and any identifying or contact information
provided in the body of a comment will be included as part of the
comment that is placed in the official public docket, and made
available in EPA's electronic public docket. If EPA cannot read your
comment due to technical difficulties and cannot contact you for
clarification, EPA may not be able to consider your comment.
a. EPA Dockets. Your use of EPA's electronic public docket to
submit comments to EPA electronically is EPA's preferred method for
receiving comments. Go directly to EPA Dockets at http://www.epa.gov/
edocket, and follow the online instructions for submitting comments.
Once in the system, select ``search,'' and then key in Docket ID No.
OW-2002-0043. The system is an ``anonymous access'' system, which means
EPA will not know your identity, e-mail address, or other contact
information unless you provide it in the body of your comment.
b. E-mail. Comments may be sent by electronic mail (e-mail) to OW-
Docket@epa.gov, Attention Docket ID No. OW-2002-0043. In contrast to
EPA's electronic public docket, EPA's e-mail system is not an
``anonymous access'' system. If you send an e-mail comment directly to
the Docket without going through EPA's electronic public docket, EPA's
e-mail system automatically captures your e-mail address. E-mail
addresses that are automatically captured by EPA's e-mail system are
included as part of the comment that is placed in the official public
docket, and made available in EPA's electronic public docket.
c. Disk or CD ROM. You may submit comments on a disk or CD ROM that
you mail to the mailing address identified in section I.C.2. These
electronic submissions will be accepted in WordPerfect or ASCII file
format. Avoid the use of special characters and any form of encryption.
2. By Mail. Send three copies of your comments and any enclosures
to: Water Docket, Environmental Protection Agency, Mail Code 4101T,
1200 Pennsylvania Ave., NW., Washington, DC 20460, Attention Docket ID
No. OW-2002-0043.
3. By Hand Delivery or Courier. Deliver your comments to: Water
Docket, EPA Docket Center, Environmental Protection Agency, Room B102,
1301 Constitution Ave., NW., Washington, DC, Attention Docket ID No.
OW-2002-0043. Such deliveries are only accepted during the Docket's
normal hours of operation as identified in section I.B.1.

D. What Should I Consider as I Prepare My Comments for EPA?

You may find the following suggestions helpful for preparing your
comments:
1. Explain your views as clearly as possible.
2. Describe any assumptions that you used.
3. Provide any technical information and/or data you used that
support your views.
4. If you estimate potential burden or costs, explain how you
arrived at your estimate.
5. Provide specific examples to illustrate your concerns.
6. Offer alternatives.
7. Make sure to submit your comments by the comment period
identified.
8. To ensure proper receipt by EPA, identify the appropriate docket
identification number in the subject line on the first page of your
response. It would also be helpful if you provided the name, date, and
Federal Register citation related to your comments.

Abbreviations Used in This Document

AIPC All Indian Pueblo Council
ALT Alanine aminotransferase
AST Aspartate aminotransferase
ASTM American Society for Testing and Materials
AWWA American Water Works Association
AwwaRF American Water Works Association Research Foundation
BAT Best available technology
BCAA Bromochloroacetic acid

[[Page 49550]]

BDCM Bromodichloromethane
CWS Community water system
DBAA Dibromoacetic acid
DBCM Dibromochloromethane
DBP Disinfection byproduct
DBPR Disinfectants and Disinfection Byproducts Rule
DCAA Dichloroacetic acid
DOC Dissolved organic carbon
EA Economic analysis
EC Enhanced coagulation
EDA Ethylenediamine
ED₁₀ Maximum likelihood estimate of a dose producing effects
in 10 percent of animals
EPA United States Environmental Protection Agency
FACA Federal Advisory Committee Act
FBRR Filter Backwash Recycling Rule
GAC Granular activated carbon
GC/ECD Gas chromatography using electron capture detection
GWUDI Ground water under the direct influence of surface water
HAA5 Haloacetic acids (five) (sum of monochloroacetic acid,
dichloroacetic acid, trichloroacetic acid, monobromoacetic acid, and
dibromoacetic acid)
IC Ion chromatography
ICR Information Collection Request
IC/ICP-MS Ion chromatograph--coupled to an inductively coupled plasma
mass spectrometer
IDSE Initial distribution system evaluation
ILSI International Life Sciences Institute
IESWTR Interim Enhanced Surface Water Treatment Rule
IPCS International Programme on Chemical Safety
IRIS Integrated Risk Information System (EPA)
kWh/yr Kilowatt hours per year
LED₁₀ Lower 95 percent confidence bound of the maximum
likelihood estimate of the dose producing effects in 10 percent of
animals
LH Luteinizing hormone
LOAEL Lowest observed adverse effect level
LRAA Locational running annual average
LT1ESWTR Long Term 1 Enhanced Surface Water Treatment Rule
LT2ESWTR Long Term 2 Enhanced Surface Water Treatment Rule
MBAA Monobromoacetic acid
MCAA Monochloroacetic acid
MCL Maximum contaminant level
MCLG Maximum contaminant level goal
M-DBP Microbial and disinfection byproducts
mg/L Milligram per liter
MRL Minimum reporting level
MRDL Maximum residual disinfectant level
MRDLG Maximum residual disinfectant level goal
MTBE Methyl tertiary butyl ether
mWh Megawatt-hours
NATICH National Air Toxics Information Clearinghouse
NDIR Nondispersive infrared detection
NDMA N-nitrosodimethylamine
NDWAC National Drinking Water Advisory Council
NF Nanofiltration
NOAEL No Observed Adverse Effect Level
NODA Notice of data availability
NPDWR National primary drinking water regulation
NRWA National Rural Water Association
NTNCWS Nontransient noncommunity water system
NTP National Toxicology Program
NTTAA National Technology Transfer and Advancement Act
ODA o-dianisidine dihydrochloride
OMB Office of Management and Budget
OSTP Office of Science and Technology Policy
PAR Population attributable risk
PE Performance evaluation
PWS Public water system
QC Quality control
RAA Running annual average
RFA Regulatory Flexibility Act
RfD Reference dose
RSC Relative source contribution
RSD Relative standard deviation
SAB Science Advisory Board
SAC Selective anion concentration
SBAR Small Business Advisory Review
SBREFA Small Business Regulatory Enforcement Fairness Act
SDWA Safe Drinking Water Act, or the ``Act,'' as amended in 1996
SER Small Entity Representative
SGA Small for gestational age
SUVA Specific ultraviolet absorbance
SWAT Surface Water Analytical Tool
SWTR Surface Water Treatment Rule
TAME Tertiary amyl methyl ether
TCAA Trichloroacetic acid
TCR Total Coliform Rule
THM Trihalomethane
TOC Total organic carbon
TTHM Total trihalomethanes (sum of four THMs: chloroform,
bromodichloromethane, dibromochloromethane, and bromoform)
TWG Technical work group
UMRA Unfunded Mandates Reform Act
USDOE EIA U.S. Department of Energy, Energy Information Administration
UV 254 Ultraviolet absorption at 254 nm
WTP Willingness To Pay

Table of Contents

I. Summary
A. Why is EPA Proposing the Stage 2 DBPR?
B. What Does the Stage 2 DBPR Require?
C. What are the Economic Impacts of the Stage 2 DBPR?
II. Background
A. What is the Statutory Authority for the Stage 2 DBPR?
B. What is the Regulatory History of the Stage 2 DBPR?
C. How were Stakeholders Involved in Developing the Stage 2
DBPR?
1. Federal Advisory Committee process
2. Other outreach processes
III. Public Health Risk
A. Reproductive and Developmental Epidemiology
1. Reif et al. 2000
a. Fetal growth
b. Fetal viability
c. Fetal malformations and other developmental anomalies
2. Bove et al. 2002
a. Fetal growth
b. Fetal viability
c. Fetal malformations
3. Nieuwenhuijsen et al. 2000
4. Additional epidemiology studies
B. Reproductive and Developmental Toxicology
1. EPA analysis and research
2. Tyl, 2000
a. Developmental defects
b. Whole litter resorption
c. Fetal toxicity
d. Male reproductive effects
3. World Health Organization review of the reproductive and
developmental toxicology literature (2000)
4. New Studies
C. Conclusions Drawn from the Reproductive and Developmental
Health Effects Data
D. Cancer Epidemiology
1. Population Attributable Risk analysis
2. New epidemiological cancer studies
a. New bladder cancer studies
b. New colon cancer studies
c. New rectal cancer studies
d. Other cancers
3. Review of the cancer epidemiology literature (WHO 2000)
E. Cancer and Other Toxicology
1. EPA criteria documents
2. Other byproducts with carcinogenic potential
a. 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone) (MX)--
multisite cancer
b. N-nitrosodimethylamine (NDMA)--multisite cancer
3. Other toxicological effects
4. WHO review of the cancer toxicology literature (2000)
F. Conclusions Drawn from the Cancer Epidemiology and Toxicology
G. Request for Comment
IV. DBP Occurrence within Distribution Systems
A. Data Sources
1. Information Collection Rule Data
2. Other Data Sources Used to Support the Proposal
B. DBPs in Distribution Systems

[[Page 49551]]

1. DBPs above the MCL occur at some locations in a substantial
number of plants
2. Specific locations in distribution systems are not protected
to MCL levels
3. Stage 1 DBPR maximum residence time location may not reflect
the highest DBP occurrence levels
C. Request for Comment
V. Discussion of Proposed Stage 2 DBPR Requirements
A. MCLG for Chloroform
1. What is EPA proposing today?
2. How was this proposal developed?
a. Background
b. Basis of the new chloroform MCLG
i. Mode of action
ii. Metabolism
c. How the MCLG is derived
i. Reference dose
ii. Relative source contribution
iii. Water ingestion and body weight assumptions
iv. MCLG calculation
v. Other considerations
d. Feasibility of other options
3. Request for comment
B. MCLGs for THMs and HAAs
1. What is EPA proposing today?
2. How was this proposal developed?
a. Trichloroacetic acid
b. Monochloroacetic acid
3. Request for comment
C. Consecutive Systems
1. What is EPA proposing today?
a. Definitions
b. Monitoring
c. Compliance schedules
d. Treatment
e. Violations
f. Public notice and consumer confidence reports
g. Recordkeeping and reporting
h. State special primacy conditions
2. How was this proposal developed?
3. Request for comment
D. MCLs for TTHM and HAA5
1. What is EPA proposing today?
2. How was this proposal developed?
a. Definition of an LRAA
b. Consideration of regulatory alternatives
c. Basis for the LRAA
d. Basis for phasing LRAA compliance
e. TTHM and HAA5 as Indicators
3. Request for comment
E. Requirements for Peak TTHM and HAA5 Levels
1. What is EPA proposing today?
2. How was this proposal developed?
3. Request for comment
F. BAT for TTHM and HAA5
1. What is EPA proposing today?
2. How was this proposal developed?
a. Basis for the BAT
i. BAT analysis using the Information Collection Rule treatment
studies
ii. BAT analysis using the SWAT
b. Basis for the Consecutive System BAT
3. Request for comment
G. MCL, BAT, and Monitoring for Bromate
1. What is EPA proposing today?
2. How was this proposal developed?
a. Bromate MCL
b. Bromate in hypochlorite solutions
c. Criterion for reduced bromate monitoring
3. Request for comment
H. Initial Distribution System Evaluation (IDSE)
1. What is EPA proposing today?
a. Applicability
b. Data collection
i. Standard monitoring program
ii. System specific study
iii. 40/30 certification
c. Implementation
2. How was this proposal developed?
a. Applicability
b. Data collection
c. Implementation
3. Request for comment
a. Applicability
b. Data collection
c. Implementation
I. Monitoring Requirements and Compliance Determination for
Stage 2A and Stage 2B TTHM and HAA5 MCLs
1. What is EPA proposing today?
a. Stage 2A
b. IDSE
c. Stage 2B
i. Subpart H systems serving 10,000 or more people
ii. Subpart H systems serving 500 to 9,999 people
iii. Subpart H systems serving fewer than 500 people
iv. Ground water systems serving 10,000 or more people
v. Ground water systems serving fewer than 10,000 people
vi. Consecutive systems
2. How was this proposal developed?
a. Sampling intervals for quarterly monitoring
b. Reduced monitoring frequency
c. Different IDSE sampling locations by disinfectant type
d. Population-based monitoring requirements for certain
consecutive systems
3. Request for comment
a. Proposed IDSE and Stage 2B monitoring requirements
b. Plant-based vs. population-based monitoring requirements
i. Issues with plant-based monitoring requirements
ii. Approaches to addressing issues with plant-based monitoring
J. Compliance Schedules
1. What is EPA proposing?
2. How did EPA develop this proposal?
3. Request for comments
K. Public Notice Requirements
1. What is EPA proposing?
2. Request for comments
L. Variances and Exemptions
1. Variances
2. What are the affordable treatment technologies for small
systems?
M. Requirements for Systems to Use Qualified Operators
N. System Reporting and Recordkeeping Requirements
1. Confirmation of applicable existing requirements
2. Summary of additional reporting requirements
3. Request for comment
O. Analytical Method Requirements
1. What is EPA proposing today?
2. How was this proposal developed?
3. Which new methods are proposed for approval?
a. EPA Method 327.0 for chlorine dioxide and chlorite.
b. EPA Method 552.3 for HAA5 and dalapon
c. ASTM D 6581-00 for bromate, chlorite, and bromide
d. EPA Method 317.0 revision 2 for bromate, chlorite, and
bromide
e. EPA Method 326.0 for bromate, chlorite, and bromide
f. EPA Method 321.8 for bromate
g. EPA 415.3 for TOC and SUVA (DOC and UV₂₅₄)
4. What additional regulated contaminants can be monitored by
extending approval of EPA Method 300.1?
5. Which methods in the 20th edition and 2003 On-Line Version of
Standard Methods are proposed for approval?
6. What is the updated citation for EPA Method 300.1?
7. How is the HAA5 sample holding time being standardized?
8. How is EPA clarifying which methods are approved for
magnesium determinations?
9. Which methods can be used to demonstrate eligibility for
reduced bromate monitoring?
10. Request for comments
P. Laboratory Certification and Approval
1. What is EPA proposing today?
2. What changes are proposed for the PE acceptance criteria?
3. What minimum reporting limits are being proposed?
4. What are the requirements for analyzing IDSE samples?
5. Request for comments
VI. State Implementation
A. State Primacy Requirements for Implementation Flexibility
B. State Recordkeeping Requirements
C. State Reporting Requirements
D. Interim Primacy
E. IDSE Implementation
F. State Burden
VII. Economic Analysis
A. Regulatory Alternatives Considered by the Agency
B. Rationale for the Proposed Rule Option
1. Reducing peak exposure
2. Reducing average exposure
C. Benefits of the Proposed Stage 2 DBPR
1. Non-quantifiable health and non-health related benefits
2. Quantifiable health benefits
3. Benefit sensitivity analyses
D. Costs of the Proposed Stage 2 DBPR
1. National cost estimates
2. Water system costs
3. State costs
4. Non-quantifiable
E. Expected System Treatment Changes
1. Pre-Stage 2 DBPR baseline conditions
2. Predicted technology distributions post-Stage 2 DBPR
F. Estimated Household Costs of the Proposed Rule
G. Incremental Costs and Benefits of the Proposed Stage 2 DBPR
H. Benefits From the Reduction of Co-Occurring Contaminants

[[Page 49552]]

I. Are there Increased Risks From Other Contaminants?
J. Effects on General Population and Subpopulation Groups
K. Uncertainties in Baseline, Risk, Benefit, and Cost Estimates
L. Benefit/Cost Determination for the Proposed Stage 2 DBPR
M. Request for Comment
VIII. Statutory and Executive Order Reviews
A. Executive Order 12866: Regulatory Planning and Review
B. Paperwork Reduction Act
C. Regulatory Flexibility Act
D. Unfunded Mandates Reform Act
E. Executive Order 13132: Federalism
F. Executive Order 13175: Consultation and Coordination with
Indian Tribal Governments
G. Executive Order 13045: Protection of Children from
Environmental Health and Safety Risks
H. Executive Order 13211: Actions That Significantly Affect
Energy Supply, Distribution, or Use
I. National Technology Transfer and Advancement Act
J. Executive Order 12898: Federal Actions to Address
Environmental Justice in Minority Populations or Low Income
Populations
K. Consultations with the Science Advisory Board, National
Drinking Water Advisory Council, and the Secretary of Health and
Human Services
L. Plain Language
IX. References

I. Summary

A. Why Is EPA Proposing the Stage 2 DBPR?

The Environmental Protection Agency is committed to ensuring that
all public water systems provide clean and safe drinking water.
Disinfectants are often an essential element of drinking water
treatment because of the barrier they provide against harmful
waterborne microbial pathogens. However, disinfectants react with
naturally occurring organic and inorganic matter in source water and
distribution systems to form disinfection byproducts (DBPs) that may
pose health risks. The Agency is proposing the Stage 2 Disinfectants
and Disinfection Byproduct Rule (DBPR) to reduce potential cancer,
reproductive, and developmental risks from DBPs.
The Stage 2 DBPR augments the Stage 1 DBPR that was finalized in
1998. The proposed Stage 2 DBPR focuses on monitoring and reducing
concentrations of two classes of DBPs: total trihalomethanes (TTHM) and
haloacetic acids (HAA5). In part, these two groups of DBPs are used as
indicators of the various byproducts that are present in disinfected
water. This means that concentrations of TTHM and HAA5 are monitored
for compliance, but their presence in drinking water is representative
of many other DBPs that may also be present in the water; likewise, a
reduction in TTHM and HAA5 indicates a reduction of total DBPs.
The Stage 2 DBPR is designed to reduce the level of exposure from
disinfectants and DBPs without undermining the control of microbial
pathogens. The Long Term 2 Enhanced Surface Water Treatment Rule
(LT2ESWTR) will be finalized and implemented simultaneously with the
Stage 2 DBPR to ensure that drinking water is microbiologically safe at
the limits set for disinfectants and DBPs.
New information on health effects, occurrence, and treatment has
become available since the Stage 1 DBPR, which supports the need for
the Stage 2 DBPR. Several reproductive and developmental studies have
recently become available, and EPA has completed a more extensive
analysis of reproductive and developmental effects associated with DBPs
since the Stage 1 DBPR. Both human epidemiology studies and animal
toxicology studies have shown associations between chlorinated drinking
water and reproductive and developmental endpoints such as spontaneous
abortion, stillbirth, neural tube defects, pre-term delivery,
intrauterine growth retardation, and low birth weight. New epidemiology
and toxicology studies evaluating bladder and rectal cancers have also
increased the weight of evidence linking these health effects to DBP
exposure. The large number of people (254 million Americans) exposed to
DBPs and the identified potential cancer, reproductive, and
developmental risks played a significant role in EPA's decision to move
forward with regulatory changes that target lowering DBP exposures
beyond the requirements of the Stage 1 DBPR.
While the Stage 1 DBPR provided a major reduction in DBP exposure,
new national survey data suggest that some customers are receiving
drinking water with elevated, or peak DBP concentrations even when
their distribution systems are in compliance with the Stage 1 DBPR.
Some of these peak concentrations can be substantially greater than the
Stage 1 DBPR maximum contaminant levels (MCLs). The new survey results
also showed that Stage 1 DBPR monitoring sites may not be
representative of peak DBP concentrations that occur in distribution
systems. In addition, the new information indicates that cost-effective
technologies including ultraviolet light (UV) and granular activated
carbon (GAC) may be very effective at lowering DBP levels. EPA's
analysis of this new information concludes that significant public
health benefits may be achieved through further cost-effective
reduction of DBPs in distribution systems.
Congress required EPA to promulgate the Stage 2 DBPR as part of the
1996 Safe Drinking Water Act (SDWA) Amendments (section 1412(b)(2)(C)).
Today's proposal reflects consensus recommendations from the Stage 2
Microbial/Disinfection Byproducts (M-DBP) Federal Advisory Committee
(the Advisory Committee). These recommendations are set forth in the M-
DBP Agreement in Principle (USEPA 2000g), which can be accessed on the
edocket Web site (www.epa.gov/edocket).
After considering the new occurrence and health effects data and
analyses, EPA has determined that there is an opportunity to further
reduce potential risks from DBPs. The Stage 2 DBPR being proposed today
presents a cost-effective, risk targeting approach to reduce risks from
DBPs. The new requirements provide for more consistent protection from
DBPs across the entire distribution system and the reduction of DBP
peaks. New risk targeting provisions require only those systems with
the greatest risk to make capital improvements. The Stage 2 DBPR, in
conjunction with the LT2ESWTR, will help public water systems deliver
safer water to Americans with the benefits of disinfection to control
pathogens but with fewer risks from DBPs.

B. What Does the Stage 2 DBPR Require?

The Stage 2 DBPR applies to community or nontransient noncommunity
water systems that add a primary or residual disinfectant other than
ultraviolet light or deliver water that has been treated with a primary
or residual disinfectant other than ultraviolet light. The TTHM and
HAA5 MCL values will remain the same as in the Stage 1 DBPR, although
compliance calculations will be different. The proposed Stage 2 DBPR
includes new MCLGs for chloroform, monochloroacetic acid, and
trichloroacetic acid, but these new MCLGs do not affect the MCLs for
TTHM or HAA5.
The risk targeting components of the Stage 2 DBPR will focus the
greatest amount of change where the greatest amount of risk may exist.
The provisions of the Stage 2 DBPR focus on identifying and reducing
exposure by reducing DBP peaks in distribution systems. The first
provision, designed to address significant variations in exposure, is
the Initial Distribution System Evaluation (IDSE). The purpose

[[Page 49553]]

of the IDSE is to identify Stage 2 DBPR compliance monitoring sites for
capturing peaks. Because Stage 2 DBPR compliance will be determined at
these new monitoring sites, distribution systems that identify elevated
concentrations of TTHM and HAA5 will need to make treatment or process
changes to bring the system into compliance with the Stage 2 DBPR. By
identifying compliance monitoring sites with elevated concentrations of
TTHM and HAA5, the IDSE will offer increased assurance that MCLs are
being met across the distribution system. Both treatment changes and
awareness of TTHM and HAA5 levels resulting from the IDSE will allow
systems to better control for distribution system peaks.
The IDSE is designed to offer flexibility to public water systems.
The IDSE requires TTHM and HAA5 monitoring for one year on a regular
schedule that is determined by source water type and system size.
Systems have the option of performing a site-specific study based on
historical data, water distribution system models, or other data; and
waivers are available under certain circumstances. The proposed IDSE
requirements are discussed in sections V.H., V.I., and V.J. of this
preamble and in subpart U of the proposed rule.
The second provision of the Stage 2 DBPR, which is designed to
address variations in temporal and spatial exposure, is the new
compliance calculation of the MCLs. The Stage 1 DBPR running annual
average (RAA) calculation allows some locations within a distribution
system to have higher DBP annual averages than others as long as the
system-wide average is below the MCL. The Stage 2 DBPR will base
compliance on a locational running annual average (LRAA) calculation
where the annual average at each sampling location in the distribution
system will be used to determine compliance with the MCLs. The LRAA
will reduce exposures to peak DBP concentrations by ensuring that each
monitoring site is in compliance with the MCLs as an annual average,
and it will provide all customers drinking water that more consistently
meets the MCLs.
EPA is proposing that systems comply with the Stage 2 DBPR MCLs in
two phases, designated as Stage 2A and Stage 2B. In Stage 2A, beginning
three years after the rule is final, all systems must comply with MCLs
of 0.120 mg/L for TTHM and 0.100 mg/L for HAA5 as LRAAs at Stage 1 DBPR
sampling sites, in addition to continuing to comply with the Stage 1
DBPR MCLs of 0.080 mg/L and 0.060 mg/L as RAAs for TTHM and HAA5,
respectively. In Stage 2B, systems must comply with MCLs of 0.080 mg/L
and 0.060 mg/L as LRAAs for TTHM and HAA5, respectively, based on
sampling sites identified through the IDSE. A more detailed discussion
of the proposed Stage 2 DBPR MCL requirements can be found in sections
V.D., V.I., and V.J. of this preamble and in Sec. 141.64(b)(2) and
(3), and Sec. 141.136, and subpart V of the rule language.
The IDSE and LRAA calculation will lead to overall reductions in
DBP concentrations and reduce short term exposures to high DBP
concentrations, but even with this strengthened approach to regulating
DBPs it will be possible for individual DBP samples to exceed the MCLs
when systems are in compliance with the Stage 2 DBPR. The Stage 2 DBPR
requires systems that experience significant excursions to evaluate
distribution system operational practices and identify opportunities to
reduce DBP concentrations in the distribution system. This provision
will curtail peaks and reduce exposure to high DBP levels. Significant
excursions are discussed in greater detail in section V.E.
The Stage 2 DBPR also contains provisions for regulating
consecutive systems, defined in the Stage 2 DBPR as public water
systems that buy or otherwise receive some or all of their finished
water from another public water system on a regular basis. Uniform
regulation of consecutive systems provided by the Stage 2 DBPR will
ensure that consecutive systems deliver drinking water that meets
applicable DBP standards. More information on regulation of consecutive
systems can be found in sections V.C., V.H., V.I. and V.J.
Today's document proposes plant-based monitoring requirements for
non-consecutive systems and certain consecutive systems. Plant-based
monitoring means that the number of compliance monitoring locations
within a distribution system is based on the number of plants,
population served, and type of source water used by the distribution
system. EPA is proposing population-based monitoring for consecutive
systems that buy all their finished water from other public water
systems. EPA is also requesting comment on whether this approach should
be extended to all systems covered by today's rule. Under a population-
based monitoring structure, the number of compliance monitoring
locations is based only on the population served and source water type.
Section V.I. describes population-based monitoring and how it might
affect systems complying with this rule.

C. What Are the Economic Impacts of the Stage 2 DBPR?

EPA quantified the potential benefits of the Stage 2 DBPR by
estimating the reduction in bladder cancer cases that may result from
the decrease in average DBP concentrations in disinfected water.
Estimated reductions in DBP-related bladder cancers (including both
fatal and non-fatal cases) result in annualized benefits ranging from
$0 to $986 million (using a three percent discount rate), depending on
the risk level assumed.
There may also be a number of important nonquantifiable benefits
associated with reducing DBPs in drinking water, the primary ones being
reduced potential risk of adverse reproductive and developmental
effects including miscarriage, stillbirth, neural tube defects, heart
defects, and cleft palate. Although a number of studies have found an
association between reproductive and developmental endpoints and short-
term exposure to elevated DBP levels, a causal link has not yet been
established and information is not yet available to quantify potential
effects. As a result, the Agency has not included an estimate of the
potential benefits from reducing reproductive and developmental risks
in its primary economic impact analysis of the Stage 2 DBPR. However,
an illustrative calculation of potential fetal loss risk is discussed
in Section VII and presented in more detail in the Economic Analysis
(USEPA 2003i) to illustrate the benefits that could be associated with
this rule. Reduction in other cancers potentially associated with DBP
exposure represent additional unquantified health benefits.
EPA estimates the total annualized costs of the Stage 2 DBPR to be
$54 to $64 million. This estimate includes costs associated with
treatment changes, the Initial Distribution System Evaluation, changes
in compliance monitoring, and rule implementation activities for both
public water systems and States. EPA estimates that approximately 2.8
percent of all plants will need to convert to chloramines or add
advanced treatment to comply with the Stage 2 DBPR.
Table I-1 presents the estimated quantified and unquantified
benefits of the Stage 2 DBPR and the estimated costs. Analyses of
unquantified benefits suggest that the total benefits associated with
the Stage 2 DBPR might be much greater than these estimates. By
targeting risks and building on the solid foundation of the Stage 1
DBPR, the

[[Page 49554]]

Stage 2 DBPR will deliver cost-effective reductions in DBP levels and
associated potential public health risks.

Table I-1.--Costs and Benefits of the Stage 2 DBPR Based on Annualization Discount Rate of 3%
----------------------------------------------------------------------------------------------------------------
Costs Benefits Unquantified benefits
----------------------------------------------------------------------------------------------------------------
$54-64 M................................. $0-986 M Reduction in potential reproductive and developmental
health effects, potential reduction in colon and
rectal cancer, improved taste and odor of drinking
water, control of contaminants that may be regulated
in the future.
----------------------------------------------------------------------------------------------------------------

II. Background

A combination of factors have influenced the development of the
proposed Stage 2 DBPR. These include the initial 1992-1994 Microbial
and Disinfection Byproduct (M-DBP) stakeholder deliberations and EPA's
Stage 1 DBPR proposal; the 1996 Safe Drinking Water Act (SDWA)
Amendments; the 1996 Information Collection Rule; the 1998 Stage 1
DBPR; other new data, research, and analysis on disinfection byproduct
(DBP) occurrence, treatment, and health effects since the Stage 1 DBPR;
and the Stage 2 DBPR Microbial and Disinfection Byproducts Federal
Advisory Committee. The following shows how EPA arrived at this
proposal for regulating disinfection byproducts.

A. What Is the Statutory Authority for the Stage 2 DBPR?

The SDWA, as amended in 1996, authorizes EPA to promulgate a
national primary drinking water regulation (NPDWR) and publish a
maximum contaminant level goal (MCLG) for contaminants the
Administrator determines ``may have an adverse effect on the health of
persons,'' is ``known to occur or there is a substantial likelihood
that the contaminant will occur in public water 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)). MCLGs
are non-enforceable health goals set at a level at which ``no known or
anticipated adverse effects on the health of persons occur and which
allows an adequate margin of safety''. These health goals are published
at the same time as the NPDWR (sections 1412(b)(4) and 1412(a)(3)).
The Agency may also consider additional health risks from other
contaminants and establish an MCL ``at a level other than the feasible
level, if the technology, treatment techniques, and other means used to
determine the feasible level would result in an increase in the health
risk from drinking water by--(i) increasing the concentration of other
contaminants in drinking water; or (ii) interfering with the efficacy
of drinking water treatment techniques or processes that are used to
comply with other national primary drinking water regulations''
(section 1412(b)(5)(A)). When establishing an MCL or treatment
technique under this authority, ``the level or levels of treatment
techniques shall minimize the overall risk of adverse health effects by
balancing the risk from the contaminant and the risk from other
contaminants the concentrations of which may be affected by the use of
a treatment technique or process that would be employed to attain the
MCL or levels'' (section 1412(b)(5)(B)).
Finally, section 1412(b)(2)(C) of the Act requires EPA to
promulgate a Stage 2 DBPR 18 months after promulgation of the Long Term
1 Enhanced Surface Water Treatment Rule (LT1ESWTR). Consistent with
statutory requirements for risk balancing (section 1412(b)(5)(B)), EPA
will finalize the LT2ESWTR concurrently with the Stage 2 DBPR to ensure
simultaneous protection from microbial and DBP risks.

B. What Is the Regulatory History of the Stage 2 DBPR?

The first rule to regulate DBPs was promulgated on November 29,
1979. The Total Trihalomethanes Rule (44 FR 68624) (USEPA 1979) set an
MCL of 0.10 mg/L for total trihalomethanes (TTHMs). Compliance was
based on the running annual average (RAA) of quarterly averages of all
samples collected throughout the distribution system. This TTHM
standard applied only to community water systems using surface water
and/or ground water that served at least 10,000 people and added a
disinfectant to the drinking water during any part of the treatment
process.
Under the Surface Water Treatment Rule (SWTR) (54 FR 27486, June
29, 1989) (USEPA 1989a), EPA set MCLGs of zero for Giardia lamblia,
viruses, and Legionella; and promulgated NPDWRs for all public water
systems 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 other pathogenic
organisms.
EPA also promulgated the Total Coliform Rule (TCR) on June 29, 1989
(54 FR 27544)(USEPA 1989b) to provide protection from microbial
contamination in distribution systems of all types of public water
supplies. The TCR established an MCLG of zero for total and fecal
coliform bacteria, and an MCL based on the percentage of positive
samples collected during a compliance period. Under the TCR, no more
than 5 percent of distribution system samples collected in any month
may contain coliform bacteria.
Together, the SWTR and the TCR were intended to address risks
associated with microbial pathogens that might be found in source
waters or associated with distribution systems. However, while reducing
exposure to pathogenic organisms, the SWTR also increased the use of
disinfectants in some public water systems and, as a result, exposure
to DBPs in those systems.
In 1992, prompted by concerns about health risk tradeoffs between
disinfection byproducts and microbial pathogens, EPA initiated a
negotiated rulemaking with a wide range of stakeholders. The
negotiators included representatives of State and local health and
regulatory agencies, public water systems, elected officials, consumer
groups, and environmental groups. The Regulatory Negotiating Committee
met from November 1992 through June 1993. Following months of intensive
discussions and technical analyses, the Regulatory Negotiating
Committee recommended the development of three sets of rules: an
Information Collection Rule, a two-staged approach for regulating DBPs,
and an ``interim'' Enhanced Surface Water Treatment Rule (IESWTR) to be
followed by a ``final'' Enhanced Surface Water Treatment Rule (USEPA
1996a, USEPA 1998c, USEPA 1998d). EPA took the first step towards
implementing this strategy by proposing

[[Page 49555]]

the Stage 1 DBPR and IESWTR in 1994. Congress affirmed the phased
microbial and disinfection byproduct rulemaking strategy in the 1996
SDWA Amendments by requiring that EPA develop these three sets of rules
on a specific schedule that stipulates simultaneous promulgation of
requirements governing microbial protection and DBPs.
In March 1997, the Agency established the Microbial and
Disinfection Byproduct (M-DBP) Advisory Committee under the Federal
Advisory Committee Act (FACA) to collect, share, and analyze new
information and data available since the 1994 proposals of the Stage 1
DBPR and the IESWTR, as well as to build consensus on the regulatory
implications of the new information. The Advisory 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
Advisory Committee met five times in March through July 1997 to discuss
issues related to the IESWTR and the Stage 1 DBPR. The Advisory
Committee reached consensus on a number of major issues that were
incorporated into the Stage 1 DBPR and the IESWTR.
The Stage 1 DBPR and IESWTR, finalized in December 1998, were the
first rules to be promulgated under the 1996 SDWA Amendments (USEPA
1998c and 1998d). The Stage 1 DBPR applies to all community and
nontransient noncommunity water systems that add a chemical
disinfectant to water. The rule established maximum residual
disinfectant level goals (MRDLGs) and enforceable maximum residual
disinfectant level (MRDL) standards for three chemical disinfectants--
chlorine, chloramine, and chlorine dioxide; maximum contaminant level
goals (MCLGs) for three THMs, two haloacetic acids (HAAs), bromate, and
chlorite; and enforceable maximum contaminant level (MCL) standards for
TTHM, five haloacetic acids (HAA5), chlorite, and bromate calculated as
running annual averages (RAAs). The Stage 1 DBPR uses TTHMs and HAA5 as
indicators of the various DBPs that are present in disinfected water.
Under the Stage 1 DBPR, 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 (TOC), that may
react with disinfectants to form DBPs. Removal is achieved through
enhanced coagulation or enhanced softening, unless a system meets
alternative compliance criteria.
EPA finalized the IESWTR at the same time as the Stage 1 DBPR to
ensure simultaneous compliance and address risk tradeoff issues. The
IESWTR applies to all water systems that use surface water or ground
water under the direct influence of surface water that serve at least
10,000 people. The purpose of the IESWTR is to improve control of
microbial pathogens in drinking water, specifically the protozoan
Cryptosporidium.
The Filter Backwash Recycle Rule (FBRR) and the Long Term 1
Enhanced Surface Water Treatment Rule (LT1ESWTR) round out the first
group of regulations balancing microbial and DBP risks. EPA promulgated
the FBRR in 2001 (USEPA 2001c) and the LT1ESWTR in 2002 (USEPA 2002b)
to increase protection of finished drinking water supplies from
contamination by Cryptosporidium and other microbial pathogens. The
LT1ESWTR extends protection against Cryptosporidium and other disease-
causing microbes to water systems that use surface water or ground
water under the direct influence of surface water that serve fewer than
10,000 people. While the Ground Water Rule, proposed in May 2000,
(USEPA 2000h) will add significant protection from pathogens in
vulnerable ground water systems, it does not pose as many risk-risk
tradeoff considerations as the surface water rules because only a small
percentage of ground water systems subject to the Stage 2 DBPR have
high DBP levels.
EPA reconvened the Advisory Committee in March 1999 to develop
recommendations on issues pertaining to the Stage 2 DBPR and LT2ESWTR.
The Advisory Committee collected, developed, and evaluated new
information that became available after the Stage 1 DBPR was published.
The Information Collection Rule provided new data on DBP exposure, and
control; it also included new data on occurrence and treatment of
pathogens. The unprecedented amount of information collected under the
Information Collection Rule was supplemented by a survey conducted by
the National Rural Water Association, data provided by various States,
the Water Utility Database (which contains data collected by the
American Water Works Association), and Information Collection Rule
Supplemental Surveys. This large body of data allowed the Advisory
Committee to reach new conclusions regarding DBP exposure and new
treatment options.
After analyzing the data, the Advisory Committee reached three
significant conclusions that led the Advisory Committee to recommending
further control of DBPs in public water systems. The data from the
Information Collection Rule show that the RAA compliance calculation
allows elevated DBP levels to regularly occur at some locations in the
system when the overall average at all locations is below the MCL.
Customers served at those sampling locations that regularly exceed the
MCLs are experiencing higher exposure compared to customers served at
locations that consistently meet the MCLs.
Second, the new data demonstrated how single samples can be
substantially above the MCLs. The new information showed that it is
possible for customers to receive drinking water with concentrations of
DBPs up to 75% above the MCLs even when their water system is in
compliance with the Stage 1 DBPR. Studies have shown that DBP exposure
during short, critical time windows may adversely impact reproductive
and developmental health.
Third, data from the Information Collection Rule revealed that the
highest TTHM and HAA5 levels are not always located at the maximum
residence time monitoring sites specified by the Stage 1 DBPR. These
sites were required for monitoring by the Stage 1 DBPR because previous
data suggested that water in the distribution system for the maximum
residence time would have the highest TTHM levels. The fact that the
locations with the highest DBP levels varied in different public water
systems indicates that the Stage 1 DBPR monitoring sites may not be
representative of the high DBP concentrations that actually exist in
distribution systems, and additional monitoring is needed to identify
distribution system locations with elevated DBP levels. This
information encouraged the Advisory Committee to recommend additional
measures to identify locations with high LRAAs. Section IV provides a
complete discussion of the new occurrence data.
The analysis of the new data also indicates that certain
technologies are effective at reducing DBP concentrations. Bench- and
pilot-scale studies for granular activated carbon (GAC) and membrane
technologies required by the Information Collection Rule provided
information on the effectiveness of the two technologies. Other studies
found UV light to be highly effective for inactivating Cryptosporidium
and Giardia at low doses without promoting the formation of DBPs
(Malley et al. 1996; Zheng et al.

[[Page 49556]]

1999). This new treatment information added to the treatment options
available to utilities for controlling DBPs beyond the requirements of
the Stage 1 DBPR.
New data on the health effects of DBPs also influenced the Advisory
Committee's recommendation to further regulate DBPs. Although bladder
cancer risks were the focus of the Stage 1 M-DBP negotiations,
potential reproductive and developmental health effects were central to
the Stage 2 M-DBP Advisory Committee discussions. Recent human
epidemiology studies and animal toxicology studies have both shown
associations between chlorinated drinking water and reproductive and
developmental health effects such as spontaneous abortion, stillbirth,
neural tube defects, pre-term delivery, intrauterine growth
retardation, and low birth weight. A critical review of the
epidemiology literature pertaining to reproductive and developmental
effects of exposure to DBPs completed in 2000 (Reif et al. 2000)
concluded that ``the weight of evidence from the epidemiological
studies also suggests that they [DBPs]
are likely to be reproductive
toxicants in humans under appropriate exposure conditions * * * and
that measures aimed at reducing the concentrations of byproducts could
have a positive impact on public health.''
While there has been substantial research to date, the Advisory
Committee recognized that significant uncertainty remains regarding the
risk associated with DBPs in drinking water. The Advisory Committee
carefully considered the analyses described previously, as well as
costs and potential impacts on public water systems, and concluded that
a targeted protective public health approach should be taken to address
exposure to DBPs beyond the requirements of the Stage 1 DBPR. After
reaching this conclusion, the Advisory Committee developed an Agreement
in Principle (USEPA 2000g) that laid out their recommendations on how
to further control DBPs in public water systems.
In the Agreement in Principle, the Advisory Committee recommended
maintaining the MCLs for TTHM and HAA5 at 0.080 mg/L and 0.060 mg/L
respectively, but changing the compliance calculation in two phases to
facilitate systems moving from the running annual average (RAA)
calculation to a locational running annual average (LRAA) calculation.
In the first phase, systems would continue to comply with the Stage 1
DBPR MCLs as RAAs and, at the same time, comply with MCLs of 0.120 mg/L
for TTHM and 0.100 mg/L for HAA5 calculated as LRAAs. RAA calculations
average all samples collected within a distribution system over a one-
year period, but LRAA calculations average all samples taken at each
individual sampling location in a distribution system during a one-year
period. Systems would also carry out an Initial Distribution System
Evaluation (IDSE) to select new compliance monitoring sites that more
accurately reflect higher TTHM and HAA5 levels occurring in the
distribution system. The second phase of compliance would require MCLs
of 0.080 mg/L for TTHM and 0.060 mg/L for HAA5 calculated as LRAAs at
individual monitoring sites identified through the IDSE.
The Agreement in Principle also provided recommendations for
simultaneous compliance with the LT2ESWTR so that the reduction of
potential health hazards of DBPs does not compromise microbial
protection. The recommendations for the LT2ESWTR included treatment
requirements for Cryptosporidium based on the results of source water
monitoring, a toolbox of options for providing additional treatment at
high risk facilities, use of microbial indicators to reduce
Cryptosporidium monitoring burden on small systems, and future
monitoring to determine if source water quality remains constant after
completion of initial monitoring. The Agreement also encouraged EPA to
develop guidance and criteria to facilitate the use of UV light for
compliance with drinking water disinfection requirements. The complete
text of the Agreement in Principle (USEPA 2000g) can be found at the
edocket Web site (http://www.epa.gov/edocket).
After extensive analysis and investigation of available data and
rule options considered by the Advisory Committee, EPA is proposing a
Stage 2 DBPR control strategy that is consistent with the key elements
of the Agreement in Principle signed in September 2000 by the
participants in the Stage 2 M-DBP Advisory Committee. EPA determined
that the risk-targeting measures recommended in the Agreement in
Principle will require only those systems with the greatest risk to
make treatment and operational changes and will maintain simultaneous
protection from the potential health hazards of DBPs and microbial
contaminants. EPA has carefully evaluated and expanded upon the
recommendations of the Advisory Committee to more fully develop today's
proposal. EPA also made simplifications where possible to minimize
complications for public water systems as they transition to compliance
with the Stage 2 DBPR while expanding public health protection. The
proposed requirements of the Stage 2 DBPR are described in detail in
section V of this preamble.

C. How Were Stakeholders Involved in Developing the Stage 2 DBPR?

1. Federal Advisory Committee Process
The Stage 2 M-DBP Advisory Committee consisted of 21 organizational
members representing EPA, State and local public health and regulatory
agencies, local elected officials, Native American Tribes, large and
small drinking water suppliers, chemical and equipment manufacturers,
environmental groups, and other stakeholders. Technical support for the
Advisory Committee's discussions was provided by a technical working
group established by the Advisory Committee. The Advisory Committee
held ten meetings to discuss issues pertaining to the Stage 2 DBPR and
LT2ESWTR from September 1999 to July 2000 which were open to the
public. There was also an opportunity for public comment at each
meeting.
In September 2000, the Advisory Committee signed the Agreement in
Principle, a full statement of the consensus recommendations of the
group. The agreement was published by EPA in a December 29, 2000
Federal Register notice (65 FR 83015), together with the list of
committee members and their organizations. The Agreement is divided
into Parts A and B. The recommendations in each part stand alone and
are independent of one another. The entire Advisory Committee reached
consensus on Part A, which contains provisions that directly apply to
the proposed Stage 2 DBPR and LT2ESWTR. The full Advisory Committee,
with the exception of the National Rural Water Association (NRWA), also
agreed to Part B, which has recommendations for future activities by
EPA in the areas of distribution systems and microbial water quality
criteria.
2. Other Outreach Processes
EPA received valuable input from small system operators as part of
an Agency outreach initiative under the Regulatory Flexibility Act
(RFA). EPA also conducted outreach conference calls to solicit feedback
and information from Small Entity Representatives (SERs) on issues
related to Stage 2 DBPR impacts on small systems. The Agency consulted
with State, local, and Tribal governments on the proposed Stage 2 DBPR.
Section VIII includes a complete

[[Page 49557]]

description of the many stakeholder activities which contributed to the
development of the Stage 2 DBPR.
The Agency held two meetings to discuss consecutive system issues
relevant to the proposal (February 22-23, 2001 in Denver, CO and March
28, 2001 in Washington, DC). Representatives from States, EPA Regions,
and public water systems participated in the discussions. EPA also
briefed the National Drinking Water Advisory Committee at their
November 2001 meeting on consecutive system issues associated with the
rule to receive input on the implementation strategy selected. This
Advisory Committee generally supported EPA's approach. Section V
describes EPA's analysis of consecutive system issues, comments and
input received during these sessions, and how the proposed requirements
will apply to consecutive systems. EPA also consulted with the Science
Advisory Board in December 2001 on the requirements of the Stage 2
DBPR.
Finally, EPA posted a pre-proposal draft of the Stage 2 DBPR
preamble and regulatory language on an EPA Internet site (http://
www.epa.gov/safewater/mdbp/st2dis.html) on October 17, 2001. This
public review period allowed readers to comment on the Stage 2 DBPR's
consistency with the Agreement in Principle of the Stage 2 M-DBP
Advisory Committee. EPA received important suggestions on this pre-
proposal draft from 14 commenters which included public water systems,
State governments, laboratories, and other stakeholders. While EPA will
not formally respond to these comments, EPA has carefully considered
them in developing today's proposal.

III. Public Health Risk

Chlorine has been widely used as a chemical disinfectant, serving
as a principal barrier to microbial contaminants in drinking water.
However, the microbial risk reduction attributes of chlorination have
been increasingly scrutinized due to concerns about potential increased
health risks from exposure to disinfection byproducts, which are formed
when certain disinfectants interact with organic and inorganic material
in source waters. Since the discovery of chlorination byproducts in
drinking water in 1974, numerous toxicological studies have shown
several DBPs (e.g., bromodichloromethane, bromoform, chloroform,
dichloroacetic acid, trichloroacetic acid and bromate) to be
carcinogenic in laboratory animals. These findings of carcinogenicity
influenced EPA to promulgate the TTHM Rule in 1979 and the Stage 1 DBPR
in 1998. The Stage 1 DBPR primarily addressed possible carcinogenic
effects (e.g., bladder, colon and rectal cancers) reported in both
human epidemiology and laboratory animal studies. Since the Stage 1
DBPR, new health studies continue to support an association between
bladder, colon and rectal cancers from long-term exposure to
chlorinated surface water. In addition to cancer effects, recent
studies have reported associations between use of chlorinated drinking
water and a number of reproductive and developmental endpoints
including spontaneous abortion, still birth, neural tube defect, pre-
term delivery, low birth weight and intrauterine growth retardation
(small for gestational age). Short-term, high-dose animal screening
studies on individual byproducts (e.g., bromodichloromethane (BDCM),
and certain haloacetic acids) have also reported adverse reproductive
and developmental effects (e.g., whole litter resorption, reduced fetal
body weight) that are similar to those reported in the human
epidemiology studies. This section discusses the new studies that have
become available since promulgation of the Stage 1 DBPR and how they
contribute to the weight of evidence for an association between health
effects and exposure to chlorinated surface water.
While the Stage 1 DBPR was targeted primarily at reducing long-term
exposures to elevated levels of DBPs to address chronic health risks
from cancer, the Stage 2 DBPR targets reducing short-term exposures to
address potential reproductive and developmental health risks and
cancer risks.
Based on the weight of evidence from both the human epidemiology
and animal toxicology data on cancer and reproductive and developmental
health effects and consideration of the large number of people exposed
to chlorinated byproducts in drinking water (approximately 254
million), EPA concludes that: (1) Current reproductive and
developmental health effects data support a hazard concern, (2) new
cancer data strengthens the evidence of an association of chlorinated
water with bladder cancer and suggests an association for colon and
rectal cancers, and (3) the combined health data warrant regulatory
action beyond the Stage 1 DBPR.

A. Reproductive and Developmental Epidemiology

The following section briefly discusses reproductive and
developmental epidemiology information EPA analyzed, some conclusions
of these studies and reports, and implications for the Stage 2 DBPR.
Further discussion of the implications and EPA's conclusions can be
found in the Stage 2 Economic Analysis (USEPA 2003i).
EPA has evaluated recently published epidemiological studies
examining the relationship between exposure to contaminants in
chlorinated surface water and adverse reproductive and developmental
outcomes. EPA also considered critical reviews of the epidemiological
literature by Reif et al. (2000), Bove et al. (2002), and
Nieuwenhuijsen et al. (2000). Based on these evaluations, EPA believes
that the reproductive and developmental epidemiology data contribute to
the weight of evidence on the potential health risks from exposure to
chlorinated drinking water. Although the data are not suitable for a
quantitative risk assessment at this time, due in part to
inconsistencies in the findings, they do suggest that exposure to DBPs
is a potential reproductive and developmental health hazard.
1. Reif et al. 2000
Reif et al. (2000) completed a critical review of the epidemiology
literature pertaining to reproductive and developmental effects of
exposure to disinfection byproducts in drinking water as a report to
Health Canada. The review focused on 16 peer-reviewed scientific
manuscripts and published reports and evaluated associations between
DBP exposure and outcomes grouped as effects on: (1) Fetal growth--low
birth weight (<2500g); very low birth weight (<1500g); preterm delivery
(<37 weeks of gestation) and intrauterine growth retardation (or small
for gestational age); (2) fetal viability (spontaneous abortion and
stillbirth) and (3) fetal malformations (all malformations, oral cleft
defects, major cardiac defects, neural tube defects, and chromosomal
abnormalities).
a. Fetal growth. Reif et al. (2000) found inconsistent
epidemiological evidence for an association between DBPs and fetal
growth. Some studies found weak but statistically significant
associations (Gallagher et al. 1998; Bove et al. 1992 and 1995), while
two studies found no association (Dodds et al. 1999; and Savitz et al.
1995) with fetal growth.
b. Fetal viability. Reif et al. 2000's review of the literature
found inconsistencies in the epidemiological evidence for the
association between DBP exposure and fetal viability. For instance, the
study by Waller et al. 1998 found an apparent dose-dependent increase
in rates of spontaneous

[[Page 49558]]

abortions associated with TTHMs in California. On the other hand,
Savitz et al. (1995) found little evidence of an association using
either the concentration of TTHM £=81 [mu]g/L or a dose
estimate based on the amount of tap water consumed. An increased risk
of stillbirth was reported for women in Nova Scotia by Dodds et al.
1999, but in New Jersey, Bove et al. (1992, 1995) found little evidence
of an association with TTHM at 80 [mu]g/L, but did report a weak
association between stillbirth and use of surface water systems.
Aschengrau et al. (1993) found an association between stillbirth and
the use of a chlorinated vs. chloraminated surface water supply, but
not for exposure to surface water.
c. Fetal malformations and other developmental anomalies. Reif et
al. (2000) considered the data for congenital anomalies to be
inconsistent across the six studies that have explored these outcomes.
For example, two of the four studies on neural tube defects (Bove et
al. 1995; Magnus et al. 1999) reported significant excess risks, but
the remaining two studies (Dodds et al. 1999; Klotz and Pyrch et al.
1999) did not. These studies found lower risks or no evidence of an
association with TTHM. However, those studies were conducted in
locations with either very low or high concentrations of DBPs which may
have limited the contrast in exposures, thereby reducing the ability to
detect increased risks. An assessment of congenital anomalies is also
difficult due to the relatively small number of cases available for
evaluation.
Overall, Reif et al. (2000) conclude that the weight of evidence
from the epidemiological studies suggest that ``DBPs are likely to be
reproductive toxicants in humans under appropriate exposure
conditions.'' Reif et al. comment that data from animal studies of
individual DBPs provide biological plausibility for the effects
observed in epidemiological studies. Although the authors recognize
that the ``data are primarily at the stage of hazard identification,''
they conclude that ``measures aimed at reducing the concentrations of
byproducts could have a positive impact on public health.''
2. Bove et al. 2002
Bove et al. (2002) conducted a qualitative review of 14
epidemiological studies that evaluated possible developmental and
reproductive endpoints associated with exposure to chlorination
byproducts in drinking water. Similar to Reif et al., Bove et al.
evaluated associations between DBP exposure and outcomes grouped as
effects on (1) fetal growth--small for gestational age (SGA) as defined
in each study (usually defined as the fifth or tenth percentile weight
by gestational week of birth); (2) fetal viability--spontaneous
abortion and stillbirth; and (3) fetal malformations (neural tube
defects, oral clefts, and cardiac defects).
a. Fetal growth. Bove et al. found that, although the studies that
evaluated SGA had several limitations, three studies out of eight
(Kramer et al. 1992, Bove et al. 1995, and Gallagher et al. 1998)
``provided moderate evidence for a causal relationship between a narrow
definition of SGA * * * and TTHM levels that could be found currently
in some U.S. public water systems.'' They also concluded that the study
with the best exposure assessment found the strongest association
between SGA and TTHM exposure (Gallagher et al. 1998). One study found
a very weak association (Dodds et al. 1999) and the other four did not
observe an association (Yang et al. 2000, Kanitz et al. 1996, Kallen et
al. 2000, and Jaakkola et al. 2001).
b. Fetal viability. Bove et al. evaluated three studies on
spontaneous abortion and three studies on stillbirth. Again, Bove et
al. found that the study employing the best methods found the strongest
association between TTHM exposure and spontaneous abortions (Waller et
al. 1998). The other two studies (Savitz et al. 1995 and Aschengrau et
al. 1989) found weak associations. Two of the studies investigating
stillbirths found an association between stillbirths and chlorinated
surface water (Dodds et al. 2001 and Aschengrau et al. 1993). The third
study (Bove et al. 1995) found no association, however this study did
not evaluate individual THM levels or cause of death information.
c. Fetal malformations. Bove et al. evaluated seven studies that
investigated the relationship between birth defects and DBP exposure.
This evaluation found ``consistency among these studies in the findings
for neural tube defects and oral cleft defects, but not for cardiac
defects. Associations were found for neural tube defects in all three
studies that examined neural tube defects. These studies also evaluated
levels of THM exposure (Bove et al. 1995; Dodds et al. 1999; Klotz et
al. 1999).'' Two studies evaluated oral cleft defects and levels of
THMs; one found an association with TTHM (Bove et al. 1995) and the
other found an association with chloroform (Dodds et al. 2001). A third
study that did not evaluate THM levels did not identify an association
with oral cleft defects (Jaakkola et al. 2001). Bove et al. 1995 found
an association between cardiac defects and TTHM, but Dodds et al. 1999,
2001 and Shaw et al. 1991 did not. An association between chlorination
and urinary tract defects was found in the three studies that evaluated
that endpoint (K[auml]ll[eacute]n et al. 2000; Magnus et al. 1999;
Aschengrau et al. 1993).
Bove et al. (2002) concluded that the current reproductive and
developmental epidemiological database for exposure to chlorinated
byproducts in drinking water presents moderate evidence for
associations between DBP exposure and SGA, neural tube defects and
spontaneous abortion. The authors acknowledged the difficulties in
assessing exposure with any precision in the studies reviewed, but held
the opinion that misclassification of exposure would tend to
underestimate rather than overestimate the risk.
3. Nieuwenhuijsen et al. 2000
Nieuwenhuijsen et al. (2000) reviewed the toxicological and
epidemiological literature and evaluated the potential risk of
chlorination DBPs on human reproductive health. The authors state that
``some studies have shown associations for DBPs and other outcomes such
as spontaneous abortions, stillbirths and birth defects, and although
the evidence for these associations is weaker it is gaining weight.''
Nieuwenhuijsen et al. also concluded that, ``although studies report
small risks that are difficult to interpret, the large number of people
exposed to chlorinated water supplies constitutes a public health
concern.''
4. Additional Epidemiology Studies
Three new reproductive and developmental epidemiological studies
were completed that were not included in the Reif et al. 2000, Bove et
al. 2002, or Nieuwenhuijsen et al. 2000 literature reviews.
Waller et al. 2001, recalculated the total trihalomethane exposures
from their original publication (Waller et al. 1998) to evaluate two
exposure assessment methods (closest site and utility-wide average).
The new calculations were intended to reduce exposure misclassification
by employing weighting factors and subset analyses. As in the 1998
publication, the new methods found a relationship between spontaneous
abortion and THM exposure, although the unweighted utility-wide point
estimate was lower than reported in the original manuscript.
Hwang et al. 2002, assessed the effect of water chlorination
byproducts on specific birth defects in Norway by

[[Page 49559]]

classifying exposure on the basis of chlorination (yes/no) and amount
of natural organic matter in the water. Statistically significant
associations with exposure were found for risks of any birth defect,
cardiac, respiratory, and urinary tract defects. For specific birth
defects, a statistically significant association was found for a defect
of the septum in the heart.
Windham et al., 2003, assessed the relationship between exposure to
THMs in drinking water and characteristics of the menstrual cycle among
403 women who provided daily urine samples for an average of 5.6
cycles. Women whose tap water had TTHM levels more than 0.060 mg/l had
statistically significantly shorter menstrual cycles than women whose
tap water had lower TTHMs. On average, the menstrual cycles of women
with the higher levels of TTHMs were one day shorter than cycles of
women with the lower levels (adjusted difference: -1.1 days, 95%
confidence interval: -1.8 days to -0.4 days). This shortening occurred
during the first half of the cycle, before ovulation (adjusted
difference: -0.9 days; 95% confidence interval: -1.6 days to -0.2
days). There were no changes in bleed length or in the regularity of
the cycles. Based on their study, Windham et al., 2003, suggested that
THM exposure may affect ovarian function, but since this is the first
study to examine human menstrual cycle variation in relation to THM
exposure, more research is needed to confirm the relationship. The
public health implication of a small reduction in menstrual cycle
length is not clear, but if THMs are related to disturbances in ovarian
function, that might provide insight into the observed associations
between THMs and a variety of adverse reproductive outcomes.
EPA's epidemiology research program continues to examine the
relationship between exposure to DBPs and adverse developmental and
reproductive effects. The Agency is supporting several studies using
improved study designs to provide better information for characterizing
potential risks. Details on EPA's epidemiology research program can be
found at http://cfint.rtpnc.epa.gov/dwportal/cfm/dwMDBP.cfm.

B. Reproductive and Developmental Toxicology

Several new reproductive and developmental toxicology studies have
become available since the December 1998 Stage 1 DBPR. This discussion
presents some conclusions derived from these studies and reports,
including hazard identification, as well as implications for the Stage
2 DBPR.
EPA conducted a literature search of animal toxicology studies on
chronic and subchronic DBP exposures associated with reproductive and
developmental health effects, evaluated the current reproductive and
developmental toxicological database for several individual DBPs, and
assessed two independent reviews (Tyl 2000 and WHO 2000). As a result
of these analyses, EPA has concluded that although the database is not
strong enough to quantify risk, it is sufficient to support a hazard
concern. This hazard concern supports the need to address potential
reproductive and developmental health effects in the Stage 2 DBPR. The
following section describes how this conclusion was reached.
1. EPA Analysis and Research
Since the Stage 1 DBPR, EPA has continued to support reproductive
and developmental toxicological research on various disinfection
byproducts through extramural and intramural research programs.
Information on EPA's toxicology programs can be found at http://
www.epa.gov/nheerl/. These studies, along with data on several DBPs
published after the 1998 Stage 1 DBPR, are summarized in the updated
children's health document, ``Health Risks to Fetuses, Infants, and
Children: A Review'' (USEPA 2003a).
In addition to this compilation of data, EPA has also prepared
individual health criteria documents that provide detailed summaries of
the relevant new information, as well as an overall characterization of
the human health risks from exposure to certain DBPs (USEPA 2003b-USEPA
2003h, USEPA 2003l). From these new evaluations, EPA has concluded that
several new studies on individual byproducts contribute to the weight
of evidence for an association between DBP exposure and adverse effects
on the developing fetus and reproduction. These effects include fetal
loss, cardiovascular effects, and male reproductive effects and are
associated with bromodichloromethane (BDCM), dichloroacetic acid
(DCAA), trichloroacetic acid (TCAA), bromochloroacetic acid (BCAA), and
dibromoacetic acid (DBAA). The data from these new studies do not
change the MCLGs that were established as a part of the Stage 1 DBPR.
2. Tyl 2000
Tyl (2000) conducted a comprehensive review of the reproductive and
developmental toxicology literature on DBPs representing over thirty-
five studies. Adverse effects reported by these studies include
developmental effects, whole litter resorption, reduced fetal body
weights, and male reproductive effects (e.g., inhibited spermiation,
increased abnormal sperm). Many of these studies are categorized as
high-dose, short-term screening studies that can be used to assess
potential hazard (Table III-1), while the long term, two-generation
reproduction studies could be an appropriate basis for quantitative
risk assessment.

----------------------------------------------------------------------------------------------------------------
Developmental
Disinfectant/DBP Screening \1\ \2\ Two-generation \3\ reproductive
----------------------------------------------------------------------------------------------------------------
Chlorine................................ ............... [bcheck]
....................................
Chlorine Dioxide........................ [bcheck]
[bcheck]
....................................
Chloramine.............................. ............... [bcheck]
....................................
Chloroform.............................. [bcheck]
[bcheck]
[bcheck]
Bromoform............................... [bcheck]
[bcheck]
[bcheck]
Bromodichloromethane.................... [bcheck]
[bcheck]
in progress
Dibromochloromethane.................... [bcheck]
[bcheck]
....................................
Monochloroacetic acid................... [bcheck]
[bcheck]
....................................
Dichloroacetic acid..................... [bcheck]
[bcheck]
....................................
Trichloroacetic acid.................... [bcheck]
[bcheck]
....................................
Monobromoacetic acid.................... [bcheck]
[bcheck]
....................................
Dibromoacetic acid...................... [bcheck]
[bcheck]
in progress
Tribromoacetic acid..................... [bcheck]
............... ....................................
Bromochloroacetic acid.................. [bcheck]
............... in planning stage
Bromodichloroacetic acid................ [bcheck]
............... ....................................
Dibromochloroacetic acid................ [bcheck]
............... ....................................

[[Page 49560]]

Chloroacetonitrile...................... [bcheck]
............... ....................................
Dichloroacetonitrile.................... [bcheck]
[bcheck]
....................................
Trichloroacetonitrile................... [bcheck]
[bcheck]
....................................
Bromoacetonitrile....................... [bcheck]
[bcheck]
....................................
Dibromoacetonitrile..................... [bcheck]
............... ....................................
Tribromoacetonitrile.................... ............... ............... ....................................
Bromochloroacetonitrile................. [bcheck]
[bcheck]
....................................
Propanal................................ [bcheck]
[bcheck]
....................................
1,1 Dichloropropanone................... [bcheck]
............... ....................................
Hexachloropropanone..................... [bcheck]
............... ....................................
Dichloromethane......................... [bcheck]
............... ....................................
MX...................................... [bcheck]
[bcheck]
....................................
Bromate................................. [bcheck]
............... ....................................
Chlorite................................ [bcheck]
[bcheck]
[bcheck]
----------------------------------------------------------------------------------------------------------------
[bcheck]
denotes the availability of at least one study in the following categories.
\1\ Screening studies are for hazard identification. These types of studies include the following: whole embryo
culture, NTP 35-day screening studies, Chernoff-Kavlock and its modified version, and short-term male
reproductive toxicity screen.
\2\ Developmental studies are used for dose-response determinations.
\3\ Two-generation reproductive studies are multi-generation reproductive toxicity studies used for dose-
response determinations.

Tyl concluded that, ``The screening studies, performed for a number
of DBPs, are `adequate' and `sufficient' only to detect potent
reproductive/developmental toxicants for hazard identification.'' Tyl
further confirms that the database identifies certain DBPs with
potential reproductive or developmental effects (Table III-2) and these
are discussed further in the next section.

Table III-2.--Potential Hazards of DBPs for Reproductive and
Developmental Effects (Adapted From Tyl, 2000)
------------------------------------------------------------------------
Type of hazard Disinfection byproducts
------------------------------------------------------------------------
Developmental defects.................. TCAA, DCAA, MCAA and chlorite.
Whole litter resorption................ Chloroform, bromoform, BDCM,
DBCM, DCAA, TCAA, DCAN, and
TCAN.
Fetotoxicity (reduced fetal body Chloroform, BDCM, DBCM, DCAA,
weights, increased variations). TCAA, DCAN, TCAN, DBAN, BCAN,
MCAN.
Male reproductive effects DCAA, DBAA, BDCM.
(spermatotoxic).
------------------------------------------------------------------------

a. Developmental defects. Tyl noted that adverse developmental
effects that were reported from whole embryo culture tests on the
developing heart, neural tube, eye, pharyngeal arch, and somites tended
to be associated with haloacetic acids tested at high doses (Hunter et
al. 1996; Saillenfait et al. 1995, Smith et al. 1989). Cardiovascular
effects were also observed in vivo for TCAA and DCAA from developmental
segment II toxicity studies at high doses (Smith et al. 1988, 1990).
b. Whole litter resorption. Whole litter resorption, likened to
miscarriage or spontaneous abortion by Tyl 2000, was also observed at
high doses in vivo for a range of DBPs as indicated in Table III-2
(Murray et al. 1979, Balster and Borzellca, 1982, Narotsky et al. 1992;
1997 a, b; Bielmeier et al. 2001; Smith et al. 1990; Smith et al.
1988). Tyl noted that similar effects were observed in several
epidemiology studies.
c. Fetal toxicity. Fetal toxic effects such as reduced fetal body
weights and increased variation were observed at high doses in vivo for
a range of DBPs (e.g., chloroform, BDCM, DBCM, DCAA, TCAA, DCAN, TCAN,
DBAN, BCAN) (Thompson et al. 1974; Schwetz et al. 1974; Murray et al.
1979; Ruddick et al. 1983; Narotsky et al. 1992, Balster and
Borzelleca, 1982; Smith et al. 1990). Again, Tyl noted a similarity in
effects observed in epidemiology studies.
d. Male reproductive effects. Animal toxicology studies report
increased risks of adverse effects on the male reproductive system from
high doses of haloacetic acids and other DBPs that have not been
studied in human epidemiology studies. Male reproductive effects (e.g.,
inhibited spermiation, reduced epididymus, sperm number and motility,
increased abnormal sperm, testicular damage and inhibited in vitro
fertilization) were reported for DCAA, DBAA, TCAA and BDCM (Toth et al.
1992, Linder et al. 1997a, b; Linder et al. 1994a, b; Cosby and Dukelow
1992). Dr. Tyl noted that the adverse effects observed in the male
reproductive toxicity screening studies (Toth et al. 1992; Linder et
al. 1994a, b; 1997a, b) are confounded by a short dosing regimen and
administration of test doses to only adult males.
From her review of the comprehensive animal toxicology database on
reproductive and developmental health effects from DBP exposure, Dr.
Tyl concludes that ``some DBPs have an intrinsic capacity to do harm,
specifically to the developing conceptus and the male (and possibly the
female) reproductive system''. She concludes that ``there is hazard to
development from the haloacetic acids (TCAA, DCAA, MCAA) and acetate;
to development from chloroform, bromoform, BDCM, DBCM, DCAA, TCAA,
DCAN, and TCAN expressed as full litter resorption (which most likely
indicates maternal endocrine/uterine effects); and fetotoxicity for
chloroform, BDCM, DBCM, DCAA, TCAA, DCAN, TCAN, DBAN, BCAN, CAN,
acetaldehyde, and possibly formaldehyde. Reproductive hazard exists for
DCAA, DBAA, and possibly formaldehyde in males and for TCE and possibly
formaldehyde in females.''

[[Page 49561]]

3. World Health Organization Review of the Reproductive and
Developmental Toxicology Literature (2000)
The International Programme on Chemical Safety (IPCS) published an
evaluation of Disinfectants and DBPs in its Environmental Health
Criteria monograph series (WHO 2000). In this review of the toxicology
data on reproductive and developmental effects from DBP exposure, the
World Health Organization (WHO) concludes that although the data on
these effects are not as robust as the cancer database, these effects
are of potential health concern. The WHO concludes that reproductive
effects in females have been principally embryolethality and fetal
resorptions associated with the haloacetonitriles
(trichloroacetonitrile, dichloroacetonitrile, bromochloroacetonitrile,
and dibromoacetonitrile) and the dihaloacetates, while DCAA and DBAA
have both been associated with adverse effects on male reproduction.
4. New Studies
Christian et al. (2001) conducted a developmental toxicity study
with pregnant New Zealand White rabbits exposed to BDCM in drinking
water at concentrations of 0, 15, 150, 450, and 900 ppm in drinking
water on gestation days 6-29. The no observed adverse effect level
(NOAEL) and lowest observed adverse effect level (LOAEL) identified for
maternal toxicity in this study were 13.4 mg/kg-day (150 ppm) and 35.6
mg/kg-day (450 ppm), respectively, based on decreased body weight gain.
The developmental NOAEL was 55.3 mg/kg-day (900 ppm) based on absence
of statistically significant, dose-related effects at any tested
concentration. Christian et al. (2001) also conducted a developmental
study of BDCM in a second species, Sprague-Dawley rats. Rats were
exposed to BDCM in the drinking water at concentrations of 0, 50, 150,
450, and 900 ppm on gestation days 6 to 21. The concentration-based
maternal NOAEL and LOAEL for this study were 150 ppm and 450 ppm,
respectively, based on statistically significant, persistent reductions
in maternal body weight and body weight gains. Based on the mean
consumed dosage of bromodichloromethane, these concentrations
correspond to doses of 18.4 mg/kg-day and 45.0 mg/kg-day, respectively.
The concentration-based developmental NOAEL and LOAEL were 450 ppm and
900 ppm, respectively, based on a significantly decreased number of
ossification sites per fetus for the forelimb phalanges (bones of the
hand or the foot) and the hindlimb metatarsals and phalanges. These
concentrations correspond to mean consumed doses of 45.0 mg/kg-day and
82.0 mg/kg-day, respectively.
Christian et al. (2002b) summarized the results of a two-generation
reproductive toxicity study on bromodichloromethane conducted in
Sprague-Dawley rats. Bromodichloromethane was continuously provided to
test animals in the drinking water at concentrations of 0, 50, 150, or
450 ppm. Average daily doses estimated for the 50, 150, and 450 ppm
concentrations were reportedly 4.1 to 12.6, 11.6 to 40.2, and 29.5 to
109 mg/kg-day, respectively. The parental NOAEL and LOAEL were 50 and
150 ppm, respectively, based on statistically significant reduced body
weight and body weight gain; F1 and F2 generation pup body weights were
reduced in the 150 and 450 ppm groups during the lactation period after
the pups began to drink the water provided to the dams. Body weight and
body weight gain were also reduced in the 150 and 450 ppm F1 generation
males and females. A marginal effect on estrous cyclicity was observed
in F1 females in the 450 ppm exposure group. Small (<=6%), but
statistically significant, delays in F1 generation sexual maturation
occurred at 150 (males) and 450 ppm (males and females) as determined
by timing of vaginal patency or preputial separation. The study's
authors considered these effects to be a secondary response associated
with reduced body weight, which appears to be dehydration brought about
by taste aversion to the compound. The results of this study identify
NOAEL and LOAEL values for reproductive effects of 50 ppm (4.1 to 12.6
mg/kg-day) and 150 ppm (11.6 to 40.2 mg/kg-day), respectively, based on
delayed sexual maturation.
Bielmeier et al. (2001) conducted a series of experiments to
investigate the mode of action in bromodichloromethane-induced full
litter resorption (FLR). The study included a strain comparison of F344
and Sprague-Dawley (SD) rats. In the strain comparison experiment,
female SD rats (13 to 14/dose group) were dosed with 0, 75, or 100 mg/
kg-day by aqueous gavage in 10% Emulphor[reg]
on GD 6 to 10. F344 rats
(12 to 14/dose group) were dosed with 0 or 75 mg/kg-day administered in
the same vehicle. The incidence of FLR in the bromodichloromethane-
treated F344 rats was 62%, while the incidence of FLR in SD rats
treated with 75 or 100 mg/kg-day of bromodichloromethane was 0%. Both
strains of rats showed similar signs of maternal toxicity, and the
percent body weight loss after the first day of dosing was comparable
for SD rats and the F344 rats that resorbed their litters. The rats
were allowed to deliver and pups were examined on postnatal days 1 and
6. Surviving litters appeared normal and no effect on post-natal
survival, litter size, or pup weight was observed. The series of
experiments conducted by Bielmeier et al. (2001) identified a LOAEL of
75 mg/kg-day (the lowest dose tested) based on FLR in F344 rats. A
NOAEL was not identified. Mechanistic studies indicate that BDCM-
induced pregnancy loss is likely to be luteinizing hormone (LH)-
mediated (Bielmeier et al., 2001). It is possible that BDCM alters LH
levels by disrupting the hypothalamic-pituitary-gonadal axis or by
altering the responsiveness of the corpora lutea to LH. Since these
possible mechanisms are potentially relevant to pregnancy maintenance
in humans, EPA believes the finding of BDCM-induced pregnancy loss in
F344 rats is relevant to risk assessment, and may provide insight into
the epidemiological finding of increased risk of spontaneous abortion
associated with consumption of BDCM (Waller et al. 1998, 2001).
Christian et al. (2002a) recently completed a two-generation
drinking water study of DBA in rats. Male and female Sprague-Dawley
rats (30/sex/exposure group) were administered DBA in drinking water at
concentrations of 0, 50, 250, or 650 ppm continuously from initiation
of exposure of the parental (P) generation male and female rats through
weaning of the F₂ offspring. Based on testicular
histomorphology indicative of abnormal spermatogenesis in P and
F₁ males, the parental and reproductive/developmental
toxicity LOAEL and NOAEL are 250 and 50 ppm, respectively.
Previous studies by EPA have reported adverse effects of DBA,
administered via oral gavage, on spermatogenesis that impacted male
fertility (Linder et al. 1994a, 1995, 1997a) at doses-comparable to
those achieved in the Christian et al. (2002a) study. Based on these
studies collectively, it is clear that DBA is spermatotoxic. Moreover,
Veeramachaneni et al. (2000) reported in an abstract that sperm from
male rabbits exposed to DBA in utero from gestation days 15 and
throughout life reduced the fertility of artificially inseminated
females as evidenced by reduced conceptions. When published, this study
may support the evidence that DBA is a male reproductive system
toxicant .
In addition, research on DBA by Klinefelter et al. (2001) has

[[Page 49562]]

demonstrated statistically significant delays in both vaginal opening
and preputial separation using the body weight on the day of
acquisition (postnatal day 45) as the co-variant. This was not found by
Christian et al (2002a) using the body weight at weaning as the
statistical covariant. However, the authors analyzed the data for
preputial separation and vaginal opening with body weight on the day of
weaning as a co-variant rather than body weight on the day of
acquisition, i.e., the day that the prepuce separates or the day the
vagina opens. It is likely that there was an increase in body weight
from postnatal day 21 (weaning) until preputial separation (day 45)
that was independent of the delay in sexual maturation.
Although the Christian et al. (2002a) study was conducted in
accordance with EPA's 1998 testing guidelines, EPA has incorporated
newer, more sophisticated measures into recent intramural and
extramural studies that have not yet been incorporated into the testing
guidelines. Such measures include measuring changes in specific
proteins in the sperm membrane proteome and fertility assessments via
in utero insemination. EPA believes that additional research is needed,
utilizing these newer toxicological measures, to clarify the extent to
which DBA poses human reproductive or developmental risk. The database
on male reproductive effects from exposure to DBA is incomplete and is
not suitable for quantitative risk assessment at this time. It does,
however, identify reproductive effects as an area of concern.

C. Conclusions Drawn From the Reproductive and Developmental Health
Effects Data

EPA believes that the weight of evidence of the best available
science, in conjunction with the widespread exposure, supports
regulatory changes that target peak DBP exposures specifically through
the Stage 2 DBPR. Several epidemiology studies found statistically
significant associations between exposure to chlorinated drinking water
and fetal growth, spontaneous abortion, stillbirth, and neural tube
defects. Although uncertainties remain and the current database does
not support a quantitative reproductive and developmental risk
assessment for most of the DBPs, the weight of evidence provides an
indication of a hazard concern that warrants additional regulatory
action beyond the Stage 1 DBPR.
Biological plausibility for the effects observed in epidemiological
studies has been demonstrated through various toxicological studies.
Tyl 2000 states that ``effects observed in animal studies included
embryonic heart and neural tube defects from haloacetic acids in vitro
and in vivo, and full litter resorption, reduced numbers of implants
per litter, and reduced fetal body weight per litter were also observed
from exposure to specific trihalomethanes. Comparable effects were also
observed in children in some (but not all) epidemiological studies,
with exposure to trihalomethanes (THMs) usually used as a surrogate for
specific DBP classes or individual DBPs, as follows: increased
incidences of cardiac defects (Bove et al. 1995) and of neural tube
defects in children (Bove et al. 1995; Dodds et al. 1999; Klotz and
Pyrch 1998) were reported. Intrauterine growth retardation (IUGR,
approximately equivalent to reduced fetal body weights per litter) was
reported to be associated with waterborne chloroform (Kramer et al.
1992; Bove et al. 1995; Gallagher et al. 1998). Miscarriage or
spontaneous abortion, or stillbirth (approximately equivalent to whole
litter resorption, reduced numbers of total and/or live implants per
litter, and increased resorptions per litter) were observed by Waller
et al., 1998; Dodds et al., 1999; and Bove et al., 1995.''
Similarity of effects between animals and humans lends credence to
and strengthens the weight of evidence for an association between
adverse reproductive and developmental health effects and exposure to
chlorinated surface water. EPA believes that the weight of evidence of
both the reproductive and developmental toxicological and
epidemiological databases suggests that exposure to DBPs may induce
potential adverse health effects on reproduction and fetal development
at some DBP exposures. However, additional toxicological work is
necessary to identify the mode of action for the effects observed.

D. Cancer Epidemiology

Epidemiological studies on cancer provide valuable information that
contributes to the overall evidence on the potential human health
hazards from exposure to chlorinated drinking water. In the area of
epidemiology, a number of 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, some studies have
found an association between bladder, rectal and colon cancer and
exposure to chlorinated surface water.
1. Population Attributable Risk Analysis
Some epidemiological studies have linked the consumption of
chlorinated surface waters to an increased risk of two major causes of
human mortality in the United States, colorectal and bladder cancers
(Cantor 1998). Bladder cancer was chosen as the primary endpoint of
concern in the Stage 1 DBPR (USEPA 1998f) economic analysis because it
had the most consistent database for a possible association to
chlorinated surface water exposure. More studies have considered
bladder cancer than any other cancer. EPA used the published mean risk
estimates from five studies to quantify the potential range of risk for
bladder cancer from DBP exposure. These risks were expressed as a range
of population attributable risks (PAR) of 2-17% (USEPA 1998f). This
means that if the associations reported in the studies turn out to
reflect a causal link, between 2 and 17% of new bladder cancer cases
could be attributable to DBPs. This PAR range also represents that
portion of the bladder cancer cases that would not have occurred if the
exposure to chlorinated drinking water were absent. A complete
discussion of the Stage 1 DBPR bladder cancer PAR evaluation, including
uncertainties and assumptions, can be found in the Stage 2 DBPR
Economic Analysis (USEPA 2003i).
While EPA recognized the limitations of the epidemiological
database for making risk estimates, the Agency believed that it was
useful for developing an estimate of bladder cancer risk. The PARs were
derived from measured risks (Odds Ratios and Relative Risk) based on
the number of years exposed to chlorinated surface water. The
uncertainties associated with these PAR estimates are largely due to
the common prevalence of both the disease (bladder cancer) and exposure
(chlorinated drinking water). EPA recognizes that risks from
chlorinated drinking water may be lower or higher than those estimated
from the epidemiological literature, and that the PAR range could
include zero or be higher than 17%.
Using the PARs of 2% and 17%, EPA estimated that the number of
possible bladder cancer cases per year potentially associated with
exposures to DBPs in chlorinated drinking water could range from 1,100
to 9,300 cases. This was based on the estimate of 54,500 new bladder
cancer cases per year nationally, as projected by the National Cancer
Institute for 1997. A thorough discussion of cancer studies published
prior to 1998 and possible

[[Page 49563]]

associations with DBP exposure can be found in the Stage 1 DBPR (USEPA
1998c).
2. New Epidemiological Cancer Studies
New studies published since the Stage 1 DBPR continue to support an
association between bladder, colon and rectal cancers and exposure to
chlorinated surface water (Yang et al. 1998; Koivusalo et al. 1998;
King et al. 2000b). Based on the weight of evidence provided by the
cancer epidemiology database, EPA has chosen to use the same PAR
analysis to estimate the primary benefits from bladder cancer cases
potentially avoided as a consequence of reducing the DBP levels from
the Stage 2 DBPR (see section VII). For the Stage 2 DBPR analysis, EPA
updated the 1997 estimate of new bladder cancer cases per year
nationally from 54,500 to 56,500 (projected by the American Cancer
Society, 2002) and accounted for the reductions in DBP exposure that
were projected for the Stage 1 DBPR.
a. New bladder cancer studies. Bladder cancer and chlorinated DBP
exposure has historically been the most strongly supported association
of all the possible cancers, based on human evidence. Two new studies
(Yang et al. 1998 and Koivusalo et al. 1998) also suggest an
association of DBP exposure with bladder cancer. Yang et al. 1998 found
a positive association between consumption of chlorinated drinking
water and bladder cancer. Koivusalo et al. (1998) found evidence of
increased risk as a function of increasing DBP exposure duration. Long
exposure durations (£=45 years for Koivusalo et al. 1998)
were associated with about a two-fold increase in risk. The new bladder
cancer studies continue to support an association and potential for a
causal relationship between exposure to chlorination byproducts and
risk for bladder cancer.
A new publication by C.M. Villanueva et al. (Villanueva et al.
2003) reports on their meta-analysis of case-control and cohort
studies. This meta-analysis may be useful for improving the estimate of
national population attributable risk (fraction of bladder cancer cases
in the U.S. that may be attributed to chlorinated drinking water).
Compared to EPA's current approach (i.e., providing a range of
population attributable risks (PAR)), use of the meta-estimate would
provide a more stable result because:
? It provides a single (meta) estimate of the odds ratio from
which to calculate the PAR, thereby summarizing the results across
studies, thus reducing the influence of geographic and temporal
differences.
? It uses three additional high-quality studies not included
in the PAR range analysis conducted by EPA (i.e., studies by Koivusalo
et al. 1998, Doyle et al. 1997, and Vena et al. 1993).
? It weights the individual studies according to their
precision, so more precise estimates (due principally to greater
numbers of cases) carry greater statistical weight and therefore have
greater influence on the meta-estimate.
? In addition to the primary analysis, the authors conducted
an evaluation of the robustness of their conclusions. They examined the
sensitivity of estimates to decisions made with respect to exposure
definitions, cut points defining exposure groups, inclusion/exclusion
of individual studies, and potential publication bias.
The meta-analysis provided at least two meta-estimates that may be
useful for estimating national population attributable risk:
? A combined odds ratio for ever-exposure, with confidence
intervals and
? A combined dose-response regression slope coefficient,
relating increasing odds ratios to additional years of chlorinated
drinking water consumption.
EPA conducted an estimate of the impact of using the meta-analysis
to provide a perspective on the national population attributable risk.
This estimate is based on the author's correction of a minor
transcription error in their published manuscript (the appropriate
estimate for the King study yields corrected over-all odds ratio for
ever-consumers of 1.2 with 95% confidence interval of 1.091 to 1.320,
personal communication from M. Kogevinas to M. Messner, 5/19/2003).
Assuming 70% of the U.S. population is in the ever-consumed category
(based on the chlorinated surface water exposed population), a point
estimate of the population attributable risk using the odds ratio from
the meta-analysis is 12% (95% interval 6% to 18%). Although EPA's
population attributable risk range (2% to 17%) was not intended to
convey a quantified level of confidence, it is not vastly different
from the meta-analysis' 95% confidence range of 6% to 18%. EPA regards
the meta-range as additional support for EPA's population attributable
risk range. The meta-analysis provides continued support for an
association between exposure to chlorinated surface water and bladder
cancer.
EPA requests comment on the use of a meta-estimated odds ratios to
estimate national population attributable risk for the purpose of
supporting the benefit analysis for this rule, either based
specifically on the Villanueva et al. publication or on the application
of a similar approach. EPA also solicits comments and suggestions for
use of the combined dose-response regression slope coefficient
associated with the increased risk of bladder cancer for each
additional year's exposure to DBPs in drinking water for estimating the
drop in risk associated with a reduction in DBPs as part of the benefit
analysis of this rule. EPA provides further discussion and solicitation
of comment on how the slope factor might further be considered in
estimating the benefits of this rule in the economic section of this
preamble.
b. New colon cancer studies. Colorectal cancer is the third most
common type of new cancer cases and deaths in both men and women in the
U.S. It is estimated that 148,300 new colorectal cancer cases will be
diagnosed in 2002, with 56,600 resulting in deaths (American Cancer
Society, 2002). Human epidemiology studies on chlorinated surface water
have reported associations with colorectal cancer. Since the Stage 1
DBPR, two new human epidemiology studies (Yang et al. 1998 and King et
al. 2000b) have been conducted to investigate the relationship between
colon cancer and exposure to chlorinated surface water. Yang et al.
1998 did not identify an association between consumption of chlorinated
drinking water and colon cancer. The King et al. (2000b) study found
evidence of a DBP association with colon cancer among males, but no
association was observed among females.
Similarity of effects reported in animal toxicity and human
epidemiology studies strengthen the weight of evidence for an
association between DBP exposure and colon cancer. Effects observed in
animal studies which included tumors in BDCM exposed rats and mice at
several sites (NTP 1987); colon tumors in bromoform exposed rats (NTP
1989); and development of aberrant crypt foci, a preneoplastic lesion
of colon cancer in animals exposed to DBP mixtures (DeAngelo et al.
2002), are comparable to observations in some cancer epidemiological
studies showing an association with colorectal cancer and consumption
of chlorinated water (King et al. 2000b).
Even with the additional study showing an association, the
epidemiological database on colon cancer as a whole is not as strong as
that for bladder cancer. However, this new study increases the weight
of evidence of an association between DBP exposure

[[Page 49564]]

and colon cancer. The Stage 1 DBPR (USEPA 1998c) includes additional
discussion of colon cancer risks associated with DBP exposure.
c. New rectal cancer studies. The evidence for an association
between DBPs and rectal cancer is stronger than for colon cancer. Yang
et al. (1998) and Hildesheim et al. (1998) both found associations
between chlorinated drinking water exposure and rectal cancer, and the
associations had a similar magnitude in both sexes. Hildesheim et al.
also found an association in both sexes with lifetime average THM
concentration. The consistency of the dose-response trends, the
consistency between sexes, and the apparent control of important
potential confounders in this study all support the observed
associations.
d. Other cancers. Two new human epidemiology studies support the
possibility of an association between DBPs and kidney cancer. Yang et
al. (1998) found a positive association for both males and females
between consumption of chlorinated drinking water and kidney cancer.
Koivusalo et al. (1998) found a small, statistically significant,
exposure-related excess risk for kidney cancer for males. The
association for females was not significant in the Koivusalo et al.
1998 study. The current database for this endpoint of cancer, however,
is insufficient to conclude an association.
Cantor et al. (1999) studied brain cancer, focusing on gliomas.
None of the exposure variables were related to brain cancer among
females, but males showed a statistically significant, monotonically
increasing risk associated with duration of exposure to chlorinated
surface water. This study suggests a possible association between
chlorination byproducts and gliomas; however, the evidence from this
study is not strong enough to support a conclusion of a causal
association.
Infante-Rivard et al. (2001) conducted a population-based case-
control study in Quebec Province, Canada, to examine possible
associations between childhood acute lymphoblastic leukemia and THMs.
There were no associations with leukemia for any of the exposure
indices for total THM, or specific THMs. Therefore, the study does not
provide evidence of an association between any of the exposure
variables and childhood leukemia.
3. Review of the Cancer Epidemiology Literature (WHO 2000)
The International Programme on Chemical Safety (IPCS) report on
disinfectants and disinfection byproducts (WHO 2000) concludes that
results of analytical epidemiological cancer studies are insufficient
to support a causal relationship for bladder, colon, rectal, or any
other cancer and chlorinated drinking water or THMs. The report notes
that there is better evidence for an association between exposure to
chlorinated surface water and bladder cancer than for other types of
cancer. The WHO also concludes that based on the large number of people
exposed to chlorinated drinking water, there is a need to address this
potential health concern.

E. Cancer and Other Toxicology

Few new cancer toxicology studies have been completed since the
Stage 1 DBPR was finalized in December 1998. The information provided
in the following sections adds to the toxicology database and provides
additional support for the Stage 2 DBPR to control DBP peaks (e.g, high
TTHM and HAA5 levels) throughout distribution systems, but does not
change the quantitative assessment of the MCLGs.
1. EPA Criteria Documents
To date, EPA has established lifetime cancer risk levels for four
DBPs (bromoform, bromodichloromethane, bromate, and dichloroacetic
acid) classified as ``probable'' carcinogens, as promulgated in the
Stage 1 DBPR and reported in the Integrated Risk Information System
(IRIS). Although researchers have continued to assess the cancer risks
of DBPs, there has been little change in the overall DBP
carcinogenicity database since the Stage 1 DBPR.
The most significant new publication since the Stage 1 DBPR was a
study of DCAA tumorigenicity in mice by DeAngelo et al. (1999). The
Agency has used the data from this study to revise the slope factor for
DCAA and a drinking water 10-6 lifetime cancer risk
concentration. The slope factor is a measure of the potency of a
carcinogen while the 10-6 lifetime cancer risk concentration
provides an estimate of the concentration of a contaminant in drinking
water that is associated with an estimated excess lifetime cancer risk
of one in a million (Table III-3).
Another significant advancement beyond the Stage 1 DBPR was the
evaluation of the chloroform tumorigenicity data on the basis of its
nonlinear mode of action following the draft 1999 proposed Guidelines
for Carcinogen Risk Assessment (USEPA 1999a). The new chloroform
assessment became available on IRIS (2001) in October, 2001 (see
section V for a more detailed discussion).
The Criteria Documents for bromoform, bromodichloromethane,
dibromochloromethane, and dichloroacetic acid that support the Stage 2
proposal include cancer slope factors and 10-6 lifetime
cancer risk concentrations that have been modified from their Stage 1
values in order to reflect the methodology proposed in the 1996/1999
draft cancer guidelines (USEPA 1999a) (Table III-3). These include the
values based on the Maximum Likelihood Estimate of the dose producing
effects in 10 percent of the animals (ED₁₀) and from the
lower 95 percent confidence bound on that value (LED₁₀).
Except for dibromochloromethane, which is classified as a possible
human carcinogen, the DBPs in Table III-3 (and bromate as noted
previously) are classified as probable human carcinogens.

Table III--3.--Quantification of Cancer Risk
----------------------------------------------------------------------------------------------------------------
Risk factors from LED₁₀ Risk factors from ED₁₀
----------------------------------------------------------------------------------------------------------------
10-6 Risk 10-6 Risk
Disinfection byproduct Slope factor concentration Slope factor concentration
(mg/kg/day)-1 (mg/L) (mg/kg/day)-1 (mg/L)
----------------------------------------------------------------------------------------------------------------
Bromodichloromethane............................ 0.034 0.001 0.022 0.002
Bromoform....................................... 0.0045 0.008 0.0034 0.01
Dibromochloromethane............................ 0.04 0.0009 0.017 0.002
Dichloroacetic Acid............................. 0.048 0.0007 0.014 0.003
----------------------------------------------------------------------------------------------------------------

[[Page 49565]]

EPA believes that it is important to pursue additional research on
cancer from DBPs. EPA has several ongoing studies in addition to a
collaboration with the National Toxicology Program of the National
Institute of Environmental Health Sciences. More information on EPA's
toxicology research program can be found at http://www.epa.gov/nheerl.
2. Other Byproducts with Carcinogenic Potential
a. 3-chloro-4- (dichloromethyl)-5-hydroxy-2(5H) -furanone) (MX)--
multisite cancer. MX is a byproduct of chlorination that is typically
found at very low concentrations (approximately <0.000067 mg/L) in
drinking water. The information available on MX was recently compiled
in the Quantitative Cancer Assessment for MX and chlorohydroxyfuranones
(USEPA 2000i). Overall, the weight of evidence indicates that MX is a
direct-acting genotoxicant in mammals, with the ability to induce
tumors in multiple sites. The primary sites for tumor formation are the
thyroid and liver.
b. N-nitrosodimethylamine (NDMA)--multisite cancer. Health effects
data indicate that NDMA is a probable human carcinogen, as described on
IRIS (1991). Risk assessments have estimated that the 10-6
lifetime cancer risk level is 0.000007 mg/L based on induction of
tumors at multiple sites. Recent studies have produced new information
on the occurrence and mechanism of formation of NDMA but there is not
enough information at this time to draw conclusions. More research is
underway to determine the mechanism by which NDMA is formed in drinking
water, and the extent of its occurrence in chloraminated systems.
3. Other Toxicological Effects
The Agency has modified the reference dose (RfD) values for 2 of
the chlorinated acetic acids since the Stage 1 DBPR. Under the Stage 1
DBPR there was no established RfD for monochloroacetic acid (MCAA).
Data from a drinking water exposure study of MCAA in rats by DeAngelo
et al. (1997) were used to establish an RfD of 0.004 mg/kg/day based on
observed increases in spleen weight. Data from DeAngelo (1997) were
also used to calculate a new RfD of 0.03 mg/kg/day for trichloroacetic
acid (TCAA) based on observed effects on body weight and liver effects.
Detailed discussions of the new reference doses are located in section
V of this preamble.
4. WHO Review of the Cancer Toxicology Literature (2000)
The IPCS report on Disinfectants and Disinfection Byproducts (WHO
2000) emphasizes that the bulk of the toxicology data focuses primarily
on carcinogenesis. The Task Group found BDCM to be of particular
interest because it produces tumors in both rats and mice at several
sites. Although the HAAs appear to be without significant genotoxic
activity, the brominated HAAs appear to induce oxidative damage to DNA,
leading to tumor formation.

F. Conclusions Drawn From the Cancer Epidemiology and Toxicology

EPA believes that the cancer epidemiology and toxicology databases
provide important information that contributes to the weight of
evidence evaluation of the potential health risks from exposure to
chlorinated drinking water. At this time the cancer epidemiology
studies are insufficient to establish a causal relationship between
exposure to chlorinated drinking water and cancer, but EPA does believe
there is a potential association. The current database is sufficient
for quantitative analysis on the endpoint of bladder cancer, as
presented previously in the PAR analysis.
The association between DBP exposure and colon cancer remains more
tenuous than the link to bladder cancer, although similarity of effects
reported in animal toxicity and human epidemiology studies strengthens
the weight of evidence for an association between DBP exposure and
colon cancer. Studies finding potential relationships between exposure
to chlorinated drinking water and rectal, kidney, and brain cancer also
add to the weight of evidence for a public health concern. EPA believes
that the overall cancer epidemiology and toxicology data support the
decision to pursue additional DBP control measures as reflected in the
Stage 2 DBPR.

G. Request for Comment

EPA requests comment on the conclusions drawn from the new health
information summarized in this section. EPA requests comment on the
weight of evidence evaluation of the potential reproductive and
developmental hazards from DBPs and its potential implications for the
regulatory provisions for the final Stage 2 DBPR. EPA solicits any
additional data on the reproductive or developmental effects from DBPs
that need to be considered for the final Stage 2 DBPR.
EPA requests comment on EPA's conclusions regarding cancer
epidemiology and toxicology, and the new studies discussed in today's
proposal. EPA solicits any additional cancer epidemiology and
toxicology data that need to be considered for the final Stage 2 DBPR.
EPA also solicits any health information available to further
assess risk to sensitive subpopulations, especially children and the
elderly.

IV. DBP Occurrence Within Distribution Systems

New information on the occurrence of DBPs in distribution systems
raises issues about the protection provided by the Stage 1 DBPR. This
section presents the new information used to identify key issues and to
support the development of the Stage 2 DBPR. For a more detailed
discussion see the Stage 2 Occurrence Assessment for Disinfectants and
Disinfection Byproducts (USEPA 2003o).
Under the Stage 1 DBPR, compliance with the DBP MCLs is determined
by averaging, annually and system-wide, all DBP measurements. The
following discussion shows that compliance based on system averages of
DBP concentrations allows a significant number of sampling locations
within distribution systems to have DBP levels above the MCLs. These
peak DBP occurrences are masked by averaging with lower distribution
system occurrence levels. The populations served by portions of the
distribution system with higher DBP concentrations are not receiving
the same level of health protection.
The new information also shows that the highest DBP levels often do
not occur at distribution system sites identified as representing
maximum residence time. The information further shows that the highest
TTHM and HAA5 levels often do not occur at the same site within the
distribution system. These two findings suggest that it is appropriate
to reevaluate the Stage 1 DBPR compliance monitoring sites in order to
target those sites with high DBP levels. EPA believes that distribution
system compliance monitoring sites need to be reevaluated to ensure
identification of sites that reflect both high TTHM and HAA5
occurrence.

A. Data Sources

1. Information Collection Rule Data
The Information Collection Rule (USEPA 1996a) established
monitoring and data reporting requirements for large public water
systems. Under the Information Collection Rule, systems serving at
least 100,000 people were required to conduct DBP and DBP-

[[Page 49566]]

related monitoring. The 18 months of required monitoring, which began
in July 1997 and ended in December 1998, applied to 296 public water
systems (500 treatment plants).
The Information Collection Rule data show the national occurrence
of: (1) Influent water quality parameters; (2) primary and secondary
disinfectant use by the large plants; (3) occurrence of DBPs and DBP
precursors in treatment plants, finished waters, and distributions
systems; (4) microbial occurrence (in subpart H systems only); and (5)
treatment plant monthly operation, and initial as well as final
treatment plant design. The data were gathered after the Stage 1 DBPR
was finalized (USEPA 1998c) but well before systems were required to
meet Stage 1 DBPR requirements.
The Information Collection Rule required a significant investment
for the water treatment industry, as well as for the EPA to analyze the
data. Overall, the occurrence and treatment data collected under the
Information Collection Rule, excluding microbial data, was estimated to
cost systems $54 million (USEPA 1996a). In addition, systems using
source waters with high DBP precursor levels were required to conduct
bench and pilot studies to evaluate the effectiveness of granular
activated carbon (GAC) and membrane technology to control for DBPs. The
estimated cost for these studies totaled approximately $57 million
(USEPA 1996a).
In addition to the analysis of DBPs in distribution systems, EPA
used occurrence data from the Information Collection Rule to confirm
selection of TTHM and HAA5 as appropriate contaminants for monitoring
DBPs. EPA also used occurrence data from the Information Collection
Rule to confirm differences in monitoring requirements for systems
using surface water versus those using ground water, as stipulated
under the Stage 1 DBR. Analysis of the Information Collection Rule data
indicates that TTHM and HAA5 comprise on average, across all systems,
about 50% of the total mixture of chlorinated DBPs and that TTHM and
HAA5 concentrations are much lower and less variable in ground water
systems than in surface water systems. These results support the basis
for continuing the use of TTHM and HAA5 as indicators for controlling
chlorinated DBPs. The data also reconfirmed that ground water systems
require less monitoring than surface water systems based on lower and
less variable DBP occurrence. For detailed analysis, see Stage 2
Occurrence Assessment for Disinfectants and Disinfection Byproducts
(USEPA 2003o).
2. Other Data Sources Used To Support the Proposal
Table IV-1 summarizes the data sources other than the Information
Collection Rule used to support the Stage 2 DBPR. The data from the
Information Collection Rule is from large systems. To validate the
conclusions drawn from analysis of the Information Collection Rule for
small and medium systems, EPA compared these other data sources with
the Information Collection Rule data. EPA found that there are
significant similarities between large systems and medium and small
systems with regard to source water quality (affecting DBP formation)
and use of treatment technologies. Because of these similarities, EPA
expects that small and medium systems would find DBP distribution
system levels similar to those found in large systems following
compliance with the Stage 1 DBPR requirements. For detailed discussion
of this analysis, see Stage 2 Occurrence Assessment for Disinfectants
and Disinfection Byproducts (USEPA 2003o) and Economic Analysis for the
Stage 2 Disinfection Byproducts Rule (USEPA 2003i).

Table IV-1.--Summary of Non-Information Collection Rule Occurrence Survey Data
--------------------------------------------------------------------------------------------------------------------------------------------------------
Geographic
Data source Data collected representation Number of plants (By population served)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Information Collection Rule Raw source water-(Large Systems) TOC Random national 47 serving 100,000 or more.
Supplemental Survey. Raw source water-(Small & Medium Survey distribution by SW 40 serving 10,000-99,999.
Systems) TOC, UV 254, bromide, turbidity, source type \1\. 40 serving fewer than 10,000.
pH, & temperature.
WaterStats............................ Population served and flows Random national 219 serving 100,000 or more.
Raw source water--Water distribution. 623 serving 10,000-99,999.
Quality Parameters (WQPs), 30 serving fewer than 10,000.
Source water type.
Finished water-WQPs, TTHM, HAAs
Treatment-unit processes, disinfectant
used.
National Rural Water Association Population served and flows Random national 117 serving fewer than 10,000.
Survey (NRWAS). Raw source water-temperatures, turbidity, distribution.
pH, and source water type, bromide, TOC,
UV 254, alkalinity, calcium, and total
hardness.
Finished water-residence time estimate,
total and individual THMs, individual
HAAs and HAA5, HAA6, HAA9,TOC, UV 254,
Bromide, Temperature, pH, free and total
chlorine residual levels.
Treatment-unit processes, disinfectant
used.
State Data-Surface Water.............. Distribution system TTHM occurrence data. AK, CA, IL, MN, MS, NC, 562 serving fewer than 10,000.
TX, WA \2\.
State Data-Ground Water............... Distribution system TTHM occurrence data. AK, CA, FL, IL, NC, TX, 2336 serving fewer than 10,000.
WA \2\.
Ground Water Supply Survey............ TOC and TTHM (one sample for each Random national 979 total.
parameter at the entry point to distribution.
distribution system.)
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Source type designations include flowing stream and lake/reservoir (Except for 7 large plants pre-selected).
\2\ Over 50 percent of each State's systems are represented. EPA believes that the data reasonably represent a full range of source water quality in
small systems at the national level.

[[Page 49567]]

B. DBPs in Distribution Systems

EPA wanted to understand DBP occurrence in distribution systems
likely to exist after implementation of the Stage 1 DBPR. Such an
understanding would enable EPA to recognize options on how to improve
protection under the Stage 2 DBPR. The analysis of occurrence data to
support the Stage 2 DBPR is complicated because available national
occurrence data do not reflect the changes in occurrence resulting from
the implementation of the Stage 1 DBPR. Many utilities have only
recently changed their treatment to comply with the Stage 1 DBPR
(subpart H systems serving 10,000 people or more were required to
comply beginning January 2002) or are about to make changes in
treatment to comply with this rule (subpart H systems serving fewer
than 10,000 people and ground water systems are required to comply
beginning January 2004).
To address the above issue, EPA evaluated Stage 1 DBPR implications
by using Information Collection Rule data from plants that would not
exceed the Stage 1 DBPR TTHM and HAA5 MCLs as an annual average. The
TTHM and HAA5 data consist of quarterly measurements in four locations
in distribution systems associated with each Information Collection
Rule treatment plant. Two samples were collected at sites representing
average residence time (AVG1 and AVG2), one sample at a site intended
to represent the maximum residence time (MAX), and one sample was
reported as a distribution system equivalent (DSE). The DSE sample was
generally representative of average residence times. EPA believes that
the monitoring locations of the Information Collection Rule, while not
necessarily being the same as the Stage 1 DBPR compliance monitoring
sites, provide a close approximation of monitoring under the Stage 1
DBPR. EPA recognizes, however, that data for plants that are in
compliance with Stage 1 MCLs even without installing additional
treatment (perhaps because of low source water TOC) are not necessarily
reflective of plants that make treatment changes to comply with the
Stage 1 DBPR.
1. DBPs Above the MCL Occur at Some Locations in a Substantial Number
of Plants
Figure IV-1 compares the TTHM running annual average (RAA) levels
with the single highest TTHM concentration in the distribution system.
Twenty one percent (60 of 290) of the Information Collection Rule
plants had single TTHM concentrations higher than the 0.080 mg/L MCL.
Figure IV-2 makes the same comparison for HAA5. Fourteen percent (40 of
290) of the plants meeting the Stage 1 DBPR MCL had single HAA5
concentrations higher than the 0.060 mg/L MCL. In systems with a low
RAA for TTHM and HAA5, the highest single TTHM and HAA5 values are
generally not much higher than the respective Stage 1 DBPR MCLs.
However, as the RAAs increase, there is a greater likelihood of having
peak levels above the MCLs. As the RAAs approach the Stage 1 DBPR MCLs,
some of the distribution system single highest concentrations approach
levels that are double the Stage 1 DBPR MCLs.
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2. Specific Locations in Distribution Systems Are Not Protected to MCL
Levels
Data from the Information Collection Rule show that the RAA
compliance calculation may allow specific locations in a distribution
system to regularly receive water with DBP levels that exceed the MCL.
Figure IV-3 shows that five percent of plants (15 out of 290) had one
or more locations that, on average, exceeded 0.080 mg/L as a TTHM LRAA
for that same year. One of the 15 plants that exceeded a TTHM LRAA of
0.080 mg/L did so at two locations. Of the 15 plants, the highest LRAA
was between 0.080 and 0.090 mg/L at 10 plants, and between 0.090 and
0.100 mg/L at 5 plants. Customers served at these locations regularly
received water with TTHM concentrations somewhat higher than the MCL.
Figure IV-4 shows similar results based on Information Collection
Rule HAA5 data. Three percent of plants (eight of 290) exceeded 0.060
mg/L as an LRAA, and three of these eight plants did so at two or three
locations. Of the 8 plants, the highest LRAA was between 0.060 and
0.070 mg/L at 5 plants, and between 0.070 and 0.075 mg/L at 3 plants.
Among the 290 plants in the Information Collection Rule database
meeting the Stage 1 MCLs, 19 plants have a maximum TTHM LRAA of 0.080
mg/l or greater or a maximum HAA5 LRAA of 0.060 mg/l or greater (four
plants exceeded both MCLs), though in no case did DBP levels at a given
location consistently exceed the MCL by more than 20%.

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3. Stage 1 DBPR Maximum Residence Time Location May Not Reflect the
Highest DBP Occurrence Levels
The 1979 TTHM rule and Stage 1 DBPR monitoring locations must
include a site reflection maximum residence time in the distribution
system with the intent of capturing the highest DBP levels in the
distribution system. The Information Collection rule referred to this
specific location as MAX. The Information Collection rule data indicate
two important results: (1) that monitoring locations identified as the
maximum residence time locations often did not represent those
locations with the highest DBP levels and (2) the highest TTHM and HAA5
level often occurred at different points in the distribution system.
Figure IV-5 illustrates that the highest TTHM and HAA5 LRAAs could
be at any of the four Information Collection Rule sample locations in
the distribution system or, in some cases, at the finished water
location. Fifty percent of the plants evaluated have the highest TTHM
LRAA concentration occurring at a site other than the maximum residence
time monitoring site. over 60% of plants evaluated had the highest HAA5
LRAA at a location other than the maximum residence time monitoring
site.
Figure IV-6, based on data from the National Rural Water Survey
(NRWS), indicates that systems serving fewer than 10,000 people also
frequently have their highest TTHM and HAAS levels at locations other
than those intended to represent maximum residence time. The occurrence
patterns indicated in Figures IV-5 and IV-6 may be due to several
factors, such as HHA5 degrading over time in the distribution system,
maximum residence time monitoring sites not actually representing the
maximum residence time, or that using a simple estimation of maximum
residence time cannot characterize a complex distribution system.
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EPA also analyzed whether the highest LRAA for TTHM and HAA5
occurred at the same location. If TTHM and HAA5 occur at the same
location rather than different locations, fewer monitoring sites would
be needed to represent TTHM and HAA5 occurrence. However, this is not
the case. The Information Collection Rule and NRWA data sets,
respectively, indicate that 49% and 44% of plants experienced their
highest LRAA TTHM and HAA5 concentrations at different locations in the
distribution system.
For plants that did have their highest LRAA TTHM and HAA5
concentrations at the same location, it was not necessarily the maximum
residence time monitoring location. Figure IV-7 illustrates that for
the Information Collection Rule plants with the highest TTHM and HAA5
levels occurring at the same location, the highest TTHM and HAA5 LRAA
simultaneously occurred at the maximum residence time monitoring
location in 50% of the cases. Figure IV-8 illustrates that for the NRWA
plants with the highest TTHM and HAA5 levels occurring at the same
location, the highest TTHM and HAA5 LRAA simultaneously occurred at the
maximum residence time (MAX) monitoring location in 64% of the cases.

C. Request for Comment

EPA requests comment on the analysis presented in this section. Is
EPA's approach for representing post Stage 1 DBPR occurrence
appropriate? What other approaches might be used? Are the conclusions
that EPA derives from the analysis appropriate?

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V. Discussion of Proposed Stage 2 DBPR Requirements

A. MCLG for Chloroform

1. What Is EPA Proposing Today?
EPA is proposing an MCLG for chloroform of 0.07 mg/L based on a
cancer reference dose (RfD), an assumption that a person drinks 2
liters of water per day (the 90th percentile of intake rate for the
U.S. population), and a relative source contribution (RSC) of 20
percent. The MCLG is proposed at a level at which no adverse effects on
the health of persons is anticipated with an adequate margin of safety.
This conclusion is based on toxicological evidence that the
carcinogenic effects of chloroform are an ultimate consequence of
sustained tissue toxicity. The MCLG is set at a daily dose for a
lifetime at which no adverse effects will occur because the sustained
tissue toxicity, which is a key event in the cancer mode of action of
chloroform, will not occur (USEPA 2001b).
EPA believes that the RfD used for chloroform is protective of
sensitive groups, including children. This RfD was developed by the EPA
current method for developing RfDs based on animal data. The method is
designed to be protective by taking human variability into account and
assuming that the average human will be as sensitive as the most
responsive animal species. EPA's understanding of the mode of action
for chloroform does not indicate a uniquely sensitive subgroup or an
increased sensitivity in children.
2. How Was This Proposal Developed?
a. Background. EPA proposed a zero MCLG for chloroform in the 1994
Stage 1 DBPR proposal (USEPA 1994b). Following the proposal, numerous
toxicological studies on chloroform were published and were discussed
in two Notices of Data Availability (NODAs) (USEPA 1997a; USEPA 1998e).
The 1998 NODA presented substantial scientific data related to the mode
of action as part of the chloroform risk assessment and requested
comment on a chloroform MCLG of 0.3 mg/L that reflected a nonlinear
mode of action. After considering comments on the NODAs, EPA determined
that further deliberations with the Science Advisory Board (SAB) and
stakeholders were needed before changing the MCLG for chloroform. Thus,
EPA promulgated a chloroform MCLG of zero in the final Stage 1 DBPR
(USEPA 1998c) and committed to conducting additional deliberations with
the SAB and factoring the SAB's review into the Agency's Stage 2 DBPR
rulemaking

[[Page 49577]]

process. The Agency consulted with the SAB in October 1999 (USEPA
2000f).
The Stage 1 DBPR MCLG of zero for chloroform was challenged, and
the U.S. Court of Appeals for the District of Columbia Circuit issued
an order vacating the zero MCLG (Chlorine Chemistry Council and
Chemical Manufacturers Association v. EPA, 206 f.3d 1286 (D.C. Circuit
2000)). EPA committed to the Court to propose a non-zero MCLG for
chloroform in the upcoming proposed Stage 2 Disinfectants and
Disinfection Byproducts Rule. EPA removed the MCLG for chloroform from
its Stage 1 DBP NPDWR (USEPA 2000e). No other provision of the Stage 1
DBPR was affected.
b. Basis of the new chloroform MCLG. Based on an analysis of all
the available scientific data on chloroform discussed in more detail
below, EPA believes that chloroform dose-response is nonlinear and that
chloroform is likely to be carcinogenic only under high exposure
conditions. EPA's assessment of the cancer risk associated with
chloroform exposure (USEPA 2001b) uses the principles of the 1999 EPA
Proposed Guidelines for Carcinogen Risk Assessment (USEPA 1999a).
The Proposed Guidelines for Carcinogen Risk Assessment, as reviewed
by the public and the EPA SAB, reflect new science and are consistent
with, and an extension of, the existing 1986 Guidelines for Carcinogen
Risk Assessment (USEPA 1986). The 1986 guidelines provide for
departures from default assumptions such as low dose linear
extrapolation. For example, the 1986 EPA guidelines reflect the
position of the Office of Science and Technology Policy (OSTP) that
(OSTP 1985; Principle 26) ``[N]o 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 1985
guidelines go on to 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.''
i. Mode of action. EPA has fully evaluated the science on
chloroform and concludes that chloroform is likely to be carcinogenic
to humans under high exposure conditions that lead to cytotoxicity and
regenerative hyperplasia in susceptible tissue; chloroform is not
likely to be carcinogenic to humans at a dose level that does not cause
cytotoxicity and cell regeneration (USEPA 1998e, USEPA 1998b, USEPA
2001b).
Chloroform's carcinogenic potential is indicated by animal tumor
evidence (liver tumors in mice and renal tumors in both mice and rats)
from inhalation and oral exposure. Data on metabolism, toxicity,
mutagenicity and cellular proliferation contribute to an understanding
of the mode of carcinogenic action. For chloroform, sustained or
repeated cytotoxicity with secondary regenerative hyperplasia precedes,
and is a key event for, hepatic and renal neoplasia.
EPA believes that a DNA reactive mutagenic mode of action is not
likely to be the predominant influence of chloroform on the
carcinogenic process. EPA has concluded that the predominant mode of
action involves cytotoxicity produced by the oxidative generation of
highly reactive metabolites, followed by regenerative cell
proliferation (USEPA 2001b). EPA further believes that the chloroform
dose-response is nonlinear. The SAB final report states ``(t)he
Subcommittee agrees with EPA that sustained or repeated cytotoxicity
with secondary regenerative hyperplasia in the liver and/or kidney of
rats and mice precedes, and is probably a causal factor for, hepatic
and renal neoplasia'' (USEPA 2000f).
ii. Metabolism. The cytochrome P450 isoenzyme CYP 2E1 is the
primary enzyme catalyzing chloroform metabolism at low concentrations.
Chloroform's carcinogenic effects involve oxidative generation of
reactive and toxic metabolites (phosgene and hydrochloric acid [HCl])
and thus are related to its noncancer toxicities (e.g., liver or kidney
toxicities). The electrophilic metabolite phosgene could react with
macromolecules such as phosphotidyl inositols or tyrosine kinases which
in turn could potentially lead to interference with signal transduction
pathways (i.e., chemical messages controlling cell division), thus
leading to carcinogenesis. Likewise, it is also plausible that phosgene
reacts with cellular phospholipids, peptides and proteins resulting in
generalized tissue injury. Glutathione, free cysteine, histidine,
methionine and tyrosine are all potential reactants for electrophilic
agents.
At high concentrations, chloroform may undergo reductive metabolism
which forms reactive dichloromethyl free radicals. These free radicals
can contribute to lipid peroxidation and cause cytotoxicity.
c. How the MCLG is derived. EPA continues to recognize the strength
of the science in support of a nonlinear approach for estimating the
carcinogenicity of chloroform. This science was affirmed by the
Chloroform Risk Assessment Review Subcommittee of the EPA SAB Executive
Committee which met on October 27-28, 1999 (USEPA 2000f). The SAB
Subcommittee agreed that the nonlinear approach is most appropriate for
the risk assessment of chloroform.
Nonzero MCLGs are scientifically and statutorily supported. The
statute requires that the MCLG be set where no known or anticipated
adverse effects occur, allowing for an adequate margin of safety (56 FR
3533; USEPA 1991b). Historically, EPA 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. If
there is substantial scientific evidence, however, that indicates there
is a ``safe threshold'', then a nonzero MCLG can be established with an
adequate margin of safety (56 FR 3533; USEPA 1991a)).
EPA would ideally like to use the delivered dose (i.e., the amount
of key chloroform metabolites that actually reach the liver and cause
cell toxicity) for calculating an RfD to support the MCLG. However, the
required toxicokinetic data are not currently available. Thus, the RfD
is calculated using the applied dose (i.e., the amount of chloroform
ingested). The RfD is based on both the benchmark dose and the
traditional no observed adverse effect level/lowest observed adverse
effect level (NOAEL/LOAEL) approaches for hepatotoxicity in the most
sensitive species, the dog. The MCLG is based on the RfD and calculated
as follows:
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i. Reference dose. The RfD for chloroform was estimated based on
noncancer effects using both the benchmark dose and the traditional
NOAEL/LOAEL approaches. For benchmark analysis, five relevant data sets
including target organ toxicity, labeling index, histopathology in
rodents, and liver toxicity in dogs (Heywood 1979) were evaluated. The
effects seen in dogs are considered to be early signs of liver
toxicity, preceding cytotoxicity, cytolethality and regenerative
hyperplasia. Thus, the Heywood (1979) study, provides the most
sensitive end point in the most sensitive species and is the most
appropriate basis for the RfD.

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The 95% confidence lower bound on the dose associated with a 10%
extra risk (LED10) is based on the prevalence of animals demonstrating
liver toxicity. After an exposure adjustment to the LED10 (1.2 mg/kg/
day), an RfD of 0.01 mg/kg/day was calculated using an overall
uncertainty factor of 100 (10 for interspecies extrapolation and 10 for
protection of sensitive individuals) (USEPA 2001b).
Coincidentally, the benchmark dose and the traditional NOAEL/LOAEL
approaches yield the same RfD number (USEPA 2001b). The NOAEL/LOAEL
approach is also based on the Heywood study (1979) which had a LOAEL of
15 mg/kg/day for evidence of liver toxicity. After an exposure
adjustment to the LOAEL (yielding 12.9 mg/kg/day), an RfD of 0.01 mg/
kg/day was calculated using an overall uncertainty factor of 1000 (10
for interspecies extrapolation, 10 for protection of sensitive
individuals, and 10 for using a LOAEL instead of a NOAEL) (USEPA
2001b).
ii. Relative source contribution. Another factor in determining the
MCLG is the relative source contribution (RSC). The RSC is used when
the MCLG is set at a level above zero. Its purpose is to ensure that
the contribution to exposure from drinking tap water does not cause the
lifetime daily exposure of persons to a contaminant to exceed RfD. The
RSC is thus a factor used to make sure that the MCLG is protective even
if persons are exposed to the contaminant by other routes (inhalation,
dermal absorption) or other sources (e.g., food). If sufficient
quantitative data are not available on exposure by other routes and
sources, EPA has historically assumed that the RSC from drinking water
is 20 percent of the total exposure, a value considered protective. If
data indicate that contributions from other routes and sources are not
significant, EPA has historically assumed a less conservative RSC of 80
percent (54 FR 22,062, 22,069 (May 22, 1989)(USEPA 1989a), 56 FR at
3535 (Jan 30, 1990)(USEPA 1991a), 59 FR 38,668, 38,678 (July 29,
1994)(USEPA 1994b)).
Today, EPA is proposing an assumption of a 20 percent RSC. This is
in consideration of data which indicate that exposure to chloroform by
other routes and sources of exposure may potentially contribute a
substantial percentage of the overall exposure to chloroform.
In the 1998 Stage 1 DBPR NODA, EPA considered an MCLG of 0.3 mg/L
that was calculated using an RSC of 80 percent, based on the assumption
that most exposure to chloroform is likely to come from ingestion of
drinking water. In the final Stage 1 DBPR, EPA reconsidered this
assumption in response to comments and in the light of data which
indicate that exposure to chloroform by inhalation and dermal exposure
may potentially contribute a substantial percentage of the overall
exposure to chloroform depending on the activity patterns of
individuals (USEPA 1998e) e.g., during showering, bathing, swimming,
boiling water, clothes washing, and dishwashing. There is also
potential exposure to chloroform by the dietary route. There are
uncertainties regarding other possible highly exposed sub-populations,
e.g., swimmers, those who use humidifiers, hot-tubs, and outdoor
misters, persons living near industrial sources, people working in
laundromats, and persons working with pesticides employing chloroform
as a solvent (USEPA 1998b).
A 1998 International Life Sciences Institute (ILSI) report
evaluated the uptake of drinking water contaminants through the skin
and by inhalation. The report noted that ``(i)n the case of chloroform,
its high volatility leads to its rapid movement from liquid to air.
Large water-use sources, such as showers, become dominant sources with
respect to exposure'' and ``(t)he inhalation route is demonstrated to
be the primary route for higher-volatility compounds (e.g.,
chloroform)'' (ILSI 1998). Weisel and Jo (1996) found that
``approximately equivalent amounts of chloroform from water can enter
the body by three different exposure routes, inhalation, dermal
absorption, and ingestion, for typical daily activities of drinking and
bathing.''
Chloroform has been found in beverages, especially soft drinks, and
food, particularly dairy products (Wallace, 1997). Wallace states that
``ingestion (drinking tap water and soft drinks and eating certain
dairy foods), inhalation (breathing peak amounts of chloroform emitted
during showers or baths, and lower levels in indoor air from other
indoor sources), and dermal absorption (during showers, baths, and
swimming)'' each ``appear to be potentially substantial contributors to
total exposure''.
EPA estimates that for the median individual, ingestion of total
tap water (assuming certain activity patterns, habits, and home
characteristics) can contribute roughly 28 percent of the total dose of
chloroform (USEPA 2001a). With assumptions as described, tap water
ingestion is a portion of exposure through fluid intake which
contributes about 34 percent of the total dose, inhalation accounts for
about 31 percent of the total dose, ingestion of foods contributes
another 27 percent of the overall dose, and dermal absorption
(primarily during showering) adds slightly less than 8 percent of the
total dose. These exposure percentages are based on average daily doses
(mean chloroform intake for adults) for each source and route of
exposure under specific conditions. They do not take into account the
considerable variability in several factors across the population. For
instance, intake of drinking water or particular foods and length of
shower varies from day-to-day, as do home air turnover rates and
ventilation. Different areas in the United States vary with respect to
these factors and chloroform concentrations in food. Thus, although the
28 percent for the median individual is based on reasonable
assumptions, uncertainty remains.
Given the uncertainties of estimation, EPA believes available
analyses point to the RSC of 20 percent as the appropriate default
(i.e., 20 percent of exposure to chloroform comes from drinking tap
water alone). EPA also believes that this default is protective of
public health and is a more reasonable choice than choosing any
particular estimate because of the assumptions and uncertainties
involved with each estimation. Hence, EPA is proposing the MCLG based
on the RSC default of 20 percent which supports the adequacy of the
margin of safety associated with the MCLG.
iii. Water ingestion and body weight assumptions. In MCLG
calculations, EPA assumes the 90th percentile water ingestion of 2
liters (roughly equivalent to a half gallon) per day (USEPA 2000a). The
use of a conservative consumption estimate is consistent with the
objective of setting an MCLG that is protective. EPA also uses a
default adult body weight of 70 kg (equal to 154 pounds) for the RfD
since dose is calculated from lifetime studies of animals and compared
to lifetime exposure for humans.
iv. MCLG calculation. The MCLG is calculated to be 0.07 mg/L using
the following assumptions: an adult tap water consumption of 2 L per
day for a 70 kg adult, and a relative source contribution of 20%:

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EPA concludes that an MCLG of 0.07 mg/L based on protection against
liver toxicity will be protective against carcinogenicity given that
the mode of action for chloroform involves cytotoxicity as a key event
preceding tumor development. Therefore, the recommended MCLG for
chloroform is 0.07 mg/L.
v. Other considerations. The evidence supports similarity of
potential response in children and adults. The basic biology of
toxicity caused by cell damage due to oxidative damage is expected to
be the same. There is nothing about the incidence and etiology of liver
and kidney cancer in children to indicate that they would be inherently
more sensitive to this mode of action. Most importantly in this case,
children appear to be no different quantitatively in ability to carry
out the oxidative metabolism step for the induction of toxicity and
cancer and may, as fetuses, be less susceptible (USEPA 1999c).
Some commenters on the March 1998 NODA were concerned that EPA did
not take drinking water epidemiology studies into account in its
evaluation of chloroform risk. EPA believes that while the
epidemiologic evidence suggests that chlorinated drinking water may be
associated with certain cancers and reproductive, developmental effects
pertinent to the risk of disinfectant byproduct mixtures, it does not
provide insight into the risk from chloroform specifically. The SAB
noted that ``(t)he goal of the draft risk assessment (the isolation of
the effect of chloroform in drinking water) makes the extensive
epidemiologic evidence on drinking water disinfection byproducts
largely irrelevant'' to the specific question of chloroform health
risks because, in the available studies, chloroform cannot be isolated
from other disinfection byproducts that may be in the drinking water
(USEPA 2000f). The SAB noted that ``the epidemiologic evidence is quite
pertinent to the broader question of most direct regulatory concern,
namely disinfection byproducts in the aggregate''.
d. Feasibility of other options. During the development of the MCLG
for chloroform, EPA considered a number of options for both the
chloroform MCLG and the TTHM MCL. Today, EPA is proposing the preferred
option of a 0.07 mg/L MCLG for chloroform. EPA primarily considered two
other options which are discussed in more detail later: a 0.07 mg/L
MCLG for chloroform in conjunction with developing MCLs for each of the
individual TTHMs (i.e., 4 MCLs and 4 MCLGs for the THMs); and
developing a single combined MCLG for TTHM rather than developing a
separate MCLG for each of the THMs.
EPA considered developing separate MCLGs and MCLs for each THM.
Under this strategy, EPA would determine an MCL as close to the
individual MCLGs as is technically feasible, taking cost into
consideration, for each THM. EPA would propose an MCLG of 0.07 mg/L for
chloroform and maintain the Stage 1 DBPR MCLGs for BDCM, DBCM, and
bromoform (USEPA 1998c). EPA analyzed the impact such an MCL strategy
would have and ultimately rejected this option. This approach
represents a fundamental shift from the TTHM strategy agreed to by
stakeholders and EPA as part of the M-DBP negotiation process and
reflected in the 1998 Stage 1 DBPR. In addition, one important
component of the existing single MCL is that TTHMs are an indicator for
other DBPs. Developing a separate MCL for each THM would move away from
this indicator approach. Because precursor and DBP occurrence
measurements are highly variable, both temporally and geographically,
determining technical feasibility for best available technology (BAT)
would be difficult. Compliance with individual THM standards would be
very different from compliance based on a sum of the four THMs and it
is not clear what treatment technology shifts would be needed. This
problem would be particularly exacerbated in areas with high bromide,
such as California. EPA also projected that States would have a
difficult time overseeing (e.g., variances, exemptions, etc.) the more
complicated rule that would result from this option.
EPA considered establishing a single combined MCLG for TTHM. There
is precedent for using a toxicity equivalency quotient (analogous to a
combined MCLG) for dioxin and coplanar PCBs (USEPA 2000o, Draft Dioxin
Reassessment). From a scientific standpoint, a combined MCLG approach
requires that the chemicals have a similar mode of action and health
endpoint. Chemicals within each of the dioxin and coplanar PCB classes
have the same mode of action and endpoint (target tissue). Within the
PCB class, noncoplanar PCBs have a different mode of action than the
coplanar PCBs. Noncoplanar PCBs are, therefore, not included in the
toxicity equivalency quotient for coplanar PCBs. In the case of the
disinfection byproducts, EPA believes that the THMs have different
modes of action and health endpoints. One of the THMs is a liver
carcinogen (chloroform) with a mode of action dependent on
cytolethality; two are DNA-reactive carcinogens (bromodichloromethane--
large intestine and kidney tumors, and bromoform--large intestine
tumors); and one is a nonlinear non-carcinogen (dibromochloromethane)
which is a liver toxicant. EPA therefore, chose not to develop a
combined MCLG for TTHM. Consequently, after considering this
alternative option in some detail, EPA is today proposing an MCLG of
0.07 mg/L for chloroform.
3. Request for Comment
Based on the information presented previously, EPA is proposing an
MCLG for chloroform of 0.07 mg/L. EPA requests comments on the MCLG and
on EPA's cancer assessment for chloroform. EPA also requests comments
on the RfD, the default RSC of 20 percent, and the tap water
consumption and body weight assumptions used in the MCLG calculation.
EPA solicits additional data on chloroform exposure via other sources
and routes. EPA requests comment on the other options for developing
the chloroform MCLG that the Agency considered.

B. MCLGs for THMs and HAAs

1. What Is EPA Proposing Today?
Today EPA is proposing new MCLGs of 0.02 mg/L for TCAA and 0.03 mg/
L for MCAA based on new toxicological data. As a part of the Stage 1
DBPR, EPA finalized an MCLG of 0.3 mg/L for TCAA. The Stage 1 DBPR did
not include an MCLG for MCAA (although it was included as one of the
five haloacetic acids in the HAA5 MCL). With the exception of
chloroform, discussed above, and these two HAAs, EPA is not revising
any of the other MCLGs that were finalized in the Stage 1 DBPR. No
significant new studies that would change EPA's MCLG estimates for
BDCM, DBCM, bromoform, or DCAA have been published since the Stage 1
DBPR. See section III for a summary of new health effects data.
2. How Was This Proposal Developed?
EPA reviewed the available literature on BDCM, DBCM, bromoform,
DCAA and determined that there was no new

[[Page 49580]]

information that would cause EPA to revise its MCLG estimates. New
toxicology studies on reproductive and developmental effects and cancer
are summarized in sections III.B. and III.D. of today's proposal.
EPA is proposing new MCLGs for TCAA and MCAA. The health effects
information and studies described in the following two sections that
support the proposed MCLGs are summarized from the Addendum to the
Criteria Document for Monochloroacetic Acid and Trichloroacetic Acid
(USEPA 2003b). The occurrence of MCAA and TCAA are discussed in the
Stage 2 Occurrence Assessment for Disinfectants and Disinfection
Byproducts (USEPA 2003o). a. Trichloroacetic acid. In the final Stage 1
DBPR, EPA based its health effects assessment of TCAA on developmental
toxicity and limited evidence of carcinogenicity (USEPA 1998c). Since
then, the Agency has decided that the RfD based on a developmental
LOAEL yields a less conservative RfD than that based on liver toxicity
derived from the study by DeAngelo et al. (1997). Thus, the Agency has
reassessed the health effects of TCAA based on liver toxicity and
revised the RfD and MCLG.
TCAA induces systemic, noncancer effects in animals and humans that
can be grouped into three categories: metabolic alterations, liver
toxicity; and developmental toxicity. The primary site of TCAA toxicity
is the liver (USEPA1994a; Dees and Travis, 1994; Acharya et al. 1995;
Acharya et al. 1997; DeAngelo et al.1997).
The liver has consistently been identified as a target organ for
TCAA toxicity in short-term (Goldsworthy and Popp, 1987; DeAngelo et
al. 1989; Sanchez and Bull, 1990) and longer-term (Bull et al. 1990;
Mather et al. 1990; Bhat et al. 1991) studies. Peroxisome proliferation
has been a primary endpoint evaluated, with mice reported to be more
sensitive to this effect than rats. More recent studies have confirmed
these earlier findings. TCAA-induced peroxisome proliferation was
observed in B6C3F1 mice exposed for 10 weeks to doses as low as 25 mg/
kg/day (Parrish et al. 1996), while in rats exposed to TCAA for up to
104 weeks (DeAngelo et al. 1997), peroxisome proliferation was observed
at 364 mg/kg/day, but not at 32.5 mg/kg/day. Increased liver weight and
significant increases in hepatocyte proliferation have been observed in
short-term studies in mice at doses as low as 100 mg/kg/day (Dees and
Travis, 1994), but no increase in hepatocyte proliferation was noted in
rats given TCAA at similar doses (DeAngelo et al. 1997). More clearly
adverse liver toxicity endpoints, including increased serum levels of
liver enzymes (indicating leakage from cells) or histopathological
evidence of necrosis, have been reported in rats, but generally only at
high doses. For example, in a rat chronic drinking water study,
increased hepatocyte necrosis was observed at a dose of 364 mg/kg/day
(DeAngelo et al. 1997).
In the DeAngelo et al.(1997) study, groups of 50 male F344 rats
were administered TCAA in drinking water, at 0, 50, 500, or 5000 mg/L,
resulting in time-weighted mean daily doses of 0, 3.6, 32.5, or 364 mg/
kg for 104 weeks. There were no significant differences in water
consumption or survival between the control and treatment groups.
Exposure to the high dose of TCAA resulted in a significant decrease in
body weight of 11% at the end of the study. The absolute but not
relative liver weight was decreased at the high dose. Complete necropsy
and histopathology examination showed mild hepatic cytoplasmic
vacuolization in the two low-dose groups, but not in the high-dose
group. The severity of hepatic necrosis was increased mildly in the
high-dose animals. Analyses of serum aspartate aminotransferase (AST)
and alanine aminotransferase (ALT) activities at the end of exposure
showed a significant decrease in AST activity in the mid-dose group and
a significant increase in ALT level in the high-dose group. Since
increased serum ALT or AST levels reflect hepatocellular necrosis, the
increased ALT at the high dose is considered an adverse effect, while a
non-dose related decrease of AST is not. Peroxisome proliferation was
increased significantly in the high-dose animals. There was no evidence
of any exposure-related increase in hepatocyte proliferation. Based on
the significant decrease in body weight (£=10%), minimal
histopathology changes, and increased serum ALT level, the high dose of
364 mg/kg/day is considered the LOAEL and the mid dose of 32.5 mg/kg/
day is considered the NOAEL.
There are no reproductive toxicity studies of TCAA. The results of
an in vitro fertilization assay indicated that TCAA might decrease
fertilization (Cosby and Dukelow, 1992). The available data suggest
that TCAA is a developmental toxicant. TCAA increased resorptions,
decreased implantations, and increased fetal cardiovascular
malformations when administered to pregnant rats at 291 mg/kg/day
(Johnson et al. 1998) on gestation days 1-22. In another study,
decreased fetal weight and length, and increased cardiovascular
malformations were observed when pregnant rats were administered 330
mg/kg/day TCAA by gavage during gestation days 6 to 15 (Smith et al.
1989). Neither of these studies identified a NOAEL. The results of in
vitro developmental toxicity assays, including mouse and rat whole-
embryo culture (Saillenfait et al. 1995; Hunter et al. 1996) and frog
embryo teratogenesis assay--Xenopus (FETAX) (Fort et al. 1993) yielded
positive results. The Hydra test system (Fu et al. 1990) produced
negative results.
TCAA has been reported to induce liver tumors in mice but not in
rats (USEPA 1994a). This observation has also been made in more recent
drinking water studies. Pereira (1996) observed an increased incidence
of hepatocellular adenomas and carcinomas in female B6C3F1 mice at
doses of 262 mg/kg/day and higher after 82 weeks. In contrast, no
increase in neoplastic liver lesions were found in F344 rats given
doses up to 364 mg/kg/day for 104 weeks (DeAngelo et al. 1997). In
addition, a variety of recent mechanistic studies have observed that
TCAA either induced or promoted liver tumors in mice (Ferreira-Gonzalez
et al. 1995; Pereira and Phelps, 1996; Tao et al. 1996; Latendresse and
Pereira, 1997; Stauber and Bull, 1997; Tao et al. 1998).
Recent mutagenicity data have provided mixed results (Giller et al.
1997; DeMarini et al. 1994; Harrington-Brock et al. 1998). TCAA did not
induce oxidative DNA damage in mice following dosing for either 3 or 10
weeks (Parrish et al. 1996). Studies on DNA strand breaks and
chromosome damage produced mixed results (Nelson and Bull, 1988; Chang
et al. 1991; Mackay et al. 1995; Harrington-Brock et al. 1998).
According to the 1999 Draft Guidelines for Carcinogen Risk
Assessment (USEPA 1999a), a compound is appropriately classified as
``Suggestive Evidence of Carcinogenicity, but Not Sufficient to Assess
Human Carcinogenic Potential'' when ``the evidence from human or animal
data is suggestive of carcinogenicity, which raises a concern for
carcinogenic effects but is judged not sufficient for a conclusion as
to human carcinogenic potential''. Based on uncertainty surrounding the
relevance of the liver tumor data in B6C3F1 mice, TCAA can best be
described as ``Suggestive Evidence of Carcinogenicity, but Not
Sufficient to Assess Human Carcinogenic Potential'' under the 1999
Draft Guidelines for Carcinogen Risk Assessment. Thus a quantitative
estimate of cancer potency is not supported.

[[Page 49581]]

The RfD for TCAA of 0.03 mg/kg/day is based on the NOAEL of 32.5
mg/kg/day for liver histopathological changes identified by DeAngelo et
al. (1997). The RfD includes an uncertainty factor of 1000 (composite
uncertainty factor consisting of three factors of 10 chosen to account
for extrapolation from a NOAEL in animals, inter-individual variability
in humans, and insufficiencies in the database, including the lack of
full histopathological data in a second species, the lack of a
developmental toxicity study in second species, and the lack of a
multi-generation reproductive study).
The MCLG is calculated to be 0.02 mg/L using the following
assumptions: an adult tap water consumption of 2 L of tap water per day
for a 70 kg adult, a relative source contribution (RSC) of 20%, and an
additional safety factor to account for possible carcinogenicity. EPA
has traditionally applied an additional safety factor of 1-10 beyond
the uncertainty factors included in the RfD to the MCLG to account for
possible carcinogenicity in cases where there is limited evidence of
carcinogenicity from drinking water, considering weight of evidence,
pharmacokinetics, potency and exposure (USEPA 1994b, p.38678). EPA is
proposing this additional safety factor of 10 for TCAA for the
following reasons: TCAA causes liver tumors in mice but does not do so
in rats. In addition, although peroxisome proliferation (a mode of
action of limited relevance to humans) may play a role in the
development of the mouse tumors, rats also exhibit a peroxisomal
proliferative response after exposure to TCA, yet do not develop
tumors. Other data suggest that promotion of initiated cells and/or
disrupted cell signaling may be involved in the mode of action for the
mouse tumors. Together these factors argue against quantification of
the mouse liver tumors using linear extrapolation from the dose-
response curve, but are not sufficient to rule out concern for a
tumorigenic response. Accordingly, EPA has employed the ten-fold
additional safety factor in determination of the Lifetime Health
Advisory for TCAA. EPA requests comment on the use of 10 as the
additional safety factor for possible carcinogenicity.
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An RSC factor of 20% is used to account for exposure to TCAA in
sources other than tap water, such as ambient air and food. Although
TCAA is nonvolatile and inhalation while showering is not expected to
be a major contribution to total dose, rain waters contain 0.01-1.0
[mu]g/L of TCAA (Reimann et al. 1996) and it can be assumed to be
detected in the atmosphere. Limited data on concentrations of TCAA in
air (NATICH 1993) indicate inhalation of TCAA in ambient air may
contribute to overall exposure. Concentrations of TCAA that have been
measured in a limited selection of foods including vegetables, fruits,
grain and bread (Reimann et al. 1996) are comparable to that in water.
About 3 to 33% of TCAA in cooking water have been reported to be taken
up by the food during cooking in a recent research summary (Raymer et
al. 2001). In addition, there are uses of chlorine in food production
and processing, and TCAA may occur in food as a byproduct of
chlorination (USEPA 1994a). Therefore, ingestion of TCAA in food may
also contribute to the overall exposure. A recent dermal absorption
study of DCAA and TCAA from chlorinated water suggested that the dermal
contribution to the total doses of DCAA and TCAA from routine household
uses of drinking water is less than 1% (Kim and Weisel, 1998).
b. Monochloroacetic acid. Subchronic and chronic oral dosing
studies suggest that the primary targets for MCAA-induced toxicity
include the heart and nasal epithelium. In a 13-week oral gavage study,
decreased heart weight was observed at 30 mg/kg/day and cardiac lesions
progressed in severity with increasing dose. Liver and kidney toxicity
were only observed at higher doses (NTP 1992). In a two-year study,
decreased survival and nasal and forestomach hyperplasia were observed
in mice at 50 mg/kg/day (NTP 1992). A more recent study confirms the
heart and nasal cavities as target sites for MCAA. DeAngelo et al.
(1997) noted decreased body weight at 26.1 mg/kg/day and myocardial
degeneration and inflammation of the nasal cavities in rats exposed to
doses of 59.9 mg/kg/day for up to 104 weeks.
No studies were located on the reproductive toxicity of MCAA and
the potential developmental toxicity of MCAA has not been adequately
tested. Two developmental toxicity studies were identified. Johnson et
al. (1998) reported markedly decreased maternal weight gain, but no
developmental effects, in rats exposed to 193 mg/kg/day MCAA through
gestation days 1-22, only fetal heart was examined. In contrast, in a
published abstract, Smith et al. (1990) reported an increase in
cardiovascular malformations when pregnant rats were exposed to 140 mg/
kg/day; this was also the LOAEL for maternal toxicity, based on marked
decreases in weight gain. MCAA was noted as a potential developmental
toxicant in in vitro screening assays using Hydra (Fu et al. 1990; Ji
et al. 1998).
MCAA has yielded mixed results in genotoxicity assays (USEPA 1994a;
Giller et al. 1997), but has not induced a carcinogenic response in
chronic rodent bioassays (NTP 1992; DeAngelo et al. 1997). In chronic
oral gavage studies, a LOAEL of 15 mg/kg/day (the lowest dose tested)
for decreased survival was identified in rats. In mice the NOAEL was 50
mg/kg/day and the LOAEL was 100 mg/kg/day for nasal and forestomach
epithelium hyperplasia (NTP 1992). In a more recent chronic study,
DeAngelo et al. (1997) reported a LOAEL of 3.5 mg/kg/day in rats given
MCAA in their drinking water, based on increased absolute and relative
spleen weight. Although spleen weight was decreased at the mid and high
doses, this might reflect the masking effect of overt toxicity. As
evidence for this, decreased body weight (£10%), liver,
kidney, and testes weight changes were reported beginning at the next
higher dose of 26.1 mg/kg/day. No increased spleen weight was reported
in the NTP (1992) bioassays, but the lowest dose in rats caused severe
toxicity, and the lowest dose in mice was more than an order of
magnitude higher than the LOAEL in the DeAngelo et al. (1997) study.
According to the 1999 Draft Guidelines for Carcinogen Risk
Assessment (USEPA 1999a), a compound is appropriately classified as
``Not Likely to be Carcinogenic to Humans'' when it has ``been
evaluated in at least two well-conducted studies in two appropriate
animal species without demonstrating carcinogenic effects.'' MCAA can
best be described as ``Not Likely to be Carcinogenic to Humans'' under
the 1999 Draft Guidelines for Carcinogen Risk Assessment.

[[Page 49582]]

The RfD for MCAA of 0.004 mg/kg/day is based on a LOAEL of 3.5 mg/
kg/day for increased spleen weight in rats (DeAngelo et al. 1997) and
application of an uncertainty factor of 1000 (composite uncertainty
factor consisting of two factors of 10 chosen to account for
extrapolation from an animal study, and inter-individual variability in
humans; as well as two factors of 3 for extrapolation from a minimal
effect LOAEL, and insufficiencies in the database, including the lack
of adequate developmental toxicity studies in two species, and the lack
of a multi-generation reproductive study). Two developmental toxicity
studies have been reported (Johnson et al. 1998; Smith et al. 1990),
but the NOAELs yielded less conservative RfDs. The study by DeAngelo et
al (1997) is the most appropriate for derivation of the RfD because it
identifies the lowest LOAEL, and dosing was in drinking water, which is
more appropriate for human health risk assessment.
The MCLG is calculated to be 0.03 mg/L using the following
assumptions: an adult tap water consumption of 2 L of tap water per day
for a 70 kg adult, and a relative source contribution of 20 %.
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An RSC factor of 20% is used to account for exposure to MCAA in
other sources in addition to tap water. Although MCAA is nonvolatile
and inhalation while showering is not expected to be a major
contribution to total dose, rain waters contain 0.05-9 [mu]g/L of MCAA
(Reimann et al. 1996) and it can be assumed to be detected in the
atmosphere. Presence of MCAA has also been reported in rain waters;
thus, inhalation of MCAA in ambient air may contribute to overall
exposure. Concentrations of MCAA that have been measured in a limited
selection of foods including vegetables, fruits, grain and bread
(Reimann et al. 1996) are comparable to that in water. About 2.5 to 62%
of MCAA in cooking water has been reported to be taken up by food
during cooking in a recent research summary (Raymer et al. 2001). In
addition, there are uses of chlorine in food production and processing,
and MCAA may occur in food as a byproduct of chlorination (USEPA
1994a). Therefore, ingestion of MCAA in food may also contribute to the
overall exposure. Assuming dermal absorption rate of MCAA is similar to
DCAA, dermal contribution to the total doses of MCAA from routine
household uses of drinking water should be minor (see V.B.2.a.).
3. Request for Comment
EPA requests comment on the new MCLGs for TCAA (0.02 mg/L) and MCAA
(0.03 mg/L) and all the factors incorporated in the derivation of the
MCLGs, including the RfDs and RSCs. EPA also solicits health effect
information on DBAA and monobromoacetic acid (MBAA), for which MCLGs
have not yet been established.

C. Consecutive Systems

Today's proposal includes provisions for consecutive systems, which
are public water systems that purchase or otherwise receive finished
water from another water system (a wholesale system). As described in
this section, consecutive systems face particular challenges in
providing water that meets regulatory standards for DBPs and other
contaminants whose concentration can increase in the distribution
system. Moreover, current regulation of DBP levels in consecutive
systems varies widely among States. In consideration of these factors,
EPA is proposing monitoring, compliance schedule, and other
requirements specifically for consecutive systems. These requirements
are intended to facilitate compliance by consecutive systems with MCLs
for TTHM and HAA5 under the Stage 2 DBPR. Further, this approach will
help to ensure that consumers in consecutive systems receive equivalent
public health protection. This section begins with a summary of how EPA
proposes to regulate consecutive systems under the Stage 2 DBPR. The
intent of this section is to provide an overview of all consecutive
system requirements in today's proposal. Detailed explanations of these
requirements are provided in later sections of this preamble. The
overview of consecutive system requirements is followed by an
explanation of why EPA has taken this approach to consecutive systems
in today's proposal, including recommendations from the Stage 2 M-DBP
Federal Advisory Committee.
1. What Is EPA Proposing Today?
As public water systems, consecutive systems must provide water
that meets the MCLs for TTHM and HAA5 under the proposed Stage 2 DBPR,
and must carry out associated monitoring, reporting, recordkeeping,
public notification, and other requirements. The following discussion
summarizes how the Stage 2 DBPR requirements apply to consecutive
systems, beginning with a series of definitions. Later sections of this
preamble provide further details as noted.
a. Definitions. To address consecutive systems in the Stage 2 DBPR,
the Agency must define them, along with a number of related terms.
EPA is proposing to define a consecutive system in the Stage 2 DBPR
as a public water system that buys or otherwise receives some or all of
its finished water from one or more wholesale systems for at least 60
days per year. In addition to buying finished water, some consecutive
systems also operate a treatment plant (meaning a plant that treats
source water to produce finished water). As described in section V.I.,
monitoring requirements under the Stage 2 DBPR proposal differ
depending on whether a consecutive system buys all of its finished
water year-round or, alternatively, produces some of its finished water
through treating source water.
EPA proposes to define finished water as water that has been
introduced into the distribution system of a public water system and is
intended for distribution without further treatment, except that
necessary to maintain water quality (such as booster disinfection).
With this definition, water entering the distribution system is
finished water even if a system subsequently applies additional
treatment like booster disinfection to maintain a disinfectant residual
throughout the distribution system.
In today's proposal, EPA defines a wholesale system as a public
water system that treats source water and then sells or otherwise
delivers finished water to another public water system for at least 60
days per year. Delivery may be through a direct connection or through
the distribution system of another consecutive system. Under this
definition, a consecutive system that passes water from a wholesaler to
another consecutive system, and that does not also treat source water,
is not

[[Page 49583]]

a wholesale system. Rather, the system that actually produces the
finished water is responsible for wholesale system requirements under
the proposed Stage 2 DBPR.
A consecutive system entry point is defined as a location at which
finished water is delivered at least 60 days per year from a wholesale
system to a consecutive system. Section V.I. presents the relationship
between consecutive system entry points and proposed Stage 2 DBPR
monitoring requirements. The combined distribution system is the
interconnected distribution system consisting of the distribution
systems of wholesale systems and of the consecutive systems that
receive finished water from those wholesale system(s).
b. Monitoring. For consecutive systems that both purchase finished
water and treat source water to produce finished water for at least
part of the year, EPA is proposing monitoring requirements under a
treatment plant-based approach, described in section V.I. This is the
approach proposed for non-consecutive systems under the Stage 2 DBPR as
well. Under this approach, the sampling requirements for consecutive
systems will be influenced by both the number of treatment plants
operated by the system and the number of consecutive system entry
points, as well as population served and source water type.
For consecutive systems that purchase all of their finished water
year-round, EPA is proposing monitoring requirements under a
population-based approach, also described in section V.I. Under the
population-based approach, the population of the consecutive system
will determine the sampling requirements. EPA believes this approach is
more appropriate than plant-based monitoring because these consecutive
systems do not have treatment plants. As noted in section V.I., EPA is
requesting comment on extending population-based monitoring to all
systems, including non-consecutive systems. EPA has prepared draft
guidance for implementing the IDSE monitoring requirements (described
in section V.H.) using the population-based approach (USEPA 2003j).
EPA is also proposing that States have the opportunity to specify
alternative monitoring requirements for multiple consecutive systems in
a combined distribution system. This option allows States to consider
complex consecutive system configurations for which alternative
monitoring strategies might be more appropriate. As a minimum under
such an approach, each consecutive system must collect at least one
sample among the total number of samples required for the combined
distribution system and will base compliance on samples collected
within its distribution system. The consecutive system is responsible
for ensuring that required monitoring is completed and the system is in
compliance. The consecutive system may conduct the monitoring itself or
arrange for the monitoring to be done by the wholesale system or
another outside party. Whatever approach it chooses, the consecutive
system must document its monitoring strategy as part of its DBP
monitoring plan.
Finally, EPA is proposing that consecutive systems not conducting
disinfectant residual monitoring comply with the monitoring
requirements and MRDLs for chlorine and chloramines.
c. Compliance schedules. EPA is proposing that consecutive systems
of any size comply with the requirements of the Stage 2 DBPR on the
same schedule as required for the largest system in the combined
distribution system. This includes the schedule for carrying out the
IDSE, described in section V.H, and for meeting the Stage 2B MCLs for
TTHM and HAA5, described in section V.D. As discussed later in this
section, EPA is proposing simultaneous compliance schedules under the
Stage 2 DBPR for all systems (both wholesalers and consecutive systems)
in a combined distribution system because this may allow for more cost-
effective compliance with TTHM and HAA5 MCLs. This is also consistent
with the recommendations of the Stage 2 M-DBP Advisory Committee. See
section V.J for details of compliance schedule requirements.
d. Treatment. While consecutive systems often do not need to treat
finished water received from a wholesale system, they may need to
implement procedures to control the formation of DBPs in the
distribution system. For consecutive systems, EPA is proposing that the
BAT for meeting TTHM and HAA5 MCLs is chloramination with management of
hydraulic flow and storage to minimize residence time in the
distribution system. This BAT stems from the recognition that treatment
to remove already-formed DBPs or minimize further formation is
different from treatment to prevent or reduce their formation. See
section V.F for additional information on BATs and their role in
compliance with MCLs.
e. Violations. Under this proposal, monitoring and MCL violations
are assigned to the PWS where the violation occurred. Several examples
are as follows:

--If a consecutive system has hired its wholesale system under contract
to monitor in the consecutive system and the wholesale system fails to
monitor, the consecutive system is in violation because it has the
legal responsibility for monitoring under State/EPA regulations.
--If monitoring results in a consecutive system indicate an MCL
violation, the consecutive systems is in violation because it has the
legal responsibility for complying with the MCL under State/EPA
regulations. The consecutive system may set up a contract with its
wholesale system that details water quality delivery specifications.
--If a wholesale system has a violation and provides that water to a
consecutive system, the wholesale system is in violation. Whether the
consecutive system is in violation will depend on the situation. The
consecutive system will also be in violation unless it conducted
monitoring that showed that the violation was not present in the
consecutive system.
f. Public notice and consumer confidence reports. The
responsibilities for public notification and consumer confidence
reports rest with the individual system. Under the Public Notice Rule
and Consumer Confidence Report Rule, the wholesale system is
responsible for notifying the consecutive system of analytical results
and violations related to monitoring conducted by the wholesale system.
Consecutive systems are required to conduct appropriate public
notification after a violation (whether in the wholesale system or the
consecutive system). In their consumer confidence report, consecutive
systems must include results of the testing conducted by the wholesale
system unless the consecutive system conducted equivalent testing that
indicated the consecutive system was in compliance, in which case the
consecutive system reports its own compliance monitoring results.
g. Recordkeeping and reporting. Consecutive systems are required to
keep all records required of PWSs regulated under this rule. They are
also required to report to the State monitoring results, violations,
and other actions, and are required to consult with the State after a
significant excursion.
h. State special primacy conditions. EPA is aware that due to the
complicated wholesale system-consecutive system relationships that

[[Page 49584]]

exist nationally, there will be cases where the standard monitoring
framework proposed today will be difficult to implement. Therefore, the
Agency is proposing to allow States to develop, as a special primacy
condition, a program under which the State can modify monitoring
requirements for consecutive systems. These modifications must not
undermine public health protection and all systems, including
consecutive systems, must comply with the TTHM and HAA5 MCLs based on
the LRAA. However, such a program would allow the State to establish
monitoring requirements that account for complicated distribution
system relationships, such as where neighboring systems buy from and
sell to each other regularly throughout the year, water passes through
multiple consecutive systems before it reaches a user, or a large group
of interconnected systems have a complicated combined distribution
system. EPA intends to develop a guidance manual to address development
of a State program and other consecutive system issues.
2. How Was This Proposal Developed?
The practice of public water systems buying and selling water to
each other has been commonplace for many years. Reasons include saving
money on pumping, treatment, equipment, and personnel; assuring an
adequate supply during peak demand periods; acquiring emergency
supplies; selling surplus supplies; delivering a better product to
consumers; and meeting Federal and State water quality standards. EPA
estimates that there are at least 8500 consecutive systems nationally,
based on the definitions being proposed today.
Consecutive systems face particular challenges in providing water
that meets regulatory standards for contaminants that can increase in
the distribution system. Examples of such contaminants include
coliforms, which can grow if favorable conditions exist, and some DBPs,
including THMs and HAAs, which can increase when a disinfectant and DBP
precursors continue to react in the distribution system.
EPA is proposing requirements specifically for consecutive systems
because States have taken widely varying approaches to regulating DBPs
in consecutive systems. For example, some States do not regulate DBP
levels in consecutive systems that deliver disinfected water but do not
add a disinfectant. Other States determine compliance with DBP
standards based on the combined distribution system that includes both
the wholesaler and consecutive systems. In this case, sites in
consecutive systems are treated as monitoring sites within the combined
distribution system. Once fully implemented, this proposed rule will
ensure similar protection for consumers in consecutive systems.
EPA is proposing that consecutive systems and wholesale systems be
on the same compliance schedule because generally the most cost-
effective way to achieve compliance with TTHM and HAA5 MCLs is to treat
at the source, typically through precursor removal or alternative
disinfectants. For a wholesale system to make the best decisions
concerning the treatment steps necessary to meet TTHM and HAA5 LRAAs
under the Stage 2 DBPR, both in its own distribution system and in the
distribution systems of consecutive systems it serves, the wholesale
system must know the DBP levels throughout the combined distribution
system. Without this information, the wholesale system may design
treatment changes that allow the wholesale system to achieve
compliance, but leave the consecutive system out of compliance. EPA
also recognizes that there may be cases where a consecutive system
needs to add treatment even after a wholesale system has optimized its
own treatment train.
In consideration of these issues, the Stage 2 M-DBP Advisory
Committee recognized two principles related to consecutive systems: (1)
Consumers in consecutive systems should be just as well protected as
customers of all systems, and (2) monitoring provisions should be
tailored to meet the first principle. Accordingly, the Advisory
Committee recommended that all wholesale and consecutive systems comply
with provisions of the Stage 2 DBPR on the same schedule required of
the wholesale or consecutive system serving the largest population in
the combined distribution system. In addition, the Advisory Committee
recommended that EPA solicit comments on issues related to consecutive
systems that the Advisory Committee had not fully explored (USEPA
2000g). EPA agrees with these recommendations and they are reflected in
today's proposal.
3. Request for Comment
EPA requests comment on all consecutive system issues related to
this rule. Specifically, EPA requests comment on the following:

--Whether the proposed definitions adequately address various wholesale
system-consecutive system relationships and issues.
--Whether any additional terms need to be defined and, if so, what the
definition should be.
--Whether the criteria for States' use of the special primacy criteria
and other State responsibilities are appropriate and adequate.
--Whether it is necessary to require that consecutive system treatment
be installed on the same compliance schedule as the wholesale system in
cases where the size of the consecutive system might otherwise allow it
a longer compliance time frame and the consecutive system treatment
does not affect water quality in any other system.

D. MCLs for TTHM and HAA5

1. What Is EPA Proposing Today?
Today, EPA is proposing use of locational running annual averages
(LRAAs) to determine compliance with the MCLs for TTHM and HAA5.
Consistent with the Stage 2 M-DBP Advisory Committee recommendation,
EPA is proposing a phased approach for LRAA implementation to allow
systems to identify compliance monitoring locations for Stage 2B while
facilitating transition to the new compliance strategy and maintaining
simultaneous compliance schedules for the Stage 2 DBPR and the
LT2ESWTR.
In Stage 2A, all systems must comply with MCLs of 0.120 mg/L for
TTHM and 0.100 mg/L for HAA5 as LRAAs using Stage 1 DBPR compliance
monitoring sites. In addition, during this time period, all systems
must continue to comply with the Stage 1 DBPR MCLs of 0.080 mg/L TTHM
and 0.060 mg/L HAA5 as RAAs.
In Stage 2B, all systems, including consecutive systems, must
comply with MCLs of 0.080 mg/L TTHM and 0.060 mg/L HAA5 as LRAAs using
sampling sites identified under the Initial Distribution System
Evaluation (IDSE) (discussed in section V.H.).
Details of proposed monitoring requirements and compliance
schedules are discussed in preamble sections V.I. and V.J.,
respectively, and may be found in Sec. 141.136 and subpart V of
today's rule.
2. How Was This Proposal Developed?
a. Definition of an LRAA. The primary objective of the LRAA is to
reduce exposure to high DBP levels. For an LRAA, an annual average must
be computed at each monitoring site. The RAA compliance basis of the
1979 TTHM rule and the Stage 1 DBPR allows a system-wide annual average
under which high DBP concentrations in one or more locations are
averaged with, and

[[Page 49585]]

dampened by, lower concentrations elsewhere in the distribution system.
Figure V-1 illustrates the difference in calculating compliance with
the MCLs for TTHM between a Stage 1 DBPR RAA, and the proposed Stage 2
DBPR LRAA.
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[[Page 49586]]

b. Consideration of regulatory alternatives. This section will
discuss EPA's and the Stage 2 M-DBP Advisory Committee's decision-
making process as an array of alternative MCL strategies were
considered. EPA believes that the MCL alternative proposed today (MCLs
of 0.080 mg/L TTHM, 0.060 mg/L HAA5 as LRAAs) is supported by the best
available research, data, and analysis. The science related to cancer
and reproductive and developmental health effects that may be
associated with DBPs, in conjunction with occurrence data that show
that a significant number of high DBP levels occur under current
regulatory scenarios, justify a change in regulation. EPA believes that
this proposal achieves an appropriate balance between the available
science and the uncertainties. EPA believes that regulatory action is
necessary and prudent in the interest of further public health
protection and that the LRAA alternative in combination with the IDSE
is a balanced and reasonable approach. Although it will not remove all
DBP peaks (individual samples with values greater than the MCL), this
proposed regulation will ensure that DBP exposures across a system's
distribution system are further reduced, are more equitable, and may
reduce cancer and reproductive and developmental risk.
The Advisory Committee discussions primarily focused on the
relative magnitude of exposure reduction versus the expected impact on
the water industry and its customers. Initially, this analysis compared
expected reductions in DBP levels and predictions of treatment
technology changes associated with a wide variety of Stage 2 DBPR MCL
alternatives.
After initial discussions, EPA and the Advisory Committee primarily
focused on four types of alternative rule scenarios.

Preferred Alternative.--MCLs of 0.080 mg/L TTHM and 0.060 mg/L HAA5 as
LRAAs. Bromate MCL of 0.010 mg/L.
Alternative 1.--MCLs of 0.080 mg/L TTHM and 0.060 mg/L HAA5 as LRAAs.
Bromate MCL of 0.005 mg/L.
Alternative 2.--MCLs of 0.080 mg/L TTHM and 0.060 mg/L HAA5 as
individual sample maximums (i.e., no single sample could exceed the
MCL). Bromate MCL of 0.010 mg/L.
Alternative 3.--MCLs of 0.040 mg/L TTHM and 0.030 mg/L HAA5 as RAAs.
Bromate MCL of 0.010 mg/L.

EPA and the Advisory Committee, with assistance from the Technical
Workgroup, conducted an in-depth analysis of these regulatory
alternatives. In the process of evaluating alternatives, EPA and the
Advisory Committee reviewed vast quantities of data and many analyses
that addressed health effects, DBP occurrence, predicted reductions in
DBP levels, predicted technology changes, and capital, annual, and
household costs. Details of the compliance, occurrence, and cost
forecasts for the four alternative rule scenarios are described in the
Stage 2 DBPR Economic Analysis (EA) (USEPA 2003i) and the Stage 2 DBPR
Occurrence Document (USEPA 2003o).
In the end, the Advisory Committee recommended the Preferred
Alternative in combination with the IDSE which they believed would
reduce exposure to high levels of DBPs. Today, EPA is proposing the
Preferred Alternative in combination with the IDSE.
The only difference between the Preferred Alternative and
Alternative 1 is the bromate MCL. The Advisory Committee's
recommendation to maintain the Stage 1 DBPR bromate MCL of 0.010 mg/L
is discussed in section V.G. of today's proposal.
Alternatives 2 and 3 are significantly more stringent than the
Stage 1 DBPR with respect to the TTHM and HAA5 requirements.
Alternative 2 would require that all samples be below the MCL. Because
DBP occurrence is variable across the distribution system and over time
(as discussed in section IV), systems would have to base their
disinfectant and treatment strategies on controlling their highest DBP
occurrence levels. Alternative 3 maintains the Stage 1 DBPR RAA
compliance calculation, but reduces the Stage 1 DBPR MCLs by 50
percent. Both alternatives 2 and 3 would cause significant changes in
treatment for a large number of systems. The estimated costs for
Alternatives 2 and 3 are approximately an order of magnitude above the
costs for the Preferred Alternative (see section VII.B.).
Consistent with this greater stringency of alternatives 2 and 3,
the predicted DBP reductions and the resulting health benefits for them
are greater than those predicted for the Preferred Alternative.
Although all members of the Advisory Committee believed that the
science showing reproductive and developmental health effects that have
been associated with DBPs was sufficient to cause concern and warrant
regulatory action, the Advisory Committee did not believe that the
association was certain enough to justify the substantial change in
treatment technologies that would be required to meet these
alternatives. Thus, the Advisory Committee rejected Alternatives 2 and
3.
c. Basis for the LRAA. This section discusses the data and
information EPA used to determine that the LRAA is an appropriate
compliance strategy for today's proposed rule. EPA has chosen
compliance based on an LRAA due to concerns about levels of DBPs above
the MCL in some portions of the distribution system. The LRAA standard
will eliminate system-wide averaging. The individuals served in areas
of the distribution system with above average DBP occurrence levels
masked by averaging under an RAA are not receiving the same level of
health protection. Although an LRAA standard still allows averaging at
a single location over an annual period, EPA believes that changing the
basis of compliance from an RAA to an LRAA will result in decreased
exposure to above average DBP levels (see section VII.A. for
predictions of DBP reductions under the LRAA MCLs). This conclusion is
based on three considerations:
(1) There is considerable evidence that under the current RAA MCL
compliance monitoring requirements a small but significant proportion
of monitoring locations experience high DBP levels. As summarized in
section IV of this preamble, 14 and 21% of Information Collection Rule
systems currently meeting the Stage 1 DBPR RAA MCLs had TTHM and HAA5
single sample concentrations greater than the Stage 1 MCLs and ranged
up to 140 [mu]g/L and 130 [mu]g/L respectively (Figures IV-1 and IV-2),
though most of these exceedences were below 100 [mu]g/L.
(2) In some situations, the populations served by certain portions
of the distribution system consistently receive water that exceeds the
MCL even though the system is in compliance. As discussed in section IV
of this preamble, some Information Collection Rule systems meeting the
Stage 1 DBPR RAA MCLs had monitoring locations that exceeded 0.080 mg/L
TTHM and/or 0.060 mg/L HAA5 as an annual average (i.e., as LRAAs) by up
to 25% (Figures IV-3 and IV-4). Five percent of plants that achieved
compliance with the Stage 1 TTHM MCL of 0.080 mg/L based on an RAA had
a particular sampling location that exceeded 0.080 mg/L as an LRAA
(Figure IV-3). Figure IV-4 shows similar results based on Information
Collection Rule HAA5 data. Three percent of plants that met the Stage 1
HAA5 MCL of 0.060 mg/L as an RAA had a sampling location that exceeded
0.060 mg/L as an LRAA. Customers served at these locations consistently
received water with TTHM and/or HAA5 concentrations higher than the
system-wide MCL.

[[Page 49587]]

(3) Compliance based on an LRAA will remove the opportunity for
systems to average out samples from high and low quality water sources.
Some systems are able to comply with an RAA MCL even if they have a
plant with a poor quality water source (that thus produces high
concentrations of DBPs) because they have another plant that has a
better quality water source (and thus lower concentrations of DBPs).
Individuals served by the plant with the poor quality source will
usually have higher DBP exposure than individuals served by the other
plant.
d. Basis for phasing LRAA compliance. EPA believes that a phased
approach for LRAA implementation will facilitate transition to the new
compliance requirements. Stage 2A of this proposed rule does not
require systems to conduct any additional monitoring. They will
continue to monitor at Stage 1 DBPR locations. Because the LRAA
calculation is the same as the RAA calculation if there is only one
site, Stage 2A compliance only applies to systems that monitor at more
than one site and will only affect medium and large surface water
systems (serving at least 10,000 people) or systems with multiple
plants. Thus, the majority of ground water systems, small surface water
systems, and some consecutive systems are not affected by the proposed
Stage 2A requirements.
e. TTHM and HAA5 as Indicators. In part, both the TTHM and HAA5
classes are regulated because they occur at high levels and represent
chlorination byproducts that are produced from source waters with a
wide range of water quality. The combination of TTHM and HAA5 represent
a wide variety of compounds resulting from bromine substitution and
chlorine substitution reactions (i.e., bromoform has 3 bromines, TCAA
has 3 chlorines, BDCM has one bromine and two chlorines, etc). EPA
believes that the TTHM and HAA5 classes serve as an indicator for
unidentified and unregulated DBPs. EPA believes that controlling the
occurrence levels of TTHM and HAA5 will control the levels of all
chlorination DBPs to some extent.
3. Request for Comment
EPA requests comment on the alternative MCL strategies that were
considered by the Advisory Committee and the determination to propose
the Preferred Alternative in combination with the IDSE as the preferred
regulatory strategy. EPA also requests comment on whether the proposed
approach will reduce peak DBP levels.
EPA requests comment on the phased MCL strategy and whether or not
it will facilitate compliance with the LRAA. EPA also requests comment
on the Stage 2A MCLs of 0.120 mg/L TTHM and 0.100 mg/L HAA5 as LRAAs
and on the long-term MCLs of 0.080 mg/L TTHM and 0.060 mg/L HAA5 as
LRAAs.

E. Requirements for Peak TTHM and HAA5 Levels

1. What Is EPA Proposing Today?
Today, EPA is proposing that, concurrent with Stage 2B, systems
must specifically document occurrences of peak DBP levels, termed
significant excursions. In support of this provision, EPA is proposing
that States, as a special primacy condition, develop criteria for
determining whether a system has a significant excursion. EPA has
developed draft guidance for systems and States on how systems may
determine whether they have significant excursions. EPA is also
proposing that a system that has a significant excursion must: (1)
Evaluate distribution system operational practices to identify
opportunities to reduce DBP levels (such as tank management to reduce
residence time and flushing programs to reduce disinfectant demand),
(2) prepare a written report of the evaluation, and (3) no later than
the next sanitary survey, review the evaluation with their State. This
review will take place under the sanitary survey components calling for
the State to review monitoring, reporting, and data verification and
system management and operation.
2. How Was This Proposal Developed?
Because individual measurements from a location are averaged over a
four-quarter period to determine compliance, there may be occurrence
levels that exceed the MCL even when a system is in compliance with an
LRAA MCL. EPA and the Advisory Committee were concerned about these
exposures to peak levels of DBPs and the possible risk they might pose.
This concern was clearly reflected in the Agreement in Principle, which
states,
``Recognizing that significant excursions of DBP levels will
sometimes occur, even when systems are in full compliance with the
enforceable MCL, public water systems that have significant excursions
during peak periods are to refer to EPA guidance on how to conduct peak
excursion evaluations, and how to reduce such peaks. Such excursions
will be reviewed as part of the sanitary survey process. EPA guidance
on DBP level excursions will be issued prior to promulgation of the
final rule and will be developed in consultation with stakeholders.''
In evaluating this recommendation, EPA believes that the Advisory
Committee's intent was clear with regard to the need for guidance on
how to evaluate and reduce significant excursions. However, the
Agreement is less clear on how, and where, to define what constitutes a
significant excursion, and how to define the scope of the evaluation.
EPA draft guidance recommends several approaches for determining
whether significant excursions have occurred. While today's proposal
requires an evaluation only of distribution system operational
practices, EPA believes that many systems would benefit from a broader
evaluation that includes treatment plant and other system operations.
EPA recognizes that different stakeholders have different points of
view on whether specific criteria that initiate the evaluation of
significant excursions should be included in the rule or in guidance.
EPA also recognizes that different stakeholders may have different
perspectives on how to identify a significant excursion. For this
proposal, EPA has prepared draft guidance for systems and States on how
to (1) determine whether a significant excursion has occurred, using
several different options, (2) conduct significant excursion
evaluations, and (3) reduce significant excursion occurrence.
3. Request for Comment
EPA requests comment on the proposed approach for addressing
significant excursions and on the draft guidance. Is a special primacy
condition the appropriate means for allowing flexibility in identifying
significant excursions while ensuring that such evaluations occur? Is
the sanitary survey the appropriate mechanism for reviewing significant
excursion data with the State? Should a system be required to take
corrective action when significant excursions occur? Should the
required scope of the evaluation be expanded beyond distribution system
operations?
EPA also requests comment on whether specific criteria that
initiate the evaluation of significant excursions should be included in
the rule or in guidance. EPA requests comment on how to identify
significant excursions (regardless of whether the criteria are in the
rule or in guidance). For example, should the significant excursion be
based on an individual measurement, e.g., any measurement being 25 or
50% over either the TTHM or HAA5 MCLs? Alternatively, should the
determination of a significant excursion be based on a certain level of
variability among multiple measurements? For example,

[[Page 49588]]

should the significant excursion be based on the standard deviation of
the LRAA exceeding specific numerical values for either TTHM (e.g.,
0.020 mg/l) or HAA5 (e.g., 0.015 mg/L)? Or should the excursion be
based on a relative measure of variability (e.g., a relative standard
deviation exceeding 25% or 50%) with the condition of a threshold
average concentration also being exceeded (e.g., an LRAA needing to be
at least 0.040 mg/l for TTHM or 0.030 mg/l for HAA5)? EPA requests
comment on the above approaches or alternative approaches for
determining whether a significant excursion has occurred. EPA also
requests comment on whether different approaches may be appropriate for
large and small systems.

F. BAT for TTHM and HAA5

1. What Is EPA Proposing Today?
Today, EPA is proposing that the best available technology (BAT)
for the TTHM and HAA5 LRAA MCLs (0.080 mg/L and 0.060 mg/L
respectively) be one of the three following technologies:
(1) GAC adsorbers with at least 10 minutes of empty bed contact
time and an annual average reactivation/replacement frequency no
greater than 120 days, plus enhanced coagulation or enhanced softening.
(2) GAC adsorbers with at least 20 minutes of empty bed contact
time and an annual average reactivation/replacement frequency no
greater than 240 days.
(3) Nanofiltration (NF) using a membrane with a molecular weight
cut off of 1000 Daltons or less (or demonstrated to reject at least 80%
of the influent TOC concentration under typical operating conditions).
EPA is proposing a different BAT for consecutive systems than for
wholesale systems to meet the TTHM and HAA5 LRAA MCLs. The proposed
consecutive system BAT is chloramination with management of hydraulic
flow and storage to minimize residence time in the distribution system.
2. How Was This Proposal Developed?
a. Basis for the BAT. The Safe Drinking Water Act directs EPA to
specify BAT for use in achieving compliance with the MCL. Systems
unable to meet the MCL after application of BAT can get a variance (see
section V.L. for a discussion of variances). Systems are not required
to use BAT in order to comply with the MCL. They can use other
technologies as long as they meet all drinking water standards and are
approved by the State.
EPA examined BAT using two different methods: (1) EPA analyzed data
from the Information Collection Rule treatment studies and (2) EPA used
the Surface Water Analytical Tool (SWAT), a model developed to compare
alternative regulatory strategies. Both analyses support the BAT
options proposed today. The results of each analyses are presented in
the following two sections.
i. BAT analysis using the Information Collection Rule treatment
studies. EPA analyzed data from the Information Collection Rule
treatment studies (Information Collection Rule Treatment Study Database
CD-ROM, Version 1.0, USEPA 2000m; Hooper and Allgeier 2002). The
treatment studies were designed to evaluate the technical feasibility
of using GAC and NF to remove DBP precursors prior to the addition of
chlorine-based disinfectants. Systems were required to conduct an
Information Collection Rule treatment study based on TOC levels in the
source or finished water. Specifically, surface water plants with
annual average source water TOC concentrations greater than 4 mg/L and
ground water plants with annual average finished water TOC
concentrations greater than 2 mg/L were required to conduct treatment
studies. Thus, the plants required to conduct treatment studies
generally had waters with organic DBP precursor levels that were
significantly higher than the Information Collection Rule national
plant medians of 2.7 mg/L for source water at surface water plants and
0.2 mg/L for finished water at ground water plants (USEPA 2003o).
Plants that conducted GAC studies typically evaluated performance
at two empty bed contact times, 10 and 20 minutes, over a wide range of
operational run times to evaluate the variable nature of TOC removal by
GAC. This allowed GAC performance to be assessed with respect to empty
bed contact time as well as reactivation/replacement frequency. Plants
that conducted membrane treatment studies evaluated one or two
nanofiltration membranes with molecular weight cutoffs less than 1000
Daltons. Regardless of the technology evaluated, all treatment studies
evaluated DBP formation in the effluent from the advanced process under
simulated distribution system conditions representative of the average
residence time and using free chlorine as the primary and residual
disinfectant. (For more information on the Information Collection Rule
treatment study requirements and testing protocols, see USEPA 1996 a
and b.)
Based on the treatment study results, GAC is effective for
controlling DBP formation for waters with influent TOC concentrations
below approximately 6 mg/L (based on the Information Collection Rule
and NRWA data, over 90 percent of plants have average influent TOC
levels below 6 mg/L (USEPA 2003o)). Of the plants that conducted an
Information Collection Rule GAC treatment study, approximately 70% of
the surface water plants studies could meet the 0.080 mg/L TTHM and
0.060 mg/L HAA5 MCLs, with a 20% safety factor (i.e., 0.064 mg/L and
0.048 mg/L, respectively) using GAC with 10 minutes of empty bed
contact time and a 120 day reactivation frequency, and 78% of the
plants could meet the MCLs with a 20% safety factor using GAC with 20
minutes of empty bed contact time and a 240 day reactivation frequency.
As discussed previously, the treatment studies were conducted at plants
with poorer water quality than the national average. Therefore, EPA
believes that much higher percentages of plants nationwide could meet
the MCLs with the proposed GAC BATs.
Among plants using GAC, larger systems would likely realize an
economic benefit from on-site reactivation, which could allow them to
use smaller, 10-minute empty bed contact time contactors with more
frequent reactivation (i.e., 120 days or less). Most small systems
would not find it economically advantageous to install on-site carbon
reactivation facilities, and thus would opt for larger, 20-minute empty
bed contact time contactors, with less frequent carbon replacement
(i.e., 240 days or less).
The proposed reactivation/replacement interval for the 20 minute
contactor (i.e., 240 days) is double the reactivation/replacement
interval for 10 minute contactor (i.e., 120 days). This is based on the
assumption of a linear relationship between empty bed contact time and
the reactivation interval (e.g., a doubling of the empty bed contact
time will result in a doubling of the reactivation interval). The data
from the Information Collection Rule treatment studies indicates that
this linear relationship may not always hold and that doubling the
empty bed contact time generally results in more than a doubling of the
reactivation interval. While there may be some operational advantage in
using larger empty bed contact times, the larger contactors will result
in additional capital expenditures. Furthermore, the economic
optimization of a GAC process must also consider the number of smaller
contactors in parallel, since it may be advantageous to operate a
larger number of smaller contactors in parallel, allowing each
individual contactor to be

[[Page 49589]]

operated for a longer period of time. Based on these considerations,
and the analysis of subject matter experts, it was concluded that the
proposed combination of GAC empty bed contact times and reactivation/
replacement intervals were reasonable for BAT.
The Information Collection Rule treatment study results also
demonstrated that nanofiltration was the better DBP control technology
for ground water sources with high TOC concentrations (i.e., above
approximately 6 mg/L). The results of the membrane treatment studies
showed that all ground water plants could meet the 0.080 mg/L TTHM and
0.060 mg/L HAA5 MCLs, with a 20% safety factor (i.e., 0.064 mg/L and
0.048 mg/L, respectively) at the average distribution system residence
time using nanofiltration. Nanofiltration would be less expensive than
GAC for high TOC ground waters, which generally require minimal
pretreatment prior to the membrane process. Also, nanofiltration is an
accepted technology for treatment of high TOC ground waters in Florida
and parts of the Southwest, areas of the country with elevated TOC
levels in ground waters.
ii. BAT analysis using the SWAT. The second method that EPA used to
examine alternatives for BAT was the SWAT model that was developed to
compare alternative regulatory strategies. EPA modeled the following
BAT options: enhanced coagulation/softening with chlorine (the Stage 1
DBPR BAT); enhanced coagulation/softening with chlorine and no
predisinfection; enhanced coagulation and GAC10; enhanced coagulation
and GAC20; and enhanced coagulation and chloramines. Enhanced
coagulation/softening is required under the Stage 1 DBPR at subpart H
conventional filtration plants. In the model, GAC10 was defined as
granular activated carbon with an empty bed contact time of 10 minutes
and a reactivation or replacement interval of 90 days or longer. GAC20
was defined as granular activated carbon with an empty bed contact time
of 20 minutes and a reactivation or replacement interval of 90 days or
longer. EPA assumed that systems would be operating to achieve both the
Stage 2B MCLs of 0.080 mg/L TTHM and 0.060 mg/L HAA5 as an LRAA and the
SWTR removal and inactivation requirements of 3-log for Giardia and 4-
log for viruses. EPA also evaluated the BAT options under the
assumption that plants operate to achieve DBP levels 20% below the MCL
(safety factor). These assumptions along with other inputs for the SWAT
runs are consistent with those used in the Economic Analysis of today's
proposed rule (USEPA 2003i).
The compliance percentages forecasted by the SWAT model are
indicated in Table V-1. EPA estimates that more than 97% of large
systems will be able to achieve the Stage 2B MCLs regardless of post-
disinfection choice if they were to apply one of the proposed GAC BATs,
i.e., enhanced coagulation (EC) and GAC10 (Seidel Memo, 2001). As shown
in the Stage 2 DBPR Occurrence document (USEPA 2003o), the source water
quality (e.g., DBP precursor levels) in medium and small systems is
expected to be comparable to or better than that for the large systems.
Based on the large system estimate, EPA believes it is conservative to
assume that at least 90% of medium and small systems will be able to
achieve the Stage 2B MCLs if they were to apply one of the proposed GAC
BATs. EPA assumes that small systems may adopt GAC20 in a replacement
mode (with replacement every 240 days) over GAC10 because it may not be
economically feasible for some small systems to install and operate an
on-site GAC reactivation facility. Moreover, some small systems may
find nanofiltration cheaper than the GAC20 in a replacement mode if
their specific geographic locations cause a relatively high cost for
routine GAC shipment.

Table V-1.--SWAT Model Predictions of Percent of Large Plants in Compliance With TTHM and HAA5 Stage 2B MCLs After Application of Specified Treatment
Technologies
--------------------------------------------------------------------------------------------------------------------------------------------------------
Compliance with 0.080 mg/L (TTHM)/0.060 mg/L Compliance with 0.064 mg/L (TTHM)/0.048 mg/L
(HAA5) LRAAs (HAA5) LRAAs (MCLs with 20% safety factor)
-----------------------------------------------------------------------------------------------------
Technology * Residual disinfectant Residual disinfectant
---------------------------------- All systems ---------------------------------- All systems
Chlorine Chloramine Chlorine Chloramine
--------------------------------------------------------------------------------------------------------------------------------------------------------
Enhanced Coagulation (EC)......................... 73.5 76.9 74.8 57.2 65.4 60.4
EC (no predisinfection)........................... 73.4 88.0 78.4 44.1 62.7 50.5
EC & GAC10........................................ 100 97.1 99.1 100 95.7 98.6
EC & GAC20........................................ 100 100 100 100 100 100
EC & All Chloramines.............................. NA 83.9 NA NA 73.6 NA
--------------------------------------------------------------------------------------------------------------------------------------------------------
* Enhanced coagulation/softening is required under the Stage 1 DBPR for conventional plants.

b. Basis for the Consecutive System BAT. EPA believes that the best
compliance strategy for consecutive systems is to collaborate with
wholesalers on the water quality they need. For consecutive systems
that are having difficulty meeting the MCLs, EPA is proposing a BAT of
chloramination with management of hydraulic flow and storage to
minimize residence time in the distribution system. EPA is proposing a
different BAT than for wholesale systems because a consecutive system's
source water has already been disinfected and contains DBPs that cannot
be effectively removed or controlled with the BATs proposed for
wholesale systems. EPA believes the proposed consecutive system BAT is
an effective means for consecutive systems to meet the MCLs.
Chloramination has been used for residual disinfection for many
years to minimize the formation of chlorination DBPs, including TTHM
and HAA5 (Stage 2 Technology and Cost Document, USEPA 2003k). The BAT
provision to manage hydraulic flow and minimize residence time in the
distribution system is to facilitate the maintenance of the chloramine
residual and minimize the likelihood for nitrification. Nitrification,
the process by which microbes convert free ammonia to nitrate and
nitrite, is a concern for systems using chloramines. Nitrification,
however, can be controlled with appropriate chlorine to ammonia ratios,
increasing flow in low demand areas, and increasing storage tank
turnover. EPA proposes that systems implementing the consecutive system
BAT must do the following: (1) Maintain a chloramine residual
throughout the distribution system, (2) develop and submit a plan that
indicates actions that will be taken to minimize the residence time of
water

[[Page 49590]]

within the distribution system, (3) have the plan approved by the
Primacy Agency, and (4) implement the plan as approved by the Primacy
Agency. Minimum components of the management plan would include
periodic scheduled flushing of all dead end pipes and storage vessels
through which water is delivered to customers, and hydraulic flow
control procedures that routinely circulate water in all storage
vessels within the distribution system.
EPA believes that the BATs proposed for wholesale systems are not
appropriate for consecutive systems because each of these BATs, when
applied to water with DBPs, raises other concerns. GAC is not cost-
effective for removing DBPs. In addition, dioxin, a carcinogen, may be
formed during GAC regeneration if GAC has been used to adsorb
chlorinated DBPs. Nanofiltration is only moderately effective at
removing THMs or HAAs if membranes that have a very low molecular
weight cutoff and very high cost of operation are employed. Therefore,
GAC and nanofiltration are not appropriate BATs for consecutive
systems.
3. Request for Comment
EPA requests comment on the proposed BATs including the BAT for
consecutive systems.

G. MCL, BAT, and Monitoring for Bromate

1. What Is EPA Proposing Today?
EPA is proposing today that the MCL for bromate for systems using
ozone remain at 0.010 mg/L as an RAA for samples taken at the entrance
to the distribution system as established by the Stage 1 DBPR and as
provided for under the risk-balancing provisions of section 1412(b)(5)
of the SDWA. EPA's proposal is consistent with the recommendation of
the Stage 2 M-DBP Advisory Committee, which considered the potential
that reducing the bromate MCL could both increase the concentration of
other DBPs in the drinking water and interfere with the efficacy of
microbial pathogen inactivation. In addition, as required by the SDWA
and as recommended by the Advisory Committee, EPA will review the
bromate MCL as part of the 6-year review process and determine whether
the MCL should remain at 0.010 mg/L or be reduced to a lower level. As
a part of that review, EPA will consider the increased utilization of
alternative technologies, such as UV, and whether the risk/risk
concerns reflected in today's proposal remain valid.
Because EPA is not revising the Stage 1 DBPR bromate MCL, EPA is
not proposing a revised BAT for bromate. The Stage 1 DBPR BAT for
bromate is defined as control of ozone treatment processes to reduce
production of bromate. EPA also determined that it was not necessary to
regulate bromate in non-ozone systems that use hypochlorite.
Finally, EPA is proposing to modify the criterion for a system that
uses ozone (and therefore must monitor for bromate) to qualify for
reduced bromate monitoring from one sample per ozone plant per month to
one sample per plant per quarter.
2. How Was This Proposal Developed?
a. Bromate MCL. Bromate is a principal byproduct from ozonation of
bromide-containing source waters. As described in more detail later,
making the bromate MCL more stringent has the potential to decrease
current levels of microbial protection, impair the ability of systems
to control resistant pathogens like Cryptosporidium, and increase
levels of DBPs from other disinfectants that may be used instead of
ozone.
EPA estimates that the 1 in 10,000 excess lifetime cancer risk
level for bromate is 0.005 mg/L. EPA proposed and ultimately finalized
an MCL of 0.010 mg/L in the Stage 1 DBPR, primarily because available
analytical detection methods for bromate could only reliably measure to
0.01 mg/L (USEPA 1994b). Analytical methods for bromate are now
available to quantify bromate concentrations as low as 0.001 mg/L. Due
to the availability of lower detection methods for bromate, as part of
the Stage 2 M-DBP Advisory Committee deliberations, EPA considered
revising the MCL to 0.005 mg/L or lower.
As a disinfectant, ozone is highly effective against a broad range
of microbial pathogens including bacteria, viruses, and protozoa.
Moreover, ozone is one of the few disinfectants available in water
treatment that is capable of inactivating Cryptosporidium, a protozoan
which can cause severe intestinal disorders and can be deadly to those
with compromised immune systems. The oxidizing properties of ozone are
also valuable for treatment objectives like control of tastes and odors
and removal of iron and manganese. In contrast, chlorine, the most
common disinfectant and oxidant in water treatment, is substantially
less effective for controlling Cryptosporidium. Chlorine dioxide, while
capable of providing low levels of inactivation for Cryptosporidium,
typically cannot be used at high doses without violating the MCL for
chlorite, a byproduct of chlorine dioxide. UV light is highly effective
against Cryptosporidium and Giardia and most viruses, but has not been
used extensively to treat drinking water in the United States.
As of early 2000, there were 332 plants of various sizes using
ozone (Overbeck 2000) and 58 plants that were planning to install
ozonation (Rice 2000--personal communication: email 7/14/2000). A
significant percent of current ozone plants use ozone for some portion
of their disinfection objective (Rice, 2000--personal communication:
email 7/14/2000). An ozone system that could not meet a 0.005 mg/L
bromate MCL would have three primary options: decrease the ozone dose;
switch to a different disinfectant; or install an advanced filtration
process such as membranes, sometimes in combination with the first two
options. Of these three options, the third is likely effective but very
expensive, while the first two create the risk either of reducing
microbial protection for a wide range of microbial pathogens, or of
increasing formation of DBPs other than bromate.
In an attempt to achieve a lower level of bromate, some systems
might be driven to reduce the applied ozone dose to the minimum
necessary for regulatory compliance or switch to other treatment
processes. Many systems currently achieve more disinfection than is
required by the SWTR and if a system were to simply lower the ozone
dose, protection from pathogens may be compromised. In addition, since
inactivation of Cryptosporidium requires much higher ozone doses than
Giardia inactivation, systems cannot achieve Cryptosporidium
inactivation with low ozone doses.
If a system were to lower the ozone dose and supplement with an
additional disinfectant, or switch entirely to a different
disinfectant, the system may not achieve the same level of microbial
protection as is afforded by ozonation. Also, other potentially harmful
byproducts from the different disinfectant would be produced.
During the Stage 2 M-DBP Advisory Committee discussions, the TWG
evaluated the impact of reducing the bromate MCL from 0.010 mg/L to
0.005 mg/L as an annual average. The TWG concluded that many systems
currently using ozone or predicted to install ozone to inactivate
microbial pathogens would have significant difficulty maintaining
bromate levels at or below 0.005 mg/L. In the Information Collection
Rule survey of systems serving greater than 100,000 people, all of the
ozone plants had annual average

[[Page 49591]]

bromate concentrations below the 0.010 mg/L level (USEPA 2003o).
However, approximately 20% of these ozone plants did not meet the 0.005
mg/L level. Using the assumption that systems operate their plants
using a safety margin of 20% below the MCL, about 30% of ozone plants
did not reliably attain this level (0.004 mg/L). During the Information
Collection Rule, for the first half of 1998, much of the U.S. was
wetter than normal (NOAA 1998). This hydrogeological condition often
leads to lower than normal bromide concentrations due to dilution by
higher water flows. In the second half of 1998, California continued to
experience El Nino rains (40% of Information Collection Rule ozone
plants were located in California) but many other areas of the country
such as Texas and Florida experienced a drought. The percentage of
ozone systems unable to achieve 0.005 mg/L bromate would likely
increase during years in which bromide concentrations in California
were elevated as consequence of drought.
The ability of systems to use ozone to meet Cryptosporidium
treatment requirements proposed under the LT2ESWTR would be diminished
if the bromate MCL was decreased from 0.010 to 0.005 mg/L. The proposed
LT2ESWTR will require a subset of systems, based on source water
pathogen levels, to provide from 1.0 to 2.5 logs of additional
treatment for Cryptosporidium. Ozone doses required to inactivate
Cryptosporidium are substantially greater than those required for
Giardia and viruses. To assess the potential impact of a lower bromate
MCL on the ability of systems to treat for Cryptosporidium, the TWG
estimated the percentage of treatment plants that could use ozone to
inactivate from 0.5 to 2.5 log of Cryptosporidium without exceeding a
bromate MCL of either 0.005 or 0.010 mg/L (USEPA 2003i). These
estimations were based on analyses of Information Collection Rule
source water quality data, coupled with projected ozone dose
requirements for Cryptosporidium. This analysis suggests that 88% of
systems could use ozone to achieve 1 log of Cryptosporidium
inactivation and 47% could inactivate 2 log while complying with a
bromate MCL of 0.010 mg/L. With the bromate MCL reduced to 0.005 mg/L,
though, these estimates drop to 67% of systems able to inactivate 1 log
of Cryptosporidium with ozone and only 14% able to inactivate 2 log.
The number of plants predicted to be able to treat for Cryptosporidium
with ozone and meet a 0.005 mg/L standard was further reduced when
periods of higher bromide levels, similar to drought conditions, were
modeled. This trend is further exacerbated since the proposed LT2ESWTR
would require more stringent ozone operating conditions (such as higher
ozone doses and longer contact times) than under current surface water
treatment requirements for the subset of plants with higher
Cryptosporidium concentrations in their source water and would thus
result in higher bromate formation than assumed by the TWG. Thus, as
systems are required to meet more stringent inactivation requirements,
a large number of systems would be forced to select treatment processes
other than ozone if the bromate standard were lowered to 0.005 mg/L.
The Stage 2 M-DBP Advisory Committee considered that reducing the
bromate MCL to 0.005 mg/L could both increase the concentration of
other DBPs in the drinking water and interfere with the efficacy of
microbial pathogen inactivation. Therefore, the Advisory Committee
recommended, for purposes of the Stage 2 DBPR, that the bromate MCL
remain at 0.010 mg/L. EPA will review the bromate MCL as part of the
ongoing 6-year review process and determine whether the MCL should
remain at 0.010 mg/L or be reduced to a lower concentration based on
new information.
Today, EPA is proposing to leave the bromate MCL at 0.010 mg/L,
consistent with the Advisory Committee's recommendation. EPA believes
that this is a prudent step at this time, in order to preserve
microbial protection. EPA will continue to analyze any new bromate
health effects data as they become available. It is possible that EPA
may determine that the bromate MCL should be decreased to 0.005 mg/L or
lower in a future rulemaking.
b. Bromate in hypochlorite solutions. The Stage 2 M-DBP Advisory
Committee also discussed the issue of hypochlorite solutions
contaminated with bromate. This contamination can occur during the
production of hypochlorite solutions from natural salt deposits. The
range of bromate concentrations in hypochlorite stock solutions varies
widely (Bolyard et al. 1992; Chlorine Institute 1999, 2000). Moreover,
the bromate contained in the stock solution is diluted upon addition to
the drinking water. From data on Information Collection Rule ozone
systems that used hypochlorite versus those that used gaseous chlorine,
the TWG estimated that hypochlorite solutions contributed an average of
0.001 mg/L bromate.
The Advisory Committee discussed these results and, since the
bromate level resulting from hypochlorite solutions was small compared
to the MCL, did not recommend regulating bromate at systems not using
ozone (non-ozone systems). The Advisory Committee recognized that ozone
systems also using hypochlorite will have to be careful about the
quality of their stock solution.
c. Criterion for reduced bromate monitoring. Because more sensitive
bromate methods are now available, EPA is proposing a new criterion for
reduced bromate monitoring. In the Stage 1 DBPR, EPA required ozone
systems to demonstrate that source water bromide levels, as a running
annual average, did not exceed 0.05 mg/L. EPA elected to use bromide as
a surrogate for bromate in determining eligibility for reduced
monitoring because the available analytical method for bromate was not
sensitive enough to quantify levels well below the bromate MCL of 0.010
mg/L.
In section V.O., EPA is proposing several new analytical methods
for bromate that are far more sensitive than the existing method. Since
these methods can measure bromate to levels of 0.001 mg/L or lower, EPA
is proposing to replace the criterion for reduced bromate monitoring
(source water bromide running annual average not to exceed 0.05 mg/L)
with a bromate running annual average not to exceed 0.0025 mg/L.
In the past, EPA has often set the criterion for reduced monitoring
eligibility at 50% of the MCL, which would be 0.005 mg/L. However, as
discussed before, EPA is proposing that the MCL for bromate remain at
0.010 mg/L, a level that is higher than EPA's usual excess cancer risk
range of 10(-4) to 10(-6) at 2x10(-4) because of risk tradeoff
considerations. EPA believes that the decision for reduced monitoring
is separate from these risk tradeoff considerations. Risk tradeoff
considerations influence the selection of the MCL, while reduced
monitoring requirements are designed to ensure that the MCL, once
established, is reliably and consistently achieved. Requiring a running
annual average of 0.0025 mg/L for the reduced monitoring criterion
allows greater confidence that the system is achieving the MCL and thus
ensuring public health protection.
3. Request for Comment
EPA requests comment on the decision to maintain the Stage 1 DBPR
bromate BAT and MCL of 0.010 mg/L. EPA also requests comment on the
decision not to require bromate

[[Page 49592]]

monitoring at non-ozone systems that use hypochlorite.
EPA requests comment on whether the criterion for reduced bromate
monitoring should be set at a level other than 0.0025 mg/L, and a
rationale for setting it at that level.

H. Initial Distribution System Evaluation (IDSE)

The IDSE is an important part of today's proposed regulation that
is intended to identify sample locations for Stage 2B compliance
monitoring that represent distribution system sites with high DBP
concentrations.
1. What is EPA Proposing Today?
EPA is proposing a requirement for systems to perform an Initial
Distribution System Evaluation (IDSE). Systems will collect data on DBP
levels throughout their distribution system, evaluate these data to
determine which sampling locations are most representative of high DBP
levels and compile this information into a report for submission to the
primacy agency.
a. Applicability. All community water systems, and large
nontransient noncommunity water systems (those serving at least 10,000
people) that add a primary or residual disinfectant other than
ultraviolet light, or that deliver water that has been treated with a
primary or residual disinfectant other than ultraviolet light (i.e.,
consecutive systems) are required to conduct an IDSE under the proposed
rule. The IDSE requirement for systems serving fewer than 500 people
may be waived if the State determines that the monitoring site approved
for Stage 1 DBPR compliance is sufficient to represent both high HAA5
and high TTHM concentrations. The State must submit criteria for this
waiver determination to EPA as part of their primacy application.
States may decide to waive the IDSE requirement for all systems serving
fewer than 500 or some subset of all systems serving fewer than 500 if
the State determines that it is appropriate. EPA is developing an IDSE
Guidance Manual that will include guidance to States on situations for
which a waiver would be appropriate (USEPA 2003j).
b. Data collection. IDSEs are intended to help identify and select
Stage 2B compliance monitoring sites that represent high concentrations
of TTHMs and HAA5. To be able to identify these sites, systems and
States must have monitoring data collected from throughout their
distribution systems. Therefore, under today's proposed rule, systems
are required to collect monitoring data on the concentrations of these
DBPs. There are three possible approaches by which a system can meet
the IDSE requirement.
i. Standard monitoring program. The standard monitoring program
requires one year of monitoring on a specified schedule throughout the
distribution system. The frequency and number of samples required under
the standard monitoring program is determined by source water type,
number of treatment plants, and system size (see section V.J. for a
more detailed discussion of the specific monitoring requirements).
Prior to commencing the standard monitoring program, systems must
prepare a monitoring plan. EPA's IDSE Guidance Manual will provide
guidance on selecting monitoring sites and conducting the standard
monitoring program (USEPA 2003j). As recommended by the Advisory
Committee, EPA is proposing that the standard monitoring program
results are not to be used for determining compliance with MCLs and
that systems will not be required to report IDSE results in the
Consumer Confidence Report.
ii. System specific study. Under this approach, systems may choose
to perform a system-specific study based on earlier monitoring studies
or other data analysis in lieu of the standard monitoring program.
These studies must provide equivalent or better information than the
standard monitoring program for selecting sites that represent high
TTHM and HAA5 levels. Examples of alternative studies are: (1) Recent
TTHM and HAA5 monitoring data that encompass a wide range of sample
sites representative of the distribution system, including those judged
to represent high TTHM and HAA5 concentrations and (2) hydraulic
modeling studies that simulate water movement in the distribution
system. Historical TTHM and HAA5 results submitted by systems must have
been generated by certified laboratories and must include the system's
most recent data. Treatment plant and distribution system
characteristics at the time of historical data collection must reflect
the current plant operations and distribution system. EPA's IDSE
Guidance Manual will include a guidance for system-specific studies and
how to determine whether site-specific data could be sufficient to meet
the IDSE requirements (USEPA 2003j).
iii. 40/30 certification. Under this approach, systems certify to
their primacy agency that all required Stage 1 DBPR compliance samples
were properly collected and analyzed during the two years prior to the
start of the IDSE, and all individual compliance samples were <= 0.040
mg/L for TTHM and <=0.030 mg/L for HAA5. Properly collected and
analyzed compliance samples are those taken at required locations at
times specified in the system's Stage 1 DBPR monitoring plan and
analyzed by certified laboratories. Systems not required to collect
Stage 1 DBPR compliance samples can not utilize the 40/30 certification
approach because they do not have data to determine sampling locations
that represent high concentrations of TTHMs and HAA5. Systems that
qualify for reduced monitoring for the Stage 1 DBPR during the two
years prior to the start of the IDSE, may use results of both routine
and reduced Stage 1 DBPR monitoring to prepare the 40/30 certification.
Large ground water systems may not have two years of HAA5 data to
evaluate due to the timing of the Stage 1 DBPR and the IDSE
requirements. EPA is proposing that, if two years worth of HAA5 data
are not available, large ground water systems evaluate the most recent
two years of TTHM data including data collected in accordance with the
1979 TTHM rule and all available HAA5 compliance data collected up to
nine months following promulgation of this rule when making the 40/30
certification. Similarly, small wholesale and consecutive systems
required to submit their IDSE report no later than two years after
publication of the final rule will evaluate all available Stage 1 DBPR
compliance data collected up to nine months following promulgation.
c. Implementation. All systems subject to the IDSE requirement
under the proposed rule (except those receiving a very small system
waiver from the State) must submit a report to the primacy agency. The
requirements for the report depend upon the IDSE data collection
alternative that the system selects and are listed in Table V-2.

[[Page 49593]]

Table V-2.--IDSE Report Requirements
------------------------------------------------------------------------
IDSE data collection
alternative IDSE report requirements
------------------------------------------------------------------------
Standard Monitoring Program.. ? All standard monitoring program
TTHM and HAA5 analytical results, the
original monitoring plan, and an
explanation of any deviations from that
plan.
? A schematic of the distribution
system.
? Recommendations and justification
for where and during what month(s) Stage
2B monitoring should be conducted.
System Specific Study........ ? All studies, reports, analytical
results and modeling.
? A schematic of the distribution
system.
? Recommendations and justification
for where and during what month(s) Stage
2B monitoring should be conducted
40/30 Certification.......... ? A certification that all required
compliance samples were properly
collected and analyzed during the two
years prior to the start of the IDSE and
all individual compliance samples were
<= 0.040 mg/L for TTHM and <=0.030 mg/L
for HAA5.
? Results of compliance samples
taken after the IDSE was scheduled to
begin and before the IDSE report was
submitted.
? Recommendations for where and
during what month(s) Stage 2B monitoring
should be conducted.
------------------------------------------------------------------------

All IDSE reports must include recommendations for the location and
schedule for the Stage 2B monitoring. The number of sampling locations
and the criteria for their selection are described in Sec. 141.605 of
today's proposed rule, and in section V.I. Generally, a system must
recommend locations with the highest LRAAs unless it provides a
rationale (such as ensuring geographical coverage of the distribution
system instead of clustering all sites in a particular section of the
distribution system) for selecting other locations. Systems must
consider both their compliance data and IDSE data in making this
determination. In addition to specifying a protocol for identifying
recommended monitoring sites in the rule language, EPA will provide
guidance for recommending compliance monitoring sites (including
rationales for systems to recommend sites that do not have the highest
LRAA concentrations) and preparing the IDSE report. EPA will also
provide a process to address IDSE implementation issues during the
period prior to State primacy. At the time that systems serving fewer
than 10,000 people conduct their monitoring or analyze their site-
specific data, many States may have primacy.
The compliance schedules for the IDSE and other requirements of the
proposed rule are described in detail in section V.J. Systems serving
at least 10,000 people (and those smaller wholesale and consecutive
systems associated with larger systems) will be collecting data for
their IDSE prior to State primacy. EPA intends to have an IDSE Guidance
Manual available to assist systems in performing the IDSE (USEPA
2003j). Primacy agencies will specify requirements for systems that do
not submit an IDSE report, or that have not, in the determination of
the primacy agency, conducted an adequate IDSE, in addition to giving
the system a monitoring and reporting violation. These requirements may
include repeating the IDSE while conducting compliance monitoring at
Stage 1 monitoring sites or conducting Stage 2 compliance monitoring at
sites selected by the State.
Consecutive systems are subject to the IDSE requirements of today's
proposed rule. IDSE requirements for consecutive systems are largely
the same as for other systems, but with two differences. First, the
schedule for completion of the IDSE by a consecutive system is
dependent upon the population of the wholesale system. If a consecutive
system serving fewer than 10,000 buys water from a system that serves
10,000 or more people, then this consecutive system must comply within
the same schedule as that for systems £= 10,000. Conversely,
if a wholesale system serves < 10,000 but sells water to a consecutive
system serving £= 10,000, then both the wholesale system and
the consecutive system must complete the IDSE within the same schedule
as that for systems £= 10,000. The second difference for
consecutive systems is that the procedure for recommending Stage 2B
compliance monitoring locations is modified for consecutive systems
purchasing or receiving all of their finished water from a wholesale
system. These modified procedures are described in Sec. 141.605 of
today's proposed rule, and in section V.I.
2. How Was This Pr oposal Developed?
The IDSE was recommended by the Stage 2 M-DBP Advisory Committee.
The Advisory Committee believed that maintaining Stage 1 DBPR sampling
sites for the Stage 2 DBPR would not accomplish the objective of
providing consistent and equitable protection across the distribution
system.
a. Applicability. The M-DBP Advisory Committee recommended that an
IDSE be performed on all community systems to help to identify the
locations in the distribution system that represent high DBP
concentrations. EPA believes that large nontransient noncommunity water
systems (those serving at least 10,000 people) also have distribution
systems that require further evaluation to determine the most
representative locations of high DBP levels. Therefore, large
nontransient noncommunity systems and all community systems are
required to perform an IDSE under today's proposal.
States may waive the IDSE requirement for those very small systems
(systems that serve fewer than 500 people) that monitor for Stage 1
DBPR compliance at the maximum residence time site if the State
determines their maximum residence time Stage 1 compliance monitoring
site is likely to capture both the high TTHM and high HAA5 levels
within the distribution system. The Advisory Committee recommended this
waiver be included because many very small systems have small
distribution systems and the high TTHM and high HAA5 site is at the
same location. The Advisory Committee also recognized that not all very
small systems have a single monitoring site that would represent both
high TTHM and high HAA5 levels (e.g., some rural systems with large
distribution systems) and thus did not recommend a blanket IDSE waiver
for all very small systems.
b. Data collection. The data collection requirements of the IDSE
are designed to find both high TTHM and high HAA5 sites (see section
V.I. for IDSE monitoring site locations). The IDSE is intended as a
one-time requirement. High TTHM and HAA5 concentrations often occur at
different locations in the

[[Page 49594]]

distribution system. The Stage 1 DBPR monitoring sites identified as
the maximum location are selected according to residence time. Because
HAAs can degrade in the distribution system in the absence of
sufficient disinfectant residual (Baribeau et al. 2000), residence time
alone is not an ideal criterion for identifying high HAA5 sites. The
Information Collection Rule data show that of the four monitoring
locations sampled per system, the one identified as the maximum
residence time location was often not the location where the highest
DBP levels were found. In fact, over 60 percent of the highest HAA5
LRAAs and 50 percent of the highest TTHM LRAAs were found at sampling
locations in the system other than the maximum residence time location
(see section IV). Thus the method and assumptions used to select the
Information Collection Rule monitoring sites, and the Stage 1 DBPR
compliance monitoring sites, are not sufficiently reliable to select
Stage 2 DBPR compliance monitoring sites that will capture high DBP
levels.
This data analysis reveals that a reevaluation of monitoring sites
is necessary at many systems to capture sites with high DBP levels. The
Advisory Committee recommended sample locations (based on distribution
disinfectant type) at widely distributed sites (see section V.I. for
details on IDSE monitoring requirements). Monitoring at additional
sites across the distribution system increases the chance of finding
sites with high DBP levels and targets both DBPs that degrade, and DBPs
that form, as residence time increases in the distribution system. EPA
believes that the required number of monitoring locations plus Stage 1
monitoring results provides an adequate recharacterization of DBP
levels throughout the distribution system, at a reasonable cost. With a
recharacterization of distribution systems that focuses on both high
TTHM and HAA5 occurrence, EPA believes that high occurrence sites will
be better represented in this standard monitoring program. Systems will
be required to take steps to address high DBP levels at points that
might otherwise have gone undetected. EPA believes that the decrease in
DBP exposure anticipated to result from the transition from an RAA to
an LRAA will be augmented by the IDSE.
The frequency and number of samples required for the standard
monitoring program decrease as system size (population served)
decreases and depend on source water type. The Advisory Committee
believed that the number of samples required for large and medium
surface water systems was not necessary for small surface water systems
and ground water systems. The majority of small systems have
distribution systems with simpler designs than large systems. DBP
occurrence in ground water systems is generally lower and less variable
than in surface water systems due to lower and less variable precursor
levels and much less temperature variation (see section IV).
Committee members recognized that some systems have detailed
knowledge of their distribution systems by way of hydraulic modeling
and/or ongoing widespread monitoring plans (well beyond that required
for compliance monitoring) that would provide equivalent or superior
monitoring site selection compared to IDSE monitoring. Therefore, the
Advisory Committee recommended that such systems be allowed to
determine new monitoring sites using system-specific data such as
historical monitoring data.
Systems that certify to their State that all compliance samples
taken in the two years prior to the start of the IDSE were <= 0.040 mg/
L TTHM and <= 0.030 mg/L HAA5 are not required to collect additional
DBP monitoring data because the Advisory Committee determined that
these systems most likely would not have high peak DBP levels. EPA
determined that this provision needed to be more specific for three
groups of systems: (1) Those performing Stage 1 DBPR reduced
monitoring, (2) large ground water systems, and (3) small systems
required to conduct an early IDSE. Today's proposal clarifies that
these systems may use a 40/30 certification. EPA recognizes that these
systems may have less compliance data on which to base their 40/30
certifications. However, EPA believes that the data that will be
available are sufficient to make a determination on the most
appropriate Stage 2B monitoring locations.
c. Implementation. Systems are required to submit an IDSE report so
that primacy agencies may review the system's IDSE data collection
efforts and the Stage 2B monitoring locations recommended by the
system. Systems serving at least 10,000 must submit their IDSE report
two years after rule promulgation (which may be prior to primacy for
some States). The M-DBP Advisory Committee recommended an
implementation schedule that would allow systems sufficient time to
make site-specific risk determinations and decisions regarding the
simultaneous implementation of the Stage 2 DBPR and LT2ESWTR but not
stretch out the compliance time frame too far into the future. This
provision requires that medium and large systems conduct and complete
site-specific risk determinations (i.e., the IDSE and LT2ESWTR
Cryptosporidium monitoring) as soon as possible after rule
promulgation. Since small systems cannot begin their microbial
monitoring until after the results from the large system microbial
monitoring have been analyzed, small systems have a longer compliance
time frame.
Systems that submit a 40/30 certification are required to submit
that certification as part of the IDSE report and to include a
recommended Stage 2B monitoring plan. The monitoring plan is required
for these systems because the Stage 2B MCL compliance monitoring sites
proposed today have fundamentally different objectives than the Stage 1
DBPR monitoring sites. Additionally, many systems are required to have
more Stage 2 compliance monitoring sites than Stage 1 sites because
high HAA5 site may be different than high TTHM sites.
3. Request for Comment
EPA requests comments on the IDSE requirement and whether it is a
good tool to identify sites representative of high TTHM and high HAA5
levels.
a. Applicability. EPA requests comment on requiring large (serving
10,000 or more people) nontransient noncommunity water systems to
perform an IDSE. Should NTNCWSs serving fewer than 10,000 people be
required to conduct an IDSE? EPA also requests comment upon whether
States should be able to waive IDSE requirements for very small systems
(serving fewer than 500 people). Are there objective criteria that the
State should use in waiving the requirement? Should the State be
allowed to grant very small system waivers based on some other
criterion other than serving a population <500? For example, should the
State be allowed to choose a higher population cutoff? Should the State
be allowed to use a non-population criterion such as simplicity of
distribution system to grant a very small system waiver? If so, what
should this criterion be and how should qualification be demonstrated?
b. Data collection. EPA requests comment on the requirements for
each of the alternatives for data collection under the proposed IDSE
including: the standard monitoring program, the system-specific study,
and the 40/30 certification. EPA requests comment on whether systems
with less than two years of routine monitoring data should be
considered to have sufficient data to utilize the 40/30 certification.

[[Page 49595]]

Specifically EPA requests comment on whether systems on reduced
monitoring, large ground water systems, and small systems required to
conduct an IDSE within the first two years after promulgation should be
prohibited from submitting a 40/30 certification.
c. Implementation. EPA requests comment on the requirement that
large and medium systems must collect data and prepare their IDSE
report prior to State primacy. EPA requests comment from the States
regarding whether they intend to be involved in the consultations with
systems collecting data for IDSE or in the review of IDSE reports that
are submitted prior to State primacy. EPA is developing a plan to
implement the IDSE during the period prior to State primacy. EPA
requests comment on any issues that should be addressed during this
period to facilitate the IDSE.

I. Monitoring Requirements and Compliance Determination for Stage 2A
and Stage 2B TTHM and HAA5 MCLs

1. What Is EPA Proposing Today?
Today's proposal includes new requirements for how systems must
monitor TTHM and HAA5 levels in their distribution systems and how
systems must assess their monitoring results to determine compliance
with TTHM and HAA5 MCLs. The new monitoring requirements are associated
with the IDSE (described in section V.H) and Stage 2B of the proposed
rule. The new compliance determination requirements relate to use of
the locational running annual average (LRAA) for meeting proposed Stage
2A and Stage 2B MCLs for TTHM and HAA5 (described in section V.D). This
section presents these proposed monitoring and compliance determination
requirements for Stage 2A, the IDSE, and Stage 2B.
An important aspect of the proposed TTHM and HAA5 monitoring
requirements is the use of two different approaches for determining the
number of samples a system is required to collect. One approach is
plant-based. Under the plant-based approach, a system's TTHM and HAA5
sampling requirements are determined by the number of treatment plants
in the system and, in the case of consecutive systems, the number of
consecutive system entry points. The second approach is population-
based. Under the population-based approach, a system's sampling
requirements are influenced by the number of people served, but not by
the number of treatment plants. EPA is proposing population-based
sampling requirements only for IDSE and Stage 2B monitoring by
consecutive systems that purchase all of their finished water year-
round. However, EPA is requesting comment on applying a population-
based approach to all systems for the IDSE and Stage 2B compliance. The
discussion of monitoring requirements in this section provides details
on these two approaches.
A number of factors affect DBP formation, including the type and
amount of disinfectant used, water temperature, pH, amount and type of
precursor material in the water, and the length of time that water
remains in the treatment and distribution systems. For this reason, and
because DBP levels can be highly variable throughout the distribution
system (as discussed in section IV), today's proposal requires systems
to collect IDSE and Stage 2B samples at specific locations in the
distribution system and in accordance with a sampling schedule. For
purposes of determining the number of required samples, EPA intends to
maintain the provision in the Stage 1 DBPR (Sec. 141.132(a)(2)) that
multiple wells drawing raw water from a single aquifer may, with State
approval, be considered one plant, and prior approvals will remain in
force unless withdrawn.
a. Stage 2A. For Stage 2A of the proposed rule, compliance will be
based on the compliance sampling sites and frequency established under
the existing Stage 1 DBPR. Systems must continue to monitor for TTHM
and HAA5 using a plant-based approach, as required under 40 CFR
141.132. Using these monitoring results, systems must continue to
demonstrate compliance with Stage 1 MCLs of 0.080 mg/L for TTHM and
0.060 mg/L for HAA5, based on a running annual average (see 40 CFR
141.133). In addition, systems must comply with the Stage 2A MCLs of
0.120 mg/L for TTHM and 0.100 mg/L for HAA5, based on the LRAA at each
Stage 1 DBPR monitoring location. Stage 1 DBPR provisions for systems
to reduce the frequency of TTHM and HAA5 monitoring will still apply.
Stage 2A will primarily affect surface water systems serving at
least 10,000 people or systems with multiple plants, because these
systems are required to monitor at more than one location in the
distribution system. Most other systems take compliance samples at only
one location under Stage 1 and in these cases, the calculated LRAA will
be equal to the calculated RAA.
b. IDSE. IDSE monitoring requirements are designed to identify
locations within the distribution system with high TTHM and HAA5
levels, which will serve as Stage 2B monitoring sites. The following
discussion provides details on the IDSE standard monitoring program.
Section V.H identifies other approaches by which systems can meet IDSE
requirements of the rule.
For IDSE monitoring, subpart H systems serving at least 10,000
people must collect samples approximately every 60 days at eight
distribution system sites per plant (these are in addition to Stage 1
DBPR compliance monitoring sites). The distribution system residual
disinfectant type determines the location of the eight sites, as shown
in Table V-3.
Subpart H systems serving fewer than 10,000 people and all ground
water systems must collect IDSE samples at two distribution system
sites per plant (at sites that are in addition to the Stage 1 DBPR
compliance monitoring sites) as shown in Table V-3. Subpart H systems
serving 500-9,999 people and ground water systems serving at least
10,000 people must sample quarterly (approximately every 90 days);
subpart H systems serving fewer than 500 people and ground water
systems serving fewer than 10,000 people must sample semi-annually
(approximately every 180 days).
EPA is also proposing IDSE monitoring requirements for consecutive
systems. For consecutive systems that both purchase finished water and
treat source water to produce finished water, IDSE requirements are the
same as for non-consecutive systems with the same population and source
water type (see Table V-3). For these consecutive systems, each
consecutive system entry point (defined in section V.C) is counted as
one treatment plant for purposes of determining sampling requirements.
However, the State may allow a system to consider multiple consecutive
system entry points to be considered a single point.
As noted previously, for consecutive systems that purchase all of
their finished water year-round, EPA is proposing a population-based
monitoring approach (see Table V-4) instead of a plant-based approach.
Under the population-based approach, monitoring requirements are not
influenced by the number of consecutive system entry points, but are
based solely on the population served and the type of source water
used. EPA believes the population-based approach is equitable and will
provide representative DBP concentrations throughout distribution
systems.

[[Page 49596]]

Table V-3.--Proposed IDSE Monitoring Requirements
----------------------------------------------------------------------------------------------------------------
Distribution system sample locations per plant per
Distribution monitoring period \1\
System type and population system Number of ------------------------------------------------------
served disinfectant monitoring Near Average
type periods Total entry residence High TTHM High HAA5
point time locations locations
----------------------------------------------------------------------------------------------------------------
Subpart H £=10,000 Chloramines.... \2\6 8 2 2 2 2
Chlorine....... \2\6 8 1 2 3 2
Subpart H 500-9,999 or Any............ \3\ 4 2 0 0 1 1
Ground Water
£=10,000.
Subpart Any H <500 or Ground Any............ \2\ 4 2 0 0 1 1
Water <10,000.
-------------
Consecutive Systems......... Any............ --Consecutive systems that purchase 100% of their finished water
year-round--see Table V.4.
--Consecutive systems that also treat source water to produce
finished water--plant-based monitoring at same location and
frequency as a non-consecutive system with the same population
and source water.
----------------------------------------------------------------------------------------------------------------
\1\ Samples must be taken at locations other than the existing Stage 1 DBPR monitoring locations. Dual sample
sets (i.e., a TTHM and an HAA5 sample) must be taken at each site. Sampling locations should be distributed
throughout the distribution system.
\2\ Approximately every 60 days.
\3\ Approximately every 90 days.
\4\ Approximately every 180 days.

Table V-4. Population-Based Monitoring Frequencies and Locations Under IDSE for Consecutive Systems That Purchase 100% of Finished Water Year-Round
--------------------------------------------------------------------------------------------------------------------------------------------------------
Distribution system sample locations \1\
------------------------------------------------------
Monitoring periods and Near
Source water type Population size category frequency entry Average High TTHM High HAA5
Total points residence locations locations
\2\ time
--------------------------------------------------------------------------------------------------------------------------------------------------------
Subpart H............................... 0-499...................... Two 2 every 180 days)..... 2 ......... ......... 1 1
500-4,999.................. Four (every 90 days)...... 2 ......... ......... 1 1
5,000-9,999................ 4 ......... 1 2 1
10,000-24,999.............. Six (every 60 days)....... 8 1 2 3 2
25,000-49,999.............. 12 2 3 4 3
50,000-99,999.............. 16 3 4 5 4
100,000-499,999............ 24 4 6 8 6
500,000-1,499,000.......... 32 6 8 10 8
1,500,000-4,999,999........ 40 8 10 12 10
£=5,000,000...... 48 10 12 14 12
Ground Water............................ 0-499...................... Two (every 180 days)...... 2 ......... ......... 1 1
500-9,999.................. 2 ......... ......... 1 1
10,000-99,999.............. Four (every 90 days)...... 6 1 1 2 2
100,000-499,999............ 8 1 1 3 3
£=500,000........ 12 2 2 4 4
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Samples must be taken at locations other than the existing Stage 1 DBPR monitoring locations. Dual sample sets (i.e., a TTHM and an HAA5 sample)
must be taken at each site. Sampling locations should be distributed throughout the distribution system.
\2\ If the number of entry points to the distribution system is less than the specified number of sampling locations, additional samples must be taken
equally at high TTHM and HAA5 locations. If there is an odd extra location number, a sample at a high TTHM location must be taken. If the number of
entry points to the distribution system is more than the specified number of sampling locations, samples must be taken at entry points to the
distribution system having the highest water flows.

As a part of the monitoring schedule, all systems conducting IDSE
monitoring must collect samples during the peak historical month for
TTHM levels or water temperature. EPA will provide guidance to assist
systems in choosing IDSE monitoring locations, including criteria for
selecting high TTHM and HAA5 monitoring locations.
c. Stage 2B. For those systems required to conduct an IDSE, Stage
2B monitoring sites are based on the system's IDSE results and Stage 1
DBPR compliance monitoring results. For those systems not required to
conduct an IDSE, Stage 2B monitoring locations are based on the
system's Stage 1 DBPR compliance monitoring results and an evaluation
of the distribution system characteristics to identify additional
monitoring locations, if required.
Consistent with the Advisory Committee recommendations, the
monitoring frequency for Stage 2B is structured so that systems that
monitor quarterly under the Stage 1 DBPR will continue to monitor
quarterly. In addition, the monitoring schedule must include the month
with the highest historical DBP concentrations.
Many systems on reduced monitoring under the Stage 1 DBPR will
conduct Stage 2B compliance monitoring at different or additional
locations than those used for Stage 1 compliance monitoring. Such
systems must conduct routine monitoring for at least one year before
being eligible for reduced monitoring under Stage 2B. Those systems
that monitor at the same locations under both the Stage 1 DBPR and
Stage 2B DBPR and have qualified for reduced monitoring under Stage 1
may remain on reduced monitoring at the beginning of Stage 2B.

[[Continued on page 49597]]

Notices For
2009
2008
2007
2006
2005
2004
2003
2002
2001
2000
1999
1998
1997
1996
1995
1994

National Primary Drinking Water Regulations: Stage 2 Disinfectants and Disinfection Byproducts Rule; National Primary and Secondary Drinking Water Regulations: Approval of Analytical Methods for Chemical Contaminants

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