[Federal Register: January 4, 2006 (Volume 71, Number 2)]
[Rules and Regulations]
[Page 387-493]
[DOCID:fr04ja06-14]

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Part II

Environmental Protection Agency

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40 CFR Parts 9, 141, and 142

National Primary Drinking Water Regulations: Stage 2 Disinfectants and
Disinfection Byproducts Rule; Final Rule

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 9, 141, and 142

[EPA-HQ-OW-2002-0043; FRL-8012-1]
RIN 2040-AD38

National Primary Drinking Water Regulations: Stage 2
Disinfectants and Disinfection Byproducts Rule

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: The Environmental Protection Agency (EPA) is promulgating
today's final rule, the Stage 2 Disinfectants and Disinfection
Byproducts Rule (DBPR), to provide for increased protection against the
potential risks for cancer and reproductive and developmental health
effects associated with disinfection byproducts (DBPs). The final Stage
2 DBPR contains maximum contaminant level goals for chloroform,
monochloroacetic acid and trichloroacetic acid; National Primary
Drinking Water Regulations, which consist of maximum contaminant levels
(MCLs) and monitoring, reporting, and public notification requirements
for total trihalomethanes (TTHM) and haloacetic acids (HAA5); and
revisions to the reduced monitoring requirements for bromate. This
document also specifies the best available technologies for the final
MCLs. EPA is also approving additional analytical methods for the
determination of disinfectants and DBPs in drinking water. EPA believes
the Stage 2 DBPR will reduce the potential risks of cancer and
reproductive and developmental health effects associated with DBPs by
reducing peak and average levels of DBPs in drinking water supplies.
    The Stage 2 DBPR applies to public water systems (PWSs) 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.
    This rule also makes minor corrections to drinking water
regulations, specifically the Public Notification tables. New endnotes
were added to these tables in recent rulemakings; however, the
corresponding footnote numbering in the tables was not changed. In
addition, this rule makes a minor correction to the Stage 1
Disinfectants and Disinfection Byproducts Rule by replacing a sentence
that was inadvertently removed.

DATES: This final rule is effective on March 6, 2006. For judicial
review purposes, this final rule is promulgated as January 4, 2006. The
incorporation by reference of certain publications listed in the rule
is approved by the Director of the Federal Register as of March 6,
2006.

ADDRESSES: EPA has established a docket for this action under Docket ID
No. EPA-HQ-OW-2002-0043. All documents in the docket are listed on the
http://www.regulations.gov Web site.

    Although listed in the index, some information is not publicly
available, e.g., CBI or other information whose disclosure is
restricted by statute. Certain other material, such as copyrighted
material, is not placed on the Internet and will be publicly available
only in hard copy form.
    Publicly available docket materials are available either
electronically through http://www.regulations.gov or in hard copy at

the Water Docket, EPA/DC, EPA West, Room B102, 1301 Constitution Ave.,
NW., Washington, DC. The Public Reading Room is open from 10 a.m. to 4
p.m., Monday through Friday, excluding legal holidays. The telephone
number for the Public Reading Room is<PHONE_NUMBER>, and the telephone
number for the Water Docket is<PHONE_NUMBER>.

FOR FURTHER INFORMATION CONTACT: For technical inquiries, contact Tom
Grubbs, Standards and Risk Management Division, Office of Ground Water
and Drinking Water (MC 4607M), Environmental Protection Agency, 1200
Pennsylvania Ave., NW., Washington, DC 20460; telephone number: (202)
564-5262; fax number:<PHONE_NUMBER>; e-mail address:
<EMAIL_ADDRESS>For general information, contact the Safe

Drinking Water Hotline, Telephone<PHONE_NUMBER>. The Safe Drinking
Water Hotline is open Monday through Friday, excluding legal holidays,
from 10 a.m. to 4 p.m. Eastern Time.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does This Action Apply to Me?

    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.

------------------------------------------------------------------------
                                                                Examples
                                                                   of
                           Category                            regulated
                                                                entities
------------------------------------------------------------------------
Industry.....................................................  Community
                                                                 and
                                                               nontransi
                                                                 ent
                                                               noncommun
                                                               ity water
                                                               systems
                                                               that use
                                                               a primary
                                                                  or
                                                               residual
                                                               disinfect
                                                               ant other
                                                                than
                                                               ultraviol
                                                               et light
                                                                  or
                                                               deliver
                                                               water
                                                               that has
                                                                been
                                                               treated
                                                               with a
                                                               primary
                                                                  or
                                                               residual
                                                               disinfect
                                                               ant other
                                                                than
                                                               ultraviol
                                                               et light.
State, Local, Tribal, or Federal Governments.................  Community
                                                                 and
                                                               nontransi
                                                                 ent
                                                               noncommun
                                                               ity water
                                                               systems
                                                               that use
                                                               a primary
                                                                  or
                                                               residual
                                                               disinfect
                                                               ant other
                                                                than
                                                               ultraviol
                                                               et light
                                                                  or
                                                               deliver
                                                               water
                                                               that has
                                                                been
                                                               treated
                                                               with a
                                                               primary
                                                                  or
                                                               residual
                                                               disinfect
                                                               ant other
                                                                than
                                                               ultraviol
                                                               et 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 that EPA is now aware
could potentially be regulated by this action. Other types of entities
not listed in the 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 this action to a particular entity, contact the person
listed in the preceding FOR FURTHER INFORMATION CONTACT section.

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

    See the ADDRESSES section for information on how to receive a copy
of this document and related information.

Regional contacts:
I. Kevin Reilly, Water Supply Section, JFK Federal Bldg., Room 203,
Boston, MA 02203,<PHONE_NUMBER>.
II. Michael Lowy, Water Supply Section, 290 Broadway, 24th Floor, New

York, NY 10007-1866,<PHONE_NUMBER>.
III. Jason Gambatese, Drinking Water Section (3WM41), 1650 Arch Street,
Philadelphia, PA 19103-2029,<PHONE_NUMBER>.
IV. Robert Burns, Drinking Water Section, 61 Forsyth Street SW.,
Atlanta, GA 30303,<PHONE_NUMBER>.
V. Miguel Del Toral, Water Supply Section, 77 W. Jackson Blvd.,
Chicago, IL 60604,<PHONE_NUMBER>.
VI. Blake L. Atkins, Drinking Water Section, 1445 Ross Avenue, Dallas,
TX 75202,<PHONE_NUMBER>.
VII. Douglas J. Brune, Drinking Water Management Branch, 901 North 5th
Street, Kansas City, KS 66101,<PHONE_NUMBER>.
VIII. Bob Clement, Public Water Supply Section (8P2-W-MS), 999 18th
Street, Suite 500, Denver, CO 80202-2466,<PHONE_NUMBER>.
IX. Bruce Macler, Water Supply Section, 75 Hawthorne Street, San
Francisco, CA 94105,<PHONE_NUMBER>.
X. Wendy Marshall, Drinking Water Unit, 1200 Sixth Avenue (OW-136),
Seattle, WA 98101,<PHONE_NUMBER>.

Abbreviations Used in This Document

ASDWA Association of State Drinking Water Administrators
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
BDCM Bromodichloromethane
CDBG Community Development Block Grant
CWS Community water system
DBAA Dibromoacetic acid
DBCM Dibromochloromethane
DBP Disinfection byproduct
DBPR Disinfectants and Disinfection Byproducts Rule
DCAA Dichloroacetic acid
EA Economic analysis
EC Enhanced coagulation
EDA Ethylenediamine
EPA United States Environmental Protection Agency
ESWTR Enhanced Surface Water Treatment Rule
FACA Federal Advisory Committee Act
GAC Granular activated carbon
GC/ECD Gas chromatography using electron capture detection
GWR Ground Water Rule
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)
HAN Haloacetonitriles (trichloroacetonitrile, dichloroacetonitrile,
bromochloroacetonitrile, and dibromoacetonitrile)
IC Ion chromatograph
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)
LOAEL Lowest observed adverse effect level
LRAA Locational running annual average
LT1ESTWR Long Term 1 Enhanced Surface Water Treatment Rule
LT2ESTWR 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
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
OMB Office of Management and Budget
PAR Population attributable risk
PE Performance evaluation
PWS Public water system
RAA Running annual average
RFA Regulatory Flexibility Act
RfD Reference dose
RSC Relative source contribution
RUS Rural Utility Service
SAB Science Advisory Board
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
TC Total coliforms
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
UV 254 Ultraviolet absorption at 254 nm
VSL Value of Statistical Life
WTP Willingness To Pay

Table of Contents

I. General Information
    A. Does This Action Apply to Me?
    B. How Can I Get Copies of This Document and Other Related
Information?
II. Summary of the Final Rule
    A. Why is EPA Promulgating the Stage 2 DBPR?
    B. What Does the Stage 2 DBPR Require?
    1. Initial Distribution System Evaluation
    2. Compliance and monitoring requirements
    3. Operational Evaluation Levels
    4. Consecutive systems
    C. Correction of Sec.  141.132
III. Background
    A. Statutory Requirements and Legal Authority
    B. What is the Regulatory History of the Stage 2 DBPR and How
Were Stakeholders Involved?
    1. Total Trihalomethanes Rule
    2. Stage 1 Disinfectants and Disinfection Byproducts Rule
    3. Stakeholder involvement
    a. Federal Advisory Committee process
    b. Other outreach processes
    C. Public Health Concerns to be Addressed
    1. What are DBPs?
    2. DBP Health Effects
    a. Cancer health effects
    i. Epidemiology
    ii. Toxicology
    b. Reproductive and developmental health effects
    i. Epidemiology
    ii. Toxicology
    c. Conclusions
    D. DBP Occurrence and DBP Control
    1. Occurrence
    2. Treatment
    E. Conclusions for Regulatory Action
IV. Explanation of Today's Action
    A. MCLGs

    1. Chloroform MCLG
    a. Today's rule
    b. Background and analysis
    c. Summary of major comments
    2. HAA MCLGs: TCAA and MCAA
    a. Today's rule
    b. Background and analysis
    c. Summary of major comments
    B. Consecutive Systems
    1. Today's Rule
    2. Background and analysis
    3. Summary of major comments
    C. LRAA MCLs for TTHM and HAA5
    1. Today's rule
    2. Background and analysis
    3. Summary of major comments
    D. BAT for TTHM and HAA5
    1. Today's rule
    2. Background and analysis
    3. Summary of major comments
    E. Compliance Schedules
    1. Today's rule
    2. Background and analysis
    3. Summary of major comments
    F. Initial Distribution System Evaluation (IDSE)
    1. Today's rule
    a. Applicability
    b. Data collection
    i. Standard monitoring
    ii. System specific study
    iii. 40/30 certification
    c. Implementation
    2. Background and analysis
    a. Standard monitoring
    b. Very small system waivers
    c. 40/30 certifications
    d. System specific studies
    e. Distribution System Schematics
    3. Summary of major comments
    G. Monitoring Requirements and Compliance Determination for TTHM
and HAA5 MCLs
    1. Today's Rule
    a. IDSE Monitoring
    b. Routine Stage 2 Compliance Monitoring
    i. Reduced monitoring
    ii. Compliance determination
    2. Background and Analysis
    3. Summary of Major Comments
    H. Operational Evaluation Requirements initiated by TTHM and
HAA5 Levels
    1. Today's rule
    2. Background and analysis
    3. Summary of major comments
    I. MCL, BAT, and Monitoring for Bromate
    1. Today's rule
    2. Background and analysis
    a. Bromate MCL
    b. Criterion for reduced bromate monitoring
    3. Summary of major comments
    J. Public Notice Requirements
    1. Today's rule
    2. Background and analysis
    3. Summary of major comments
    K. Variances and Exemptions
    1. Today's Rule
    2. Background and Analysis
    a. Variances
    b. Affordable Treatment Technologies for Small Systems
    c. Exemptions
    3. Summary of major comments
    L. Requirements for Systems to Use Qualified Operators
    M. System Reporting and Recordkeeping Requirements
    1. Today's rule
    2. Summary of major comments
    N. Approval of Additional Analytical Methods
    1. Today's Rule
    2. Background and Analysis
    O. Laboratory Certification and Approval
    1. PE acceptance criteria
    a. Today's rule
    b. Background and analysis
    c. Summary of major comments
    2. Minimum reporting limits
    a. Today's rule
    b. Background and analysis
    c. Summary of major comments
    P. Other regulatory changes
V. State Implementation
    A. Today's rule
    1. State Primacy Requirements for Implementation Flexibility
    2. State recordkeeping requirements
    3. State reporting requirements
    4. Interim primacy
    5. IDSE implementation
    B. Background and Analysis
    C. Summary of Major Comments
VI. Economic Analysis
    A. Regulatory Alternatives Considered
    B. Analyses that Support Today's Final Rule
    1. Predicting water quality and treatment changes
    2. Estimating benefits
    3. Estimating costs
    4. Comparing regulatory alternatives
    C. Benefits of the Stage 2 DBPR
    1. Nonquantified benefits
    2. Quantified benefits
    3. Timing of benefits accrual
    D. Costs of the Stage 2 DBPR
    1. Total annualized present value costs
    2. PWS costs
    a. IDSE costs
    b. PWS treatment costs
    c. Monitoring costs
    3. State/Primacy agency costs
    4. Non-quantified costs
    E. Household Costs of the Stage 2 DBPR
    F. Incremental Costs and Benefits of the Stage 2 DBPR
    G. Benefits From the Reduction of Co-occurring Contaminants
    H. Potential Risks From Other Contaminants
    1. Emerging DBPs
    2. N-nitrosamines
    3. Other DBPs
    I. Effects of the Contaminant on the General Population and
Groups within the General Population that are Identified as Likely
To Be at Greater Risk of Adverse Health Effects
    J. Uncertainties in the Risk, Benefit, and Cost Estimates for
the Stage 2 DBPR
    K. Benefit/Cost Determination for the Stage 2 DBPR
    L. Summary of Major Comments
    1. Interpretation of health effects studies
    2. Derivation of benefits
    3. Use of SWAT
    5. Unanticipated risk issues
    6. Valuation of cancer cases avoided
VII. 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 Risks and Safety Risks
    H. Executive Order 13211: Actions Concerning Regulations 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
    M. Analysis of the Likely Effect of Compliance With the Stage 2
DBPR on the Technical, Managerial, and Financial Capacity of Public
Water Systems
    N. Congressional Review Act
VIII. References

II. Summary of the Final Rule

A. Why is EPA Promulgating the Stage 2 DBPR?

    The Environmental Protection Agency is finalizing the Stage 2
Disinfectants and Disinfection Byproduct Rule (DBPR) to reduce
potential cancer risks and address concerns with potential reproductive
and developmental risks from DBPs. The Agency is committed to ensuring
that all public water systems provide clean and safe drinking water.
Disinfectants are 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 Stage 2 DBPR is designed to reduce the level of exposure
from DBPs without undermining the control of microbial pathogens. The
Long Term 2 Enhanced Surface Water Treatment Rule (LT2ESWTR) is being
finalized and implemented simultaneously with the Stage 2 DBPR to
ensure that drinking water is microbiologically safe at the limits set
for DBPs.
    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)).
The Stage 2 DBPR augments the Stage 1 DBPR that was finalized in 1998
(63 FR 69390, December 16, 1998) (USEPA

1998a). The goal of the Stage 2 DBPR is to target the highest risk
systems for changes beyond those required for Stage 1 DBPR. Today's
rule reflects consensus recommendations from the Stage 2 Microbial/
Disinfection Byproducts (M-DBP) Federal Advisory Committee (the
Advisory Committee) as well as public comments.
    New information on health effects, occurrence, and treatment has
become available since the Stage 1 DBPR that supports the need for the
Stage 2 DBPR. EPA has completed a more extensive analysis of health
effects, particularly reproductive and developmental endpoints,
associated with DBPs since the Stage 1 DBPR. Some recent studies on
both human epidemiology and animal toxicology have shown possible
associations between chlorinated drinking water and reproductive and
developmental endpoints such as spontaneous abortion, stillbirth,
neural tube and other birth defects, intrauterine growth retardation,
and low birth weight. While results of these studies have been mixed,
EPA believes they support a potential hazard concern. New epidemiology
and toxicology studies evaluating bladder, colon, and rectal cancers
have increased the weight of evidence linking these health effects to
DBP exposure. The large number of people (more than 260 million
Americans) exposed to DBPs and the potential cancer, reproductive, and
developmental risks have 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 is predicted to provide a major reduction in
DBP exposure, national survey data suggest that some customers may
receive drinking water with elevated, or peak, DBP concentrations even
when their distribution system is in compliance with the Stage 1 DBPR.
Some of these peak concentrations are substantially greater than the
Stage 1 DBPR maximum contaminant levels (MCLs) and some customers
receive these elevated levels of DBPs on a consistent basis. The new
survey results also show that Stage 1 DBPR monitoring sites may not be
representative of higher DBP concentrations that occur in distribution
systems. In addition, new studies indicate 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 occurrence and treatment information indicates
that significant public health benefits may be achieved through
further, cost-effective reductions of DBPs in distribution systems.
    The Stage 2 DBPR presents a risk-targeting approach to reduce risks
from DBPs. The new requirements provide for more consistent, equitable
protection from DBPs across the entire distribution system and the
reduction of DBP peaks. New risk-targeting provisions require systems
to first identify their risk level; then, only those systems with the
greatest risk will need to make operational or treatment changes. 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 and with fewer risks from DBPs.

B. What Does the Stage 2 DBPR Require?

    The risk-targeting components of the Stage 2 DBPR focus the
greatest amount of change where the greatest amount of risk may exist.
Therefore, the provisions of the Stage 2 DBPR focus first on
identifying the higher risks through the Initial Distribution System
Evaluation (IDSE). The rule then addresses reducing exposure and
lowering DBP peaks in distribution systems by using a new method to
determine MCL compliance (locational running annual average (LRAA)),
defining operational evaluation levels, and regulating consecutive
systems. This section briefly describes the requirements of this final
rule. More detailed information on the regulatory requirements for this
rule can be found in Section IV.
1. Initial Distribution System Evaluation
    The first provision, designed to identify higher risk systems, is
the Initial Distribution System Evaluation (IDSE). The purpose of the
IDSE is to identify Stage 2 DBPR compliance monitoring sites that
represent each system's highest levels of DBPs. Because Stage 2 DBPR
compliance will be determined at these new monitoring sites, only those
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 the highest concentrations of TTHM and HAA5 in each system's
distribution system, the IDSE will offer increased assurance that MCLs
are being met across the distribution system and that customers are
receiving more equitable public health protection. 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.
Alternatively, 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
IDSE requirements are discussed in Sections IV.E, IV.F., and IV.G of
this preamble and in subpart U of the rule language.

2. Compliance and Monitoring Requirements

    As in Stage 1, the Stage 2 DBPR focuses on monitoring for and
reducing concentrations of two classes of DBPs: total trihalomethanes
(TTHM) and haloacetic acids (HAA5). These two groups of DBPs act as
indicators for the various byproducts that are present in water
disinfected with chlorine or chloramine. This means that concentrations
of TTHM and HAA5 are monitored for compliance, but their presence in
drinking water is representative of many other chlorination DBPs that
may also occur in the water; thus, a reduction in TTHM and HAA5
generally indicates an overall reduction of DBPs.
    The second provision of the Stage 2 DBPR is designed to address
spatial variations in DBP exposure through a new compliance calculation
(referred to as locational running annual average) for TTHM and HAA5
MCLs. The MCL values remain the same as in the Stage 1. The Stage 1
DBPR running annual average (RAA) calculation allowed some locations
within a distribution system to have higher DBP annual averages than
others as long as the system-wide average was below the MCL. The Stage
2 DBPR bases 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
of 0.080 mg/L and 0.060 mg/L for TTHM and HAA5, respectively. The LRAA
will reduce exposures to high DBP concentrations by ensuring that each
monitoring site is in compliance with the MCLs as an annual average,
while providing all customers drinking water that more consistently
meets the MCLs. A more detailed discussion of Stage 2 DBPR MCL
requirements can be found in Sections IV.C, IV.E, and IV.G of this
preamble and in Sec.  141.64(b)(2) and (3) and subpart V of the rule
language.
    The number of compliance monitoring sites is based on the

population served and the source water type. EPA believes that
population-based monitoring provides better risk-targeting and is
easier to implement. Section IV.G describes population-based monitoring
and how it affects systems complying with this rule.
    The 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.
3. Operational Evaluation Levels
    The IDSE and LRAA calculation will lead to lower DBP concentrations
overall and reduce short term exposures to high DBP concentrations in
certain areas, but this strengthened approach to regulating DBPs will
still allow individual DBP samples above the MCL even when systems are
in compliance with the Stage 2 DBPR. Today's rule requires systems that
exceed operational evaluation levels (referred to as significant
excursions in the proposed rule) to evaluate system operational
practices and identify opportunities to reduce DBP concentrations in
the distribution system. This provision will curtail peaks by providing
systems with a proactive approach to remain in compliance. Operational
evaluation requirements are discussed in greater detail in Section
IV.H.
4. Consecutive Systems
    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. Uniform regulation of
consecutive systems provided by the Stage 2 DBPR will ensure that
consecutive systems deliver drinking water that meets applicable DBP
standards, thereby providing better, more equitable public health
protection. More information on regulation of consecutive systems can
be found in Sections IV.B, IV.E, and IV.G.

C. Correction of Sec.  141.132

    Section 553 of the Administrative Procedure Act, 5 U.S.C.
553(b)(B), provides that, when an agency for good cause finds that
notice and public procedure are impracticable, unnecessary, or contrary
to the public interest, the agency may issue a rule without providing
prior notice and an opportunity for public comment. In addition to
promulgating the Stage 2 regulations, this rule also makes a minor
correction to the National Primary Drinking Water Regulations,
specifically the Stage 1 Disinfection Byproducts Rule. This rule
corrects a technical error made in the January 16, 2001, Federal
Register Notice (66 FR 3769) (see page 3770). This rule restores the
following sentence that was inadvertently removed from Sec.  141.132
(b)(1)(iii), ``Systems on a reduced monitoring schedule may remain on
that reduced schedule as long as the average of all samples taken in
the year (for systems which must monitor quarterly) or the result of
the sample (for systems which must monitor no more frequently than
annually) is no more than 0.060 mg/L and 0.045 mg/L for TTHMs and HAA5,
respectively.'' This text had been part of the original regulation when
it was codified in the CFR on December 16, 1998. However, as a result
of a subsequent amendment to that regulatory text, the text discussed
today was removed. EPA recognized the error only after publication of
the new amendment, and is now correcting the error. EPA is merely
restoring to the CFR language that EPA had promulgated on December 16,
1998. EPA is not creating any new rights or obligations by this
technical correction. Thus, additional notice and public comment is not
necessary. EPA finds that this constitutes ``good cause'' under 5
U.S.C. 553(b)(B).

III. Background

    A combination of factors influenced the development of the Stage 2
DBPR. These include the initial 1992-1994 Microbial and Disinfection
Byproduct (M-DBP) stakeholder deliberations and EPA's Stage 1 DBPR
proposal (USEPA 1994); the 1996 Safe Drinking Water Act (SDWA)
Amendments; the 1996 Information Collection Rule; the 1998 Stage 1
DBPR; 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 sections provide summary background
information on these subjects. For additional information, see the
proposed Stage 2 DBPR and supporting technical material where cited (68
FR 49548, August 18, 2003) (USEPA 2003a).

A. Statutory Requirements and Legal Authority

    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 any contaminant 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 (SDWA sections 1412(b)(4) and
1412(a)(3)).
    SDWA also requires each NPDWR for which an MCLG is established to
specify an MCL that is as close to the MCLG as is feasible (sections
1412(b)(4) and 1401(1)(C)). 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 or
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 maximum contaminant level or levels'' (section
1412(b)(5)(B)). In today's rule, the Agency is establishing MCLGs and
MCLs for certain DBPs, as described in Section IV.
    Finally, section 1412(b)(2)(C) of the Act requires EPA to
promulgate a Stage 2 DBPR. Consistent with statutory provisions for
risk balancing (section 1412(b)(5)(B)), EPA is finalizing 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 and How Were
Stakeholders Involved?

    This section first summarizes the existing regulations aimed at
controlling

levels of DBPs in drinking water. The Stage 2 DBPR establishes
regulatory requirements beyond these rules that target high risk
systems and provide for more equitable protection from DBPs across the
entire distribution system. Next, this section summarizes the extensive
stakeholder involvement in the development of the Stage 2 DBPR.
1. Total Trihalomethanes Rule
    The first rule to regulate DBPs was promulgated on November 29,
1979. The Total Trihalomethanes Rule (44 FR 68624, November 29, 1979)
(USEPA 1979) set an MCL of 0.10 mg/L for total trihalomethanes (TTHM).
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.
2. Stage 1 Disinfectants and Disinfection Byproducts Rule
    The Stage 1 DBPR, finalized in 1998 (USEPA 1998a), 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 trihalomethanes (THMs), two haloacetic acids
(HAAs), bromate, and chlorite; and enforceable maximum contaminant
level (MCL) standards for TTHM, five haloacetic acids (HAA5), bromate
(calculated as running annual averages (RAAs)), and chlorite (based on
daily and monthly sampling). The Stage 1 DBPR uses TTHM 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 one
or more alternative compliance criteria.
    The Stage 1 DBPR was one of the first rules to be promulgated under
the 1996 SDWA Amendments (USEPA 1998a). EPA finalized the Interim
Enhanced Surface Water Treatment Rule (63 FR 69477, December 16, 1998)
(USEPA 1998b) at the same time as the Stage 1 DBPR to ensure
simultaneous compliance and address risk tradeoff issues. Both rules
were products of extensive Federal Advisory Committee deliberations and
final consensus recommendations in 1997.
3. Stakeholder Involvement
    a. Federal Advisory Committee process. EPA reconvened the M-DBP
Advisory Committee in March 1999 to develop recommendations on issues
pertaining to the Stage 2 DBPR and LT2ESWTR. 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 from
September 1999 to July 2000, which were open to the public, with an
opportunity for public comment at each meeting.
    The Advisory Committee carefully considered extensive new data on
the occurrence and health effects of DBPs, as well as costs and
potential impacts on public water systems. In addition, they considered
risk tradeoffs associated with treatment changes. Based upon this
detailed technical evaluation, the committee concluded that a targeted
protective public health approach should be taken to address exposure
to DBPs beyond the requirements of the Stage 1 DBPR. While there had
been substantial research to date, the Advisory Committee also
concluded that significant uncertainty remained regarding the risk
associated with DBPs in drinking water. After reaching these
conclusions, the Advisory Committee developed an Agreement in Principle
(65 FR 83015, December 29, 2000) (USEPA 2000a) that laid out their
consensus recommendations on how to further control DBPs in public
water systems, which are reflected in today's final rule.
    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 compliance monitoring sites that 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 first phase has been dropped in
the final rule, as discussed in section IV.C.
    The Agreement in Principle also provided recommendations for
simultaneous compliance with the LT2ESWTR so that the reduction of DBPs
does not compromise microbial protection. The complete text of the
Agreement in Principle (USEPA 2000a) can be found online at
http://www.regulations.gov.

    b. Other outreach processes. EPA worked with stakeholders to
develop the Stage 2 DBPR through various outreach activities other than
the M-DBP Federal Advisory Committee process. The Agency consulted with
State, local, and Tribal governments; the National Drinking Water
Advisory Committee (NDWAC); the Science Advisory Board (SAB); and Small
Entity Representatives (SERs) and small system operators (as part of an
Agency outreach initiative under the Regulatory Flexibility Act).
Section VII includes a complete description of the many stakeholder
activities which contributed to the development of the Stage 2 DBPR.
    Additionally, EPA posted a pre-proposal draft of the Stage 2 DBPR
preamble and regulatory language on an EPA Internet site 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.

C. Public Health Concerns to be Addressed

    EPA is promulgating the Stage 2 rule to reduce the potential risks
of cancer and reproductive and developmental health effects from DBPs.
In addition, the provisions of the Stage 2 DBPR provide for more
equitable public health protection. Sections C and D describe the
general basis for this public health concern through reviewing
information in the following areas: the health effects associated with
DBPs, DBP occurrence, and the control of DBPs.
1. What Are DBPs?
    Chlorine has been widely used to kill disease-causing microbes in
drinking water. The addition of chlorine in PWSs across the U.S. to
kill microbial pathogens in the water supply has been cited as one of
the greatest public health advances of the twentieth century (Okun
2003). For example, during the decade 1880-1890, American cities
experienced an average mortality rate of 58 per 100,000 from typhoid,
which was commonly transmitted through contaminated water. By 1938,
this rate had fallen to 0.67 deaths per 100,000, largely due to
improved treatment of drinking water (Blake 1956).
    During the disinfection process, organic and inorganic material in
source waters can combine with chlorine and certain other chemical
disinfectants to form DBPs. More than 260 million people in the U.S.
are exposed to disinfected water and DBPs (USEPA 2005a). Although
chlorine is the most commonly applied disinfectant, other
disinfectants, including ozone, chlorine dioxide, chloramine, and
ultraviolet radiation, are in use. In combination with these, all
surface water systems must also use either chlorine or chloramine to
maintain a disinfectant residual in their distribution system. The kind
of disinfectant used can produce different types and levels of
disinfectant byproducts in the drinking water.
    Many factors affect the amount and kinds of DBPs in drinking water.
Areas in the distribution system that have had longer contact time with
chemical disinfectants tend to have higher levels of DBPs, such as
sites farther from the treatment plant, dead ends in the system, and
small diameter pipes. The makeup and source of the water also affect
DBP formation. Different types of organic and inorganic material will
form different types and levels of DBPs. Other factors, such as water
temperature, season, pH, and location within the water purification
process where disinfectants are added, can affect DBP formation within
and between water systems.
    THMs and HAAs are widely occurring classes of DBPs formed during
disinfection with chlorine and chloramine. The four THMs (TTHM) and
five HAAs (HAA5) measured and regulated in the Stage 2 DBPR act as
indicators for DBP occurrence. There are other known DBPs in addition
to a variety of unidentified DBPs present in disinfected water. THMs
and HAAs typically occur at higher levels than other known and
unidentified DBPs (McGuire et al. 2002; Weinberg et al. 2002). The
presence of TTHM and HAA5 is representative of the occurrence of many
other chlorination DBPs; thus, a reduction in the TTHM and HAA5
generally indicates an overall reduction of DBPs.
2. DBP Health Effects
    Since the mid 1980's, epidemiological studies have supported a
potential association between bladder cancer and chlorinated water and
possibly also with colon and rectal cancers. In addition, more recent
health studies have reported potential associations between chlorinated
drinking water and reproductive and developmental health effects.
    Based on a collective evaluation of both the human epidemiology and
animal toxicology data on cancer and reproductive and developmental
health effects discussed below and in consideration of the large number
of people exposed to chlorinated byproducts in drinking water (more
than 260 million), EPA concludes that (1) new cancer data since Stage 1
strengthen the evidence of a potential association of chlorinated water
with bladder cancer and suggests an association for colon and rectal
cancers, (2) current reproductive and developmental health effects data
do not support a conclusion at this time as to whether exposure to
chlorinated drinking water or disinfection byproducts causes adverse
developmental or reproductive health effects, but do support a
potential health concern, and (3) the combined health data indicate a
need for public health protection beyond that provided by the Stage 1
DBPR.
    This section summarizes the key information in the areas of cancer,
reproductive, and developmental health studies that EPA used to arrive
at these conclusions. Throughout this writeup, EPA uses `weight of
evidence,' `causality,' and `hazard' as follows:
     A `weight of evidence' evaluation is a collective
evaluation of all pertinent information. Judgement about the weight of
evidence involves considerations of the quality and adequacy of data
and consistency of responses. These factors are not scored mechanically
by adding pluses and minuses; they are judged in combination.
     Criteria for determining `causality' include consistency,
strength, and specificity of association, a temporal relationship, a
biological gradient (dose-response relationship), biological
plausibility, coherence with multiple lines of evidence, evidence from
human populations, and information on agent's structural analogues
(USEPA 2005i). Additional considerations for individual study findings
include reliable exposure data, statistical power and significance, and
freedom from bias and confounding.
     The term `hazard' describes not a definitive conclusion,
but the possibility that a health effect may be attributed to a certain
exposure, in this case chlorinated water. Analyses done for the Stage 2
DBPR follow the 1999 EPA Proposed Guidelines for Carcinogenic Risk
Assessment (USEPA 1999a). In March 2005, EPA updated and finalized the
Cancer Guidelines and a Supplementary Children's Guidance, which
include new considerations on mode of action for cancer risk
determination and additional potential risks due to early childhood
exposure (USEPA 2005i; USEPA 2005j). Conducting the cancer evaluation
using the 2005 Cancer Guidelines would not result in any change from
the existing analysis. With the exception of chloroform, no mode of
action has been established for other specific regulated DBPs. Although
some of the DBPs have given mixed mutagenicity and genotoxicity
results, having a positive mutagenicity study does not necessarily mean
that a chemical has a mutagenic mode of action. The extra factor of
safety for children's health protection does not apply because the new
Supplementary Children's Guidance requires application of the
children's factor only when a mutagenic mode of action has been
identified.
    a. Cancer health effects. The following section briefly discusses
cancer epidemiology and toxicology information EPA analyzed and some
conclusions of these studies and reports. Further discussion of these
studies and EPA's conclusions can be found in the proposed Stage 2 DBPR
(USEPA 2003a) and the Economic Analysis for the Final Stage 2
Disinfectants and Disinfection Byproducts Rule (Economic Analysis (EA))
(USEPA 2005a).
    Human epidemiology studies and animal toxicology studies have

examined associations between chlorinated drinking water or DBPs and
cancer. While EPA cannot conclude there is a causal link between
exposure to chlorinated surface water and cancer, EPA believes that the
available research indicates a potential association between bladder
cancer and exposure to chlorinated drinking water or DBPs. EPA also
believes the available research suggests a possible association between
rectal and colon cancers and exposure to chlorinated drinking water or
DBPs. This is based on EPA's evaluation of all available cancer
studies. The next two sections focus on studies published since the
Stage 1 DBPR. Conclusions are based on the research as a whole.
    i. Epidemiology. A number of epidemiological studies have been
conducted to investigate the relationship between exposure to
chlorinated drinking water and various cancers. These studies
contribute to the overall evidence on potential human health hazards
from exposure to chlorinated drinking water.
    Epidemiology studies provide useful health effects information
because they reflect human exposure to a drinking water DBP mixture
through multiple routes of intake such as ingestion, inhalation and
dermal absorption. The greatest difficulty with conducting cancer
epidemiology studies is the length of time between exposure and effect.
Higher quality studies have adequately controlled for confounding and
have limited the potential for exposure misclassification, for example,
using DBP levels in drinking water as the exposure metric as opposed to
type of source water. Study design considerations for interpreting
cancer epidemiology data include sufficient follow-up time to detect
disease occurrence, adequate sample size, valid ascertainment of cause
of the cancer, and reduction of potential selection bias in case-
control and cohort studies (by having comparable cases and controls and
by limiting loss to follow-up). Epidemiology studies provide extremely
useful information on human exposure to chlorinated water, which
complement single chemical, high dose animal data.
    In the Stage 1 DBPR, EPA concluded that the epidemiological
evidence suggested a potential increased risk for bladder cancer. Some
key studies EPA considered for Stage 1 include Cantor et al. (1998),
Doyle et al. (1997), Freedman et al. (1997), King and Marrett (1996),
McGeehin et al. (1993), Cantor et al. (1987), and Cantor et al. (1985).
Several studies published since the Stage 1 DBPR continue to support an
association between increased risk of bladder cancer and exposure to
chlorinated surface water (Chevrier et al. 2004; Koivusalo et al. 1998;
Yang et al. 1998). One study found no effects on a biomarker of
genotoxicity in urinary bladder cells from TTHM exposure (Ranmuthugala
et al. 2003). Epidemiological reviews and meta-analyses generally
support the possibility of an association between chlorinated water or
THMs and bladder cancer (Villanueva et al. 2004; Villanueva et al.
2003; Villanueva et al. 2001; Mills et al. 1998). The World Health
Organization (WHO 2000) found data inconclusive or insufficient to
determine causality between chlorinated water and any health endpoint,
although they concluded that the evidence is better for bladder cancer
than for other cancers.
    In the Stage 1 DBPR, EPA concluded that early studies suggested a
small possible increase in rectal and colon cancers from exposure to
chlorinated surface waters. The database of studies on colon and rectal
cancers continues to support a possible association, but evidence
remains mixed. For colon cancer, one newer study supports the evidence
of an association (King et al. 2000a) while others showed inconsistent
findings (Hildesheim et al. 1998; Yang et al. 1998). Rectal cancer
studies are also mixed. Hildesheim et al. (1998) and Yang et al. (1998)
support an association with rectal cancer while King et al. (2000a) did
not. A review of colon and rectal cancer concluded evidence was
inconclusive but that there was a stronger association for rectal
cancer and chlorination DBPs than for colon cancer (Mills et al. 1998).
The WHO (2000) review reported that studies showed weak to moderate
associations with colon and rectal cancers and chlorinated surface
water or THMs but that evidence is inadequate to evaluate these
associations.
    Recent studies on kidney, brain, and lung cancers and DBP exposure
support a possible association (kidney: Yang et al. 1998, Koivusalo et
al. 1998; brain: Cantor et al. 1999; lung: Yang et al. 1998). However,
so few studies have examined these endpoints that definitive
conclusions cannot be made. Studies on leukemia found little or no
association with DBPs (Infante-Rivard et al. 2002; Infante-Rivard et
al. 2001). A recent study did not find an association between
pancreatic cancer and DBPs (Do et al. 2005). A study researching
multiple cancer endpoints found an association between THM exposure and
all cancers when grouped together (Vinceti et al. 2004). More details
on the cancer epidemiology studies since the Stage 1 DBPR are outlined
in Table II.D-1.

                 Table II.D-1.--Summary of Cancer Epidemiology Studies Reviewed for Stage 2 DBPR
----------------------------------------------------------------------------------------------------------------
                                                       Exposure(s)         Outcome(s)
                                     Study type          studied            measured             Findings
----------------------------------------------------------------------------------------------------------------
           Author(s)
Do et al. 2005.................  Case-control       Estimated          Pancreatic cancer  No association was
                                  study in Canada,   chlorinated                           found between
                                  1994-1997.         DBPs,                                 pancreatic cancer and
                                                     chloroform, BDCM                      exposure to
                                                     concentrations.                       chlorinated DBPs,
                                                                                chloroform, or BDCM.
Chevrier et al. 2004...........  Case-control       Compared THM       Bladder cancer...  A statistically
                                  study in France,   levels, duration                      significant decreased
                                  1985-1987.         of exposure, and                      risk of bladder
                                                     3 types of water                      cancer was found as
                                                     treatment                             duration of exposure
                                                     (ozonation,                           to ozonated water
                                                     chlorination,                         increased. This was
                                                     ozonation/                            evident with and
                                                     chlorination).                        without adjustment
                                                                                for other exposure
                                                                                measures. A small
                                                                                association was
                                                                                detected for
                                                                                increased bladder
                                                                                cancer risk and
                                                                                duration of exposure
                                                                                to chlorinated
                                                                                surface water and
                                                                                with the estimated
                                                                                THM content of the
                                                                                water, achieving
                                                                                statistical
                                                                                significance only
                                                                                when adjusted for
                                                                                duration of ozonated
                                                                                water exposures.
                                                                                Effect modification
                                                                                by gender was noted
                                                                                in the adjusted
                                                                                analyses.

Vinceti et al. 2004............  Retrospective      Standardized       15 cancers         Mortality ratio from
                                  cohort study in    mortality ratios   including colon,   all cancers showed a
                                  Italy, 1987-1999.  from all causes    rectum, and        statistically
                                                     vs. cancer for     bladder.           significant small
                                                     consumers                             increase for males
                                                     drinking water                        consuming drinking
                                                     with high THMs.                       water with high THMs.
                                                                                For females, an
                                                                                increased mortality
                                                                                ratio for all cancers
                                                                                was seen but was not
                                                                                statistically
                                                                                significant. Stomach
                                                                                cancer in men was the
                                                                                only individual
                                                                                cancer in which a
                                                                                statistically
                                                                                significant excess in
                                                                                mortality was
                                                                                detected for
                                                                                consumption of
                                                                                drinking water with
                                                                                high THMs.
Ranmuthugala et al. 2003.......  Cohort study in 3  Estimated dose of  Frequency of       Relative risk
                                  Australian         TTHM,              micronuclei in     estimates for DNA
                                  communities,       chloroform, and    urinary bladder    damage to bladder
                                  1997.              bromoform from     epithelial cells.  cells for THM dose
                                                     routinely-                            metrics were near
                                                     collected THM                         1.0. The study
                                                     measurements and                      provides no evidence
                                                     fluid intake                          that THMs are
                                                     diary.                                associated with DNA
                                                                                damage to bladder
                                                                                epithelial cells, and
                                                                                dose-response
                                                                                patterns were not
                                                                                detected.
Infante-Rivard et al. 2002.....  Population-based   Estimated          Acute              Data are suggestive,
                                  case-control       prenatal and       lymphoblastic      but imprecise,
                                  study in Quebec,   postnatal          leukemia.          linking DNA variants
                                  1980-1993.         exposure to THMs                      with risk of acute
                                                     and                                   lymphoblastic
                                                     polymorphisms in                      leukemia associated
                                                     two genes.                            with drinking water
                                                                                DBPs. The number of
                                                                                genotyped subjects
                                                                                for GSTT1 and CYP2E1
                                                                                genes was too small
                                                                                to be conclusive.
Infante-Rivard et al. 2001.....  Population-based   Compared water     Acute              No increased risk for
                                  case-control       chlorination       lymphoblastic      lymphoblastic
                                  study in Quebec,   (never,            leukemia.          leukemia was observed
                                  1980-1993.         sometimes,                            for prenatal exposure
                                                     always) and                           at average levels of
                                                     exposure to                           TTHMs, metals or
                                                     TTHMs, metals,                        nitrates. However, a
                                                     and nitrates.                         non-statistically
                                                                                significant, small
                                                                                increased risk was
                                                                                seen for postnatal
                                                                                cumulative exposure
                                                                                to TTHMs and
                                                                                chloroform (both at
                                                                                above the 95th
                                                                                exposure percentile
                                                                                of the distribution
                                                                                for cases and
                                                                                controls), for zinc,
                                                                                cadmium, and arsenic,
                                                                                but not other metals
                                                                                or nitrates.
King et al. 2000a..............  Population-based   Compared source    Colon and rectal   Colon cancer risk was
                                  case-control       of drinking        cancer.            statistically
                                  study in           water and                             associated with
                                  southern           chlorination                          cumulative long term
                                  Ontario, 1992-     status.                               exposure to THMs,
                                  1994.              Estimated TTHM                        chlorinated surface
                                                     levels, duration                      water, and tap water
                                                     of exposure, and                      consumption metrics
                                                     tap water                             among males only.
                                                     consumption.                          Exposure-response
                                                                                relationships were
                                                                                evident for exposure
                                                                                measures combining
                                                                                duration and THM
                                                                                levels. Associations
                                                                                between the exposure
                                                                                measures and rectal
                                                                                cancer were not
                                                                                observed for either
                                                                                gender.
Cantor et al. 1999.............  Population-based   Compared level     Brain cancer.....  Among males, a
                                  case-control       and duration of                       statistically
                                  study in Iowa,     THM exposure                          significant increased
                                  1984-1987.         (cumulative and                       risk of brain cancer
                                                     average), source                      was detected for
                                                     of water,                             duration of
                                                     chlorination,                         chlorinated versus
                                                     and water                             non-chlorinated
                                                     consumption.                          source water,
                                                                                especially among high-
                                                                                level consumers of
                                                                                tap water. An
                                                                                increased risk of
                                                                                brain cancer for high
                                                                                water intake level
                                                                                was found in men. No
                                                                                associations were
                                                                                found for women for
                                                                                any of the exposure
                                                                                metrics examined.
Cantor et al. 1998.............  Population-based   Compared level     Bladder cancer...  A statistically
                                  case-control       and duration of                       significant positive
                                  study in Iowa,     THM exposure                          association between
                                  1986-1989.         (cumulative and                       risk of bladder
                                                     average), source                      cancer and exposure
                                                     of water,                             to chlorinated
                                                     chlorination,                         groundwater or
                                                     and water                             surface water
                                                     consumption.                          reported for men and
                                                                                for smokers, but no
                                                                                association found for
                                                                                male/female non-
                                                                                smokers, or for women
                                                                                overall. Limited
                                                                                evidence was found
                                                                                for an association
                                                                                between tapwater
                                                                                consumption and
                                                                                bladder cancer risk.
                                                                                Suggestive evidence
                                                                                existed for exposure-
                                                                                response effects of
                                                                                chlorinated water and
                                                                                lifetime THM measures
                                                                                on bladder cancer
                                                                                risk.
Hildesheim et al. 1998.........  Population-based   Compared level     Colon and rectal   Increased risks of
                                  case-control       and duration of    cancer.            rectal cancer was
                                  study in Iowa,     THM exposure                          associated with
                                  1986-1989.         (cumulative and                       duration of exposure
                                                     average), source                      to chlorinated
                                                     of water,                             surface water and any
                                                     chlorination,                         chlorinated water,
                                                     and water                             with evidence of an
                                                     consumption.                          exposure-response
                                                                                relationship. Risk of
                                                                                rectal cancer is
                                                                                statistically
                                                                                significant increased
                                                                                with >60 years
                                                                                lifetime exposure to
                                                                                THMs in drinking
                                                                                water, and risk
                                                                                increased for
                                                                                individuals with low
                                                                                dietary fiber intake.
                                                                                Risks were similar
                                                                                for men and women and
                                                                                no effects were
                                                                                observed for tapwater
                                                                                measures. No
                                                                                associations were
                                                                                detected for water
                                                                                exposure measures and
                                                                                risk of colon cancer.
Koivusalo et al. 1998..........  Population-based   Estimated          Bladder and        Drinking water
                                  case-control       residential        kidney cancer.     mutagenicity was
                                  study in           duration of                           associated with a
                                  Finland, 1991-     exposure and                          small, statistically
                                  1992.              level of                              significant, exposure-
                                                     drinking water                        related excess risk
                                                     mutagenicity.                         for kidney and
                                                                                bladder cancers among
                                                                                men; weaker
                                                                                associations were
                                                                                detected for
                                                                                mutagenic water and
                                                                                bladder or kidney
                                                                                cancer among women.
                                                                                The effect of
                                                                                mutagenicity on
                                                                                bladder cancer was
                                                                                modified by smoking
                                                                                status, with an
                                                                                increased risk among
                                                                                non-smokers.

Yang et al. 1998...............  Cross-sectional    Examined           Cancer of rectum,  Residence in
                                  study in Taiwan,   residence in       lung, bladder,     chlorinating
                                  1982-1991.         chlorinated        kidney, colon,     municipalities (vs.
                                                     (mainly surface    and 11 others.     non-chlorinating) was
                                                     water sources)                        statistically
                                                     relative to non-                      significantly
                                                     chlorinated                           associated with the
                                                     (mainly private                       following types of
                                                     well) water.                          cancer in both males
                                                                                and females: rectal,
                                                                                lung, bladder, and
                                                                                kidney cancer. Liver
                                                                                cancer and all
                                                                                cancers were also
                                                                                statistically
                                                                                significantly
                                                                                elevated in
                                                                                chlorinated towns for
                                                                                males only. Mortality
                                                                                rates for cancers of
                                                                                the esophagus,
                                                                                stomach, colon,
                                                                                pancreas, prostate,
                                                                                brain, breast, cervix
                                                                                uteri and uterus, and
                                                                                ovary were comparable
                                                                                for chlorinated and
                                                                                non-chlorinated
                                                                                residence.
Doyle et al. 1997..............  Prospective        Examined           Colon, rectum,     Statistically
                                  cohort study in    chloroform         bladder, and 8     significant increased
                                  Iowa, 1987-1993.   levels and         other cancers in   risk of colon cancer,
                                                     source of          women.             breast cancer and all
                                                     drinking water.                       cancers combined was
                                                                                observed for women
                                                                                exposed to chloroform
                                                                                in drinking water,
                                                                                with evidence of
                                                                                exposure-response
                                                                                effects. No
                                                                                associations were
                                                                                detected between
                                                                                chloroform and
                                                                                bladder, rectum,
                                                                                kidney, upper
                                                                                digestive organs,
                                                                                lung, ovary,
                                                                                endometrium, or
                                                                                breast cancers, or
                                                                                for melanomas or non-
                                                                                Hodgkin's lymphoma.
                                                                                Surface water
                                                                                exposure (compared to
                                                                                ground water users)
                                                                                was also a
                                                                                significant predictor
                                                                                of colon and breast
                                                                                cancer risk.
Freedman et al. 1997...........  Population-based   Estimated          Bladder cancer...  There was a weak
                                  case-control       duration of                           association between
                                  study in           exposure to                           bladder cancer risk
                                  Maryland, 1975-    chlorinated                           and duration of
                                  1992.              water. Compared                       exposure to municipal
                                                     exposure to                           water for male
                                                     chlorinated                           cigarette smokers, as
                                                     municipal water                       well as an exposure-
                                                     (yes/no).                             response
                                                                                relationship. No
                                                                                association was seen
                                                                                for those with no
                                                                                history of smoking,
                                                                                suggesting that
                                                                                smoking may modify a
                                                                                possible effect of
                                                                                chlorinated surface
                                                                                water on the risk of
                                                                                bladder cancer.
King and Marrett 1996..........  Case-control       Compared source    Bladder cancer...  Statistically
                                  study in           of drinking                           significant
                                  Ontario, Canada,   water and                             associations were
                                  1992-1994.         chlorination                          detected for bladder
                                                     status.                               cancer and
                                                     Estimated TTHM                        chlorinated surface
                                                     levels, duration                      water, duration or
                                                     of exposure, and                      concentration of THM
                                                     tap water                             levels and tap water
                                                     consumption.                          consumption metrics.
                                                                                Population
                                                                                attributable risks
                                                                                were estimated at 14
                                                                                to 16 percent. An
                                                                                exposure-response
                                                                                relationship was
                                                                                observed for
                                                                                estimated duration of
                                                                                high THM exposures
                                                                                and risk of bladder
                                                                                cancer.
McGeehin et al. 1993...........  Population-based   Compared source    Bladder cancer...  Statistically
                                  case-control       of drinking                           significant
                                  study in           water, water                          associations were
                                  Colorado, 1990-    treatment, and                        detected for bladder
                                  1991.              tap water versus                      cancer and duration
                                                     bottled water.                        of exposure to
                                                     Estimated                             chlorinated surface
                                                     duration of                           water. The risk was
                                                     exposure to                           similar for males and
                                                     TTHMs and levels                      females and among
                                                     of TTHMs,                             nonsmokers and
                                                     nitrates, and                         smokers. The
                                                     residual                              attributable risk was
                                                     chlorine.                             estimated at 14.9
                                                                                percent. High tap
                                                                                water intake was
                                                                                associated with risk
                                                                                of bladder cancer in
                                                                                a exposure-response
                                                                                fashion. No
                                                                                associations were
                                                                                detected between
                                                                                bladder cancer and
                                                                                levels of TTHMs,
                                                                                nitrates, and
                                                                                residual chlorine.
Cantor et al. 1987 (and Cantor   Population-based   Compared source    Bladder cancer...  Bladder cancer was
 et al. 1985).                    case-control       of drinking                           statistically
                                  study in 10        water. Estimated                      associated with
                                  areas of the       total beverage                        duration of exposure
                                  U.S., 1977-1978.   and tap water                         to chlorinated
                                                     consumption and                       surface water for
                                                     duration of                           women and nonsmokers
                                                     exposure.                             of both sexes. The
                                                                                largest risks were
                                                                                seen when both
                                                                                exposure duration and
                                                                                level of tap water
                                                                                ingestion were
                                                                                combined. No
                                                                                association was seen
                                                                                for total beverage
                                                                                consumption.
     Reviews/Meta-analyses
Villanueva et al. 2004.........  Review and meta-   Individual-based   Bladder cancer...  The meta-analysis
                                  analysis of 6      exposure                              suggests that risk of
                                  case-control       estimates to                          bladder cancer in men
                                  studies.           THMs and water                        increases with long-
                                                     consumption over                      term exposure to
                                                     a 40-year period.                     TTHMs. An exposure-
                                                                                response pattern was
                                                                                observed among men
                                                                                exposed to TTHMs,
                                                                                with statistically
                                                                                significant risk seen
                                                                                at exposures higher
                                                                                than 50 ug/L. No
                                                                                association between
                                                                                TTHMs and bladder
                                                                                cancer was seen for
                                                                                women.
Villanueva et al. 2003 (and      Review and meta-   Compared source    Bladder cancer...  The meta-analysis
 Goebell et al. 2004).            analysis of 6      of water and                          findings showed a
                                  case-control       estimated                             moderate excess risk
                                  studies and 2      duration of                           of bladder cancer
                                  cohort studies.    exposure to                           attributable to long-
                                                     chlorinated                           term consumption of
                                                     drinking water.                       chlorinated drinking
                                                                                water for both
                                                                                genders, particularly
                                                                                in men. Statistically
                                                                                significance seen
                                                                                with men and combined
                                                                                both sexes. The risk
                                                                                was higher when
                                                                                exposure exceeded 40
                                                                                years.

Villanueva et al. 2001.........  Qualitative        Compared exposure  Cancer of          Review found that
                                  review of 31       to TTHM levels,    bladder, colon,    although results for
                                  cancer studies.    mutagenic          rectum, and 5      cancer studies varied
                                                     drinking water,    other cancers..    and were not always
                                                     water                                 statistically
                                                     consumption,                          significant, evidence
                                                     source water,                         for bladder cancer is
                                                     types of                              strongest, and all 10
                                                     disinfection                          of the bladder cancer
                                                     (chlorination                         studies showed
                                                     and                                   increased cancer
                                                     chloramination),                      risks with ingestion
                                                     and residence                         of chlorinated water.
                                                     times.                                The authors felt
                                                                                associations with
                                                                                chlorinated water and
                                                                                cancer of the colon,
                                                                                rectum, pancreas,
                                                                                esophagus, brain, and
                                                                                other cancers were
                                                                                inconsistent.
WHO 2000.......................  Qualitative        Various exposures  Various cancers..  Studies reviewed
                                  reviews of         to THMs..                             reported weak to
                                  various studies                                          moderate increased
                                  in Finland,                                              relative risks of
                                  U.S., and Canada.                                        bladder, colon,
                                                                                rectal, pancreatic,
                                                                                breast, brain or lung
                                                                                cancer associated
                                                                                with long-term
                                                                                exposure to
                                                                                chlorinated drinking
                                                                                water. The authors
                                                                                felt evidence is
                                                                                inconclusive for an
                                                                                association between
                                                                                colon cancer and long-
                                                                                term exposure to
                                                                                THMs; that evidence
                                                                                is insufficient to
                                                                                evaluate a causal
                                                                                relationship between
                                                                                THMs and rectal,
                                                                                bladder, and other
                                                                                cancers. They found
                                                                                no association
                                                                                between THMs and
                                                                                increased risk of
                                                                                cardiovascular
                                                                                disease.
Mills et al. 1998..............  Qualitative        Examined TTHM      Cancer of colon,   Review suggests
                                  review of 22       levels and water   rectum, and        possible increases in
                                  studies.           consumption.       bladder.           risks of bladder
                                                     Compared source                       cancer with exposure
                                                     of water and 2                        to chlorinated
                                                     types of water                        drinking water. The
                                                     treatment                             authors felt evidence
                                                     (chlorination                         for increased risk of
                                                     and                                   colon and rectal
                                                     chloramination).                      cancers is
                                                                                inconclusive, though
                                                                                evidence is stronger
                                                                                for rectal cancer.
----------------------------------------------------------------------------------------------------------------

    Overall, bladder cancer data provide the strongest basis for
quantifying cancer risks from DBPs. EPA has chosen this endpoint to
estimate the primary benefits of the Stage 2 DBPR (see Section VI).
    ii. Toxicology. Cancer toxicology studies provide additional
support that chlorinated water is associated with cancer. In general,
EPA uses long term toxicology studies that show a dose response to
derive MCLGs and cancer potency factors. Short term studies are used
for hazard identification and to design long term studies. Much of the
available cancer toxicology information was available for the Stage 1
DBPR, but there have also been a number of new cancer toxicology and
mode of action studies completed since the Stage 1 DBPR was finalized
in December 1998.
    In support of this rule, EPA has developed health criteria
documents which summarize the available toxicology data for brominated
THMs (USEPA 2005b), brominated HAAs (USEPA 2005c), MX (USEPA 2000b),
MCAA (USEPA 2005d), and TCAA (USEPA 2005e). The 2003 IRIS assessment of
DCAA (USEPA 2003b) and an addendum (USEPA 2005k) also provides analysis
released after Stage 1. It summarizes information on exposure from
drinking water and develops a slope factor for DCAA. IRIS also has
toxicological reviews for chloroform (USEPA 2001a), chlorine dioxide
and chlorite (USEPA 2000c), and bromate (USEPA 2001b), and is currently
reassessing TCAA.
    Slope factors and risk concentrations for BDCM, bromoform, DBCM and
DCAA have been developed and are listed in Table II.D-2. For BDCM,
bromoform, and DBCM, table values are derived from the brominated THM
criteria document (USEPA 2005b), which uses IRIS numbers that have been
updated using the 1999 EPA Proposed Guidelines for Carcinogenic Risk
Assessment (USEPA 1999a). For DCAA, the values are derived directly
from IRIS.

                                  Table II.D-2.--Quantification of Cancer Risk
----------------------------------------------------------------------------------------------------------------
                                                        LED 10a                             ED 10a
                                         -----------------------------------------------------------------------
         Disinfection byproduct                                10 -6 Risk                          10 -6 Risk
                                            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           0.015 b          0.0023 b
----------------------------------------------------------------------------------------------------------------
a LED10 is the lower 95% confidence bound on the (effective dose) ED10 value. ED10 is the estimated dose
  producing effects in 10% of animals.
b The ED10 risk factors for DCAA have been changed from those given in the comparable table in the proposed
  Stage 2 DBPR to correct for transcriptional errors.

    More research on DBPs is underway at EPA and other research
institutions. Summaries of on-going studies may be found on EPA's DRINK
Web site (http://www.epa.gov/safewater/drink/intro.html). Two-year

bioassays by the National Toxicology Program (NTP) released in abstract
form have recently been completed on BDCM and chlorate. The draft
abstract on BDCM reported no evidence of carcinogenicity when BDCM was
administered via drinking

water (NTP 2005a). Another recent study, a modified two-year bioassay
on BDCM in the drinking water, reported little evidence of
carcinogenicity (George et al. 2002). In a previous NTP study, tumors
were observed, including an increased incidence of kidney, liver, and
colon tumors, when BDCM was administered at higher doses by gavage in
corn oil (NTP 1987). EPA will examine new information on BDCM as it
becomes available. In the chlorate draft abstract, NTP found some
evidence that it may be a carcinogen (NTP 2004). Chlorate is a
byproduct of hypochlorite and chlorine dioxide systems. A long-term,
two-year bioassay NTP study on DBA is also complete but has not yet
undergone peer review (NTP 2005b).
    b. Reproductive and developmental health effects. Both human
epidemiology studies and animal toxicology studies have examined
associations between chlorinated drinking water or DBPs and
reproductive and developmental health effects. Based on an evaluation
of the available science, EPA believes the data suggest that exposure
to DBPs is a potential reproductive and developmental health hazard.
    The following section briefly discusses the reproductive and
developmental epidemiology and toxicology information available to EPA.
Further discussion of these studies and EPA's conclusions can be found
in the proposed Stage 2 DBPR (USEPA 2003a) and the Economic Analysis
(USEPA 2005a).
    i. Epidemiology. As discussed previously, epidemiology studies have
the strength of relating human exposure to DBP mixtures through
multiple intake routes. Although the critical exposure window for
reproductive and developmental effects is much smaller than that for
cancer (generally weeks versus years), exposure assessment is also a
main limitation of reproductive and developmental epidemiology studies.
Exposure assessment uncertainties arise from limited data on DBP
concentrations and maternal water usage and source over the course of
the pregnancy. However, classification errors typically push the true
risk estimate towards the null value (Vineis 2004). According to Bove
et al. (2002), ``Difficulties in assessing exposure may result in
exposure misclassification biases that would most likely produce
substantial underestimates of risk as well as distorted or attenuated
exposure-response trends.'' Studies of rare outcomes (e.g., individual
birth defects) often have limited statistical power because of the
small number of cases being examined. This limits the ability to detect
statistically significant associations for small to moderate relative
risk estimates. Small sample sizes also result in imprecision around
risk estimates reflected by wide confidence intervals. In addition to
the limitations of individual studies, evaluating reproductive and
developmental epidemiology studies collectively is difficult because of
the methodological differences between studies and the wide variety of
endpoints examined. These factors may contribute to inconsistencies in
the scientific body of literature as noted below.
    More recent studies tend to be of higher quality because of
improved exposure assessments and other methodological advancements.
For example, studies that use THM levels to estimate exposure tend to
be higher quality than studies that define exposure by source or
treatment. These factors were taken into account by EPA when comparing
and making conclusions on the reproductive and developmental
epidemiology literature. What follows is a summary of available
epidemiology literature on reproductive and developmental endpoints
such as spontaneous abortion, stillbirth, neural tube and other birth
defects, low birth weight, and intrauterine growth retardation.
Information is grouped, where appropriate, into three categories on
fetal growth, viability, and malformations, and reviews are described
separately afterward. Table II.D-3 provides a more detailed description
of each study or review.
    Fetal growth. Many studies looked for an association between fetal
growth (mainly small for gestational age, low birth weight, and pre-
term delivery) and chlorinated water or DBPs. The results from the
collection of studies as a whole are inconsistent. A number of studies
support the possibility that exposure to chlorinated water or DBPs are
associated with adverse fetal growth effects (Infante-Rivard 2004;
Wright et al. 2004; Wright et al. 2003; K[auml]ll[eacute]n and Robert
2000; Gallagher et al. 1998; Kanitz et al. 1996; Bove et al. 1995;
Kramer et al. 1992). Other studies showed mixed results (Porter et al.
2005; Savitz et al. 2005; Yang 2004) or did not provide evidence of an
association (Toledano et al. 2005; Jaakkola et al. 2001; Dodds et al.
1999; Savitz et al. 1995) between DBP exposure and fetal growth. EPA
notes that recent, higher quality studies provide some evidence of an
increased risk of small for gestational age and low birth weight.
    Fetal viability. While the database of epidemiology studies for
fetal loss endpoints (spontaneous abortion or stillbirth) remains
inconsistent as a whole, there is suggestive evidence of an association
between fetal loss and chlorinated water or DBP exposure. Various
studies support the possibility that exposure to chlorinated water or
DBPs is associated with decreased fetal viability (Toledano et al.
2005; Dodds et al. 2004; King et al. 2000b; Dodds et al. 1999; Waller
et al. 1998; Aschengrau et al. 1993; Aschengrau et al. 1989). Other
studies did not support an association (Bove et al. 1995) or reported
inconclusive results (Savitz et al. 2005; Swan et al. 1998; Savitz et
al. 1995) between fetal viability and exposure to THMs or tapwater. A
recent study by King et al. (2005) found little evidence of an
association between stillbirths and haloacetic acids after controlling
for trihalomethane exposures, though non-statistically significant
increases in stillbirths were seen across various exposure levels.
    Fetal malformations. A number of epidemiology studies have examined
the relationship between fetal malformations (such as neural tube, oral
cleft, cardiac, or urinary defects, and chromosomal abnormalities) and
chlorinated water or DBPs. It is difficult to assess fetal
malformations in aggregate due to inconsistent findings and disparate
endpoints being examined in the available studies. Some studies support
the possibility that exposure to chlorinated water or DBPs is
associated with various fetal malformations (Cedergren et al. 2002;
Hwang et al. 2002; Dodds and King 2001; Klotz and Pyrch 1999; Bove et
al. 1995; Aschengrau et al. 1993). Other studies found little evidence
(Shaw et al. 2003; K[auml]ll[eacute]n and Robert 2000; Dodds et al.
1999; Shaw et al. 1991) or inconclusive results (Magnus et al. 1999)
between chlorinated water or DBP exposure and fetal malformations.
Birth defects most consistently identified as being associated with
DBPs include neural tube defects and urinary tract malformations.
    Other endpoints have also been examined in recent epidemiology
studies. One study suggests an association between DBPs and decreased
menstrual cycle length (Windham et al. 2003), which, if corroborated,
could be linked to the biological basis of other reproductive endpoints
observed. No association between THM exposure and semen quality was
found (Fenster et al. 2003). More work is needed in both areas to
support these results.
    Reviews. An early review supported an association between measures
of fetal viability and tap water (Swan et al.

1992). Three other reviews found data inadequate to support an
association between reproductive and developmental health effects and
THM exposure (Reif et al. 1996; Craun 1998; WHO 2000). Mills et al.
(1998) examined data on and found support for an association between
fetal viability and malformations and THMs. Another review presented to
the Stage 2 MDBP FACA found some evidence for an association with fetal
viability and some fetal malformations and exposure to DBPs but
reported that the evidence was inconsistent for these endpoints as well
as for fetal growth (Reif et al. 2000). Reif et al. (2000) concluded
that the weight of evidence from epidemiology studies suggests that
``DBPs are likely to be reproductive toxicants in humans under
appropriate exposure conditions,'' but from a risk assessment
perspective, data are primarily at the hazard identification stage.
Nieuwenhuijsen et al. (2000) found some evidence for an association
between fetal growth and THM exposure and concluded evidence for
associations with other fetal endpoints is weak but gaining weight. A
qualitative review by Villanueva et al. (2001) found evidence generally
supports a possible association between reproductive effects and
drinking chlorinated water. Graves et al. (2001) supports a possible
association for fetal growth but not fetal viability or malformations.
More recently, Bove et al. (2002) examined and supported an association
between small for gestational age, neural tube defects and spontaneous
abortion endpoints and DBPs. Following a meta-analysis on five
malformation studies, Hwang and Jaakkola (2003) concluded that there
was evidence which supported associations between DBPs and risk of
birth defects, especially neural tube defects and urinary tract
defects.

                    Table II.D-3.--Summary of Reproductive/Developmental Epidemiology Studies
----------------------------------------------------------------------------------------------------------------
                                                       Exposure(s)         Outcome(s)
           Author(s)                 Study type          studied            measured             Findings
----------------------------------------------------------------------------------------------------------------
Porter et al. 2005.............  Cross-sectional    Estimated THM and  Intrauterine       No consistent
                                  study in           HAA exposure       growth             association or dose-
                                  Maryland, 1998-    during pregnancy.  retardation.       response relationship
                                  2002.                                                    was found between
                                                                                exposure to either
                                                                                TTHM or HAA5 and
                                                                                intrauterine growth
                                                                                retardation. Results
                                                                                suggest an increased
                                                                                risk of intrauterine
                                                                                growth retardation
                                                                                associated with TTHM
                                                                                and HAA5 exposure in
                                                                                the third trimester,
                                                                                although only HAA5
                                                                                results were
                                                                                statistically
                                                                                significant.
Savitz et al. 2005.............  Population-based   Estimated TTHM,    Early and late     No association with
                                  prospective        HAA9, and TOC      pregnancy loss,    pregnancy loss was
                                  cohort study in    exposures during   preterm birth,     seen when looking at
                                  three              pregnancy.         small for          high exposure of TTHM
                                  communities        Indices examined   gestational age,   compared to low
                                  around the U.S.,   included           and term birth     exposure of TTHM.
                                  2000-2004.         concentration,     weight.            When examining
                                                     ingested amount,                      individual THMs, a
                                                     exposure from                         statistically
                                                     showering and                         significant
                                                     bathing, and an                       association was found
                                                     integration of                        between
                                                     all exposures                         bromodichloromethane
                                                     combined.                             (BDCM) and pregnancy
                                                                                loss. A similar, non-
                                                                                statistically
                                                                                significant
                                                                                association was seen
                                                                                between
                                                                                dibromochloromethane
                                                                                (DBCM) and pregnancy
                                                                                loss. Some increased
                                                                                risk was seen for
                                                                                losses at greater
                                                                                than 12 weeks'
                                                                                gestation for TTHM,
                                                                                BDCM, and TOX (total