Lead; Renovation, Repair, and Painting Program for Public and Commercial Buildings, 24848-24862 [2010-10097]

Agencies

• ENVIRONMENTAL PROTECTION AGENCY

[Federal Register Volume 75, Number 87 (Thursday, May 6, 2010)]
[Proposed Rules]
[Pages 24848-24862]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2010-10097]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 745

[EPA-HQ-OPPT-2010-0173; FRL-8823-6]
RIN 2070-AJ56


Lead; Renovation, Repair, and Painting Program for Public and 
Commercial Buildings

AGENCY: Environmental Protection Agency (EPA).

ACTION: Advance notice of proposed rulemaking.

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SUMMARY: EPA is giving advance notice of the Agency's intention to 
regulate the renovation, repair, and painting of public and commercial 
buildings under section 402(c)(3) of the Toxic Substances Control Act 
(TSCA). This notice announces the commencement of proceedings to 
propose lead-safe work practices and other requirements for renovations 
on the exteriors of public and commercial buildings and to determine 
whether lead-based paint hazards are created by interior renovation, 
repair, and painting projects in public and commercial buildings. For 
those renovations in the interiors of public and commercial buildings 
that create lead-based paint hazards, EPA will propose regulations to 
address these hazards.

DATES: Comments must be received on or before July 6, 2010.

ADDRESSES: Submit your comments, identified by docket identification 
(ID) number EPA-HQ-OPPT-2010-0173, by one of the following methods:
     Federal eRulemaking Portal: https://www.regulations.gov. 
Follow the online instructions for submitting comments.
     Mail: Document Control Office (7407M), Office of Pollution 
Prevention and Toxics (OPPT), Environmental Protection Agency, 1200 
Pennsylvania Ave., NW., Washington, DC 20460-0001.
     Hand Delivery: OPPT Document Control Office (DCO), EPA 
East Bldg., Rm. 6428, 1201 Constitution Ave., NW., Washington, DC; 
Attention: Docket ID Number EPA-HQ-OPPT-2010-0173. The DCO is open from 
8 a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The 
telephone number for the DCO is (202) 564-8930. Such deliveries are 
only accepted during the DCO's normal hours of operation, and special 
arrangements should be made for deliveries of boxed information.
    Instructions: Direct your comments to docket ID number EPA-HQ-OPPT-
2010-0173. EPA's policy is that all comments received will be included 
in the docket without change and may be made available online at https://www.regulations.gov, including any personal information provided, 
unless the comment includes information claimed to be Confidential 
Business Information (CBI) or other information whose disclosure is 
restricted by statute. Do not submit information that you consider to 
be CBI or otherwise protected through regulations.gov or e-mail. The 
regulations.gov Web site is an ``anonymous access'' system, which means 
EPA will not know your identity or contact information unless you 
provide it in the body of your comment. If you send an e-mail comment 
directly to EPA without going through regulations.gov, your e-mail 
address will be automatically captured and included as part of the 
comment that is placed in the docket and made available on the 
Internet. If you submit an electronic comment, EPA recommends that you 
include your name and other contact information in the body of your 
comment and with any disk or CD-ROM you submit. If EPA cannot read your 
comment due to technical difficulties and cannot contact you for 
clarification, EPA may not be able to consider your comment. Electronic 
files should avoid the use of special characters, any form of 
encryption, and be free of any defects or viruses.
    Docket: All documents in the docket are listed in the docket index 
available at https://www.regulations.gov. 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, will be publicly available only 
in hard copy. Publicly available docket materials are available 
electronically at https://www.regulations.gov, or, if only available in 
hard copy, at the OPPT Docket. The OPPT Docket is located in the EPA 
Docket Center (EPA/DC) at Rm. 3334, EPA West Bldg., 1301 Constitution 
Ave., NW., Washington, DC. The EPA/DC Public Reading Room hours of 
operation are 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding 
legal holidays. The telephone number of the EPA/DC Public Reading Room 
is (202) 566-1744, and the telephone number for the OPPT Docket is 
(202) 566-0280. Docket visitors are required to show photographic 
identification, pass through a metal detector, and sign the EPA visitor 
log. All visitor bags are processed through an X-ray machine and 
subject to search. Visitors will be provided an EPA/DC badge that must 
be visible at all times in the building and returned upon departure.

FOR FURTHER INFORMATION CONTACT:
    For technical information contact: Hans Scheifele, National Program 
Chemicals Division, Office of Pollution Prevention and Toxics, 
Environmental Protection Agency, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460-0001; telephone number: (202) 564-3122; e-mail 
address: scheifele.hans@epa.gov.
    For general information contact: The TSCA-Hotline, ABVI--Goodwill, 
422 South Clinton Ave., Rochester, NY 14620; telephone number: (202) 
554-1404; e-mail address: TSCA-Hotline@epa.gov.

SUPPLEMENTARY INFORMATION: 

I. General Information

A. Does this action apply to me?

    This document is directed to the public in general. However, this 
document may be of particular interest to the following entities:
     Building construction (North American Industrial 
Classification System (NAICS) code 236), e.g., commercial building 
construction, industrial building construction, commercial and 
institutional building construction, building finishing contractors, 
drywall and insulation contractors, painting and wall covering 
contractors, finish carpentry contractors, other building finishing 
contractors.
     Specialty trade contractors (NAICS code 238), e.g., 
plumbing, heating, and air-conditioning contractors, painting and wall 
covering contractors, electrical contractors, finish carpentry 
contractors, drywall and insulation contractors, siding contractors, 
tile and terrazzo contractors, glass and glazing contractors.
     Real estate (NAICS code 531), e.g., lessors of non-
residential buildings and dwellings, non-residential property managers.
     Facilities support services (NAICS code 561210).
     Other general government support (NAICS code 921) e.g., 
general services departments, government, public property management 
services, government.

[[Page 24849]]

    This listing is not intended to be exhaustive, but rather provides 
a guide for readers regarding entities likely to be affected by this 
action. Other types of entities not listed in this unit could also be 
affected. The NAICS codes have been provided to assist you and others 
in determining whether this action might apply to certain entities. If 
you have any questions regarding the applicability of this action to a 
particular entity, consult the technical person listed under FOR 
FURTHER INFORMATION CONTACT.

B. What should I consider as I prepare my comments for EPA?

    1. Submitting CBI. Do not submit this information to EPA through 
regulations.gov or e-mail. Clearly mark the part or all of the 
information that you claim to be CBI. For CBI information in a disk or 
CD-ROM that you mail to EPA, mark the outside of the disk or CD-ROM 
that you mail to EPA, mark the outside of the disk or CD-ROM as CBI and 
then identify electronically within the disk or CD-ROM the specific 
information that is claimed as CBI. In addition to one complete version 
of the comment that includes information claimed as CBI, a copy of the 
comment that does not contain the information claimed as CBI must be 
submitted for inclusion in the public docket. Information so marked 
will not be disclosed except in accordance with procedures set forth in 
40 CFR part 2.
    2. Tips for preparing your comments. When submitting comments, 
remember to:
    i. Identify the document by docket ID number and other identifying 
information (subject heading, Federal Register date and page number).
    ii. Follow directions. The Agency may ask you to respond to 
specific questions or organize comments by referencing a Code of 
Federal Regulations (CFR) part or section number.
    iii. Explain why you agree or disagree; suggest alternatives and 
substitute language for your requested changes.
    iv. Describe any assumptions and provide any technical information 
and/or data that you used.
    v. If you estimate potential costs or burdens, explain how you 
arrived at your estimate in sufficient detail to allow for it to be 
reproduced.
    vi. Provide specific examples to illustrate your concerns and 
suggest alternatives.
    vii. Explain your views as clearly as possible, avoiding the use of 
profanity or personal threats.
    viii. Make sure to submit your comments by the comment period 
deadline identified.

II. Background

A. EPA's Lead-Bhased Paint Programs

    In 1992, Congress found that low-level lead poisoning was 
widespread among American children, affecting, at that time, as many as 
3,000,000 children under age 6; that the ingestion of household dust 
containing lead from deteriorating or abraded lead-based paint was the 
most common cause of lead poisoning in children; and that the health 
and development of children living in as many as 3,800,000 American 
homes was endangered by chipping or peeling lead paint, or excessive 
amounts of lead-contaminated dust in their homes. Congress further 
determined that the prior Federal response to this threat was 
insufficient and enacted Title X of the Housing and Community 
Development Act of 1992, Public Law 102-550 (also known as the 
Residential Lead-Based Paint Hazard Reduction Act of 1992) (``the Act'' 
or ``Title X''). Title X established a national goal of eliminating 
lead-based paint hazards in housing as expeditiously as possible and 
provided a leadership role for the Federal government in building the 
infrastructure necessary to achieve this goal.
    Subsequently, President Clinton created the President's Task Force 
on Environmental Health Risks and Safety Risks to Children. Co-chaired 
by the Secretary of the Department of Health and Human Services (HHS) 
and the Administrator of EPA, the Task Force consisted of 
representatives from 16 Federal departments and agencies. The Task 
Force set a Federal goal of eliminating childhood lead poisoning by the 
year 2010 (Ref. 1). In October 2001, President Bush extended the work 
of the Task Force for an additional 18 months beyond its original 
charter. Reducing lead poisoning in children was the Task Force's top 
priority. Although more work remains to be done, significant progress 
has been made towards reducing lead poisoning in children. The 
estimated percentage of children with blood lead levels above 10 
micrograms per deciliter ([mu]g/dL) declined from 4.4% between 1991 and 
1994 to 1.4% between 1999 and 2004 (Ref. 25). More information on 
Federal efforts to address lead poisoning, including the 
responsibilities of EPA and other Federal Agencies under Title X, can 
be found in Units III.A. and III.B. of the preamble to the 2006 
Renovation, Repair, and Painting Program Proposed Rule (2006 Proposal) 
(Ref. 3).
    The Act added a new title to TSCA entitled ``Title IV-Lead Exposure 
Reduction.'' Most of EPA's responsibilities for addressing lead-based 
paint hazards can be found in this title, with section 402 of TSCA 
being one source of the rulemaking authority to carry out these 
responsibilities. TSCA section 402(a) directs EPA to promulgate 
regulations covering lead-based paint activities to ensure that persons 
performing these activities are properly trained, that training 
programs are accredited, and that contractors performing these 
activities are certified. These regulations must contain standards for 
performing lead-based paint activities, taking into account 
reliability, effectiveness, and safety. On August 29, 1996, EPA 
promulgated final regulations under TSCA section 402(a) that govern 
lead-based paint inspections, lead hazard screens, risk assessments, 
and abatements in target housing and child-occupied facilities (also 
referred to as the Lead-based Paint Activities Regulations) (Ref. 4). 
``Target housing'' is defined in TSCA section 401 as any housing 
constructed before 1978, except housing for the elderly or persons with 
disabilities (unless any child under age 6 resides or is expected to 
reside in such housing) or any 0-bedroom dwelling. The Lead-based Paint 
Activities Regulations created a subset of public and commercial 
buildings called child-occupied facilities, and defined them in terms 
of the amount of time a young child might spend within them. These 
regulations, codified at 40 CFR part 745, subpart L, contain an 
accreditation program for training providers and training and 
certification requirements for lead-based paint inspectors, risk 
assessors, project designers, abatement supervisors, and abatement 
workers. Work practice standards for lead-based paint activities are 
included. Pursuant to TSCA section 404, provision was made for 
interested States, Territories, and Indian Tribes to apply for and 
receive authorization to administer their own lead-based paint 
activities programs.
    On June 9, 1999, the Lead-based Paint Activities Regulations were 
amended to include a fee schedule for training programs seeking EPA 
accreditation and for individuals and firms seeking EPA certification 
(Ref. 5). These fees were established as directed by TSCA section 
402(a)(3), which requires EPA to recover the cost of administering and 
enforcing the lead-based paint activities requirements in unauthorized 
States. The most recent amendment to the Lead-based Paint Activities 
Regulations occurred on April 8, 2004, when notification requirements 
were added to help EPA monitor compliance with the training and 
certification provisions and

[[Page 24850]]

the abatement work practice standards (Ref. 6).
    Another of EPA's responsibilities under Title X is to require that 
purchasers and tenants of target housing and occupants of target 
housing undergoing renovation are provided information on lead-based 
paint and lead-based paint hazards. As directed by TSCA section 406(a), 
the Consumer Products Safety Commission (CPSC), the Department of 
Housing and Urban Development (HUD), and EPA, in consultation with the 
Centers for Disease Control and Prevention (CDC), jointly developed a 
lead hazard information pamphlet entitled Protect Your Family From Lead 
in Your Home (PYF) (Ref. 7). This pamphlet was designed to be 
distributed as part of the disclosure requirements of section 1018 of 
Title X and TSCA section 406(b), to provide home purchasers, renters, 
owners, and occupants with the information necessary to allow them to 
make informed choices when selecting housing to buy or rent, or 
deciding on home renovation projects. The pamphlet contains information 
on the health effects of lead, how exposure can occur, and steps that 
can be taken to reduce or eliminate the risk of exposure during various 
activities in the home.
    Pursuant to the authority provided in section 1018 of Title X, on 
March 6, 1996, HUD and EPA jointly promulgated regulations requiring 
persons who are selling or leasing target housing to provide the PYF 
pamphlet and information on known lead-based paint and lead-based paint 
hazards in the housing to purchasers and renters (Ref. 8). These joint 
regulations, codified at 24 CFR part 35, subpart A, and 40 CFR part 
745, subpart F, describe in detail the information that must be 
provided before the contract or lease is signed and require that 
sellers, landlords, and agents document compliance with the disclosure 
requirements in the contract to sell or lease the property. Title X 
does not provide for these requirements to be administered by States or 
Tribes in lieu of the Federal regulations. Therefore, HUD and EPA are 
responsible for administering and enforcing these disclosure 
obligations.
    TSCA section 406(b) directs EPA to promulgate regulations requiring 
persons who perform renovations for compensation in target housing to 
provide a lead hazard information pamphlet to owners and occupants of 
the home being renovated. These regulations, promulgated on June 1, 
1998, are codified at 40 CFR part 745, subpart E (Ref. 9). The term 
``renovation'' is not defined in the statute, but the regulation, at 40 
CFR 745.83, defines a ``renovation'' as the modification of any 
existing structure, or portion of a structure, that results in the 
disturbance of painted surfaces. The regulations specifically exclude 
lead-based paint abatement projects as well as small projects that 
disturb 2 square feet or less of painted surface per component, 
emergency projects, and renovations affecting components that have been 
found to be free of lead-based paint, as that term is defined in the 
regulations, by a certified inspector or risk assessor. These 
regulations require the renovation firm to document compliance with the 
requirement to provide the owner and the occupant with the PYF 
pamphlet. TSCA section 404 also allows States to apply for, and receive 
authorization to administer, the TSCA section 406(b) requirements.
    TSCA section 403 directs EPA to promulgate regulations that 
identify, for the purposes of Title X and Title IV of TSCA, dangerous 
levels of lead in paint, dust, and soil. EPA promulgated regulations 
pursuant to TSCA section 403 on January 5, 2001, and codified them at 
40 CFR part 745, subpart D (Ref. 10). These hazard standards define 
lead-based paint hazards in target housing and child-occupied 
facilities as paint-lead, dust-lead, and soil-lead hazards. A paint-
lead hazard is defined as any damaged or deteriorated lead-based paint, 
any chewable lead-based painted surface with evidence of teeth marks, 
or any lead-based paint on a friction surface if lead dust levels 
underneath the friction surface exceed the dust-lead hazard standards. 
A dust-lead hazard is surface dust that contains a mass-per-area 
concentration of lead equal to or exceeding 40 micrograms per square 
foot ([mu]g/ft\2\) on floors or 250 [mu]g/ft\2\ on interior windowsills 
based on wipe samples. A soil-lead hazard is bare soil that contains 
total lead equal to or exceeding 400 parts per million (ppm) in a play 
area or average of 1,200 ppm of bare soil in the rest of the yard based 
on soil samples.

B. EPA's Renovation, Repair, and Painting Program

    Section 402(c) of TSCA addresses renovation and remodeling. For the 
stated purpose of reducing the risk of exposure to lead in connection 
with renovation and remodeling activities, section 402(c)(1) of TSCA 
requires EPA to promulgate and disseminate guidelines for the conduct 
of such activities that may create a risk of exposure to dangerous 
levels of lead. In response to this statutory directive, EPA developed 
the guidance document entitled ``Reducing Lead Hazards when Remodeling 
Your Home'' in consultation with industry and trade groups (Ref. 11). 
This document has been widely disseminated to renovation and remodeling 
stakeholders through the National Lead Information Center, EPA Regions, 
and EPA's State and Tribal partners and is available at https://www.epa.gov/lead/pubs/rrpamph.pdf.
    Section 402(c)(2) of TSCA directs EPA to study the extent to which 
persons engaged in various types of renovation and remodeling 
activities are exposed to lead during such activities or create a lead-
based paint hazard regularly or occasionally. EPA conducted this study 
in four phases. Phase I, the Environmental Field Sampling Study (Ref. 
12), evaluated the amount of leaded dust generated by various typical 
renovation activities. Phase II, the Worker Characterization and Blood 
Lead Study (Ref. 22), involved collecting data on blood lead and 
renovation and remodeling activities from workers. Phase III, the 
Wisconsin Childhood Blood-Lead Study (Ref. 14), was a retrospective 
study focused on assessing the relationship between renovation and 
remodeling activities and children's blood-lead levels. Phase IV, the 
Worker Characterization and Blood-Lead Study of R&R (Renovation and 
Repair) Workers Who Specialize in Renovations of Old or Historic Homes 
(Ref. 15), was similar to Phase II, but focused on individuals who 
worked primarily in old historic buildings. More information on the 
results of these peer-reviewed studies can be found in Unit III.C.1. of 
the preamble to the 2006 Proposal (Ref. 3).
    Section 402(c)(3) of TSCA directs EPA to revise the regulations 
promulgated under TSCA section 402(a), i.e., the Lead-based Paint 
Activities Regulations, to apply to renovation or remodeling activities 
in target housing, public buildings constructed before 1978, and 
commercial buildings that create lead-based paint hazards. Based 
primarily on the four-phase study conducted under TSCA section 
402(c)(2), EPA issued a proposed rule in January 2006 to cover 
renovation, repair, and painting activities that disturb painted 
surfaces in target housing and child-occupied facilities (Ref. 3). In 
the 2006 Proposal, EPA proposed to conclude that all such activities in 
the presence of lead-based paint create lead-based paint hazards 
because available information indicated that all such activities create 
dust-lead levels that exceed the hazard standards established under 
TSCA section 403.
    After the 2006 Proposal was issued, EPA conducted a field study 
entitled ``Characterization of Dust Lead Levels

[[Page 24851]]

after Renovation, Repair, and Painting Activities'' (Dust Study) to 
better characterize dust-lead levels resulting from various renovation, 
repair, and painting activities (Ref. 16). This study, completed in 
January 2007, was designed to compare environmental lead levels at 
appropriate stages after various types of renovation, repair, and 
painting preparation activities were performed on the interiors and 
exteriors of target housing units and child-occupied facilities. The 
renovation activities were conducted by local professional renovation 
firms, using personnel who received lead safe work practices training. 
The activities conducted represented a range of renovation, repair, and 
painting activities that would have been permitted under the 2006 
Proposal, including work practices that are restricted or prohibited 
under the final rule, such as the use of high-speed machines without 
high-efficiency particulate air (HEPA) filtered exhaust control to 
remove paint. Of particular interest was the impact of using specific 
work practices that renovation firms would be required to use under the 
proposed rule, such as the use of plastic to contain the work area and 
a multi-step cleaning protocol, as opposed to more typical work 
practices. The Dust Study reinforced EPA's proposed finding that 
typical renovation and remodeling activities that disturb lead-based 
paint create lead-based paint hazards.
    In April 2008, EPA issued the final Renovation, Repair and Painting 
Rule (RRP Rule) under the authority of section 402(c)(3) of TSCA to 
address lead-based paint hazards created by renovation, repair, and 
painting activities that disturb lead-based paint in target housing and 
child-occupied facilities (Ref. 17). The term ``target housing'' is 
defined in TSCA section 401 as any housing constructed before 1978, 
except housing for the elderly or persons with disabilities (unless any 
child under age 6 resides or is expected to reside in such housing) or 
any 0-bedroom dwelling. Under the RRP Rule, a child-occupied facility 
is a building, or a portion of a building, constructed prior to 1978, 
visited regularly by the same child, under 6 years of age, on at least 
two different days within any week (Sunday through Saturday period), 
provided that each day's visit lasts at least 3 hours and the combined 
weekly visits last at least 6 hours, and the combined annual visits 
last at least 60 hours. The RRP Rule establishes requirements for 
training renovators, other renovation workers, and dust sampling 
technicians; for certifying renovators, dust sampling technicians, and 
renovation firms; for accrediting providers of renovation and dust 
sampling technician training; for renovation work practices; and for 
recordkeeping. Interested States, Territories, and Indian Tribes may 
apply for and receive authorization to administer and enforce all of 
the elements of the RRP Rule.

C. Recent Renovation, Repair, and Painting Program Developments

    Shortly after the RRP Rule was published, several petitions were 
filed challenging the rule. These petitions were consolidated in the 
Circuit Court of Appeals for the District of Columbia Circuit. On 
August 24, 2009, EPA entered into an agreement with the environmental 
and children's health advocacy groups in settlement of their petitions 
(Ref. 18). In this agreement, EPA committed to propose several changes 
to the RRP Rule. EPA also agreed to commence rulemaking to address 
renovations in public and commercial buildings, other than child-
occupied facilities, to the extent those renovations create lead-based 
paint hazards. For these buildings, EPA agreed, at a minimum, to do the 
following:
     Issue a proposal to regulate renovations on the exteriors 
of public and commercial buildings other than child-occupied facilities 
by December 15, 2011 and to take final action on that proposal by July 
15, 2013.
     Consult with EPA's Science Advisory Board by September 30, 
2011, on a methodology for evaluating the risk posed by renovations in 
the interiors of public and commercial buildings other than child-
occupied facilities.
     Eighteen months after receipt of the Science Advisory 
Board's report, either issue a proposal to regulate renovations on the 
interiors of public and commercial buildings other than child-occupied 
facilities or conclude that such renovations do not create lead-based 
paint hazards.
    On August 10, 2009, EPA received a petition from several 
environmental and public health advocacy groups requesting that the EPA 
amend regulations issued under Title IV of TSCA (Ref. 20). 
Specifically, the petitioners requested that EPA lower the Agency's 
dust-lead hazard standards issued pursuant to section 403 of TSCA from 
40 [mu]g/ft\2\ to 10 [mu]g/ft\2\ or less for floors and from 250 [mu]g/
ft\2\ to 100 [mu]g/ft\2\ or less for window sills. The petitioners also 
asked EPA to modify the definition of lead-based paint in 40 CFR 
745.103 and 745.223 from 0.5 percent by weight (5,000 parts per million 
(ppm)) to 0.06 percent by weight (600 ppm) with a corresponding 
reduction in the 1.0 milligram per square centimeter standard. On 
October 22, 2009, EPA granted this petition under section 553(e) of the 
Administrative Procedures Act, 5 U.S.C. 553(e) (Ref. 21). In granting 
this petition, EPA agreed to commence the appropriate proceeding, but 
did not commit to a particular schedule or to a particular outcome. 
Because Congress gave the Department of Housing and Urban Development 
(HUD) statutory authority to establish a lower level of lead in paint 
for the purpose of the definition of the term ``lead-based paint'' in 
target housing (see 15 U.S.C. 2681(9)), EPA agreed to work with HUD in 
taking the appropriate action on the request pertaining to the 
definition of the term ``lead-based paint.''

D. Information on Lead and Its Health Effects

    Lead is a soft, bluish metallic chemical element mined from rock 
and found in its natural state all over the world. Lead is virtually 
indestructible, is persistent, and has been known since antiquity for 
its adaptability in making various useful items. In modern times, it 
has been used to manufacture many different products, including paint, 
batteries, pipes, solder, pottery, and gasoline. Through the 1940's, 
paint manufacturers frequently used lead as a primary ingredient in 
many oil-based interior and exterior house paints. Usage gradually 
decreased through the 1950's and 1960's as titanium dioxide replaced 
lead and as latex paints became more widely available.
    1. Health effects in general. Lead bioaccumulates, and is only 
slowly removed, with bone lead serving as a blood lead source for years 
after exposure and may serve as a significant source of exposure. Bone 
accounts for more than 90% of the total body burden of lead in adults 
and 70% in children (Ref. 22). In comparison to adults, bone mineral 
turns over much more quickly in children as a result of growth. Changes 
in blood lead concentration in children are thought to parallel more 
closely to changes in total body burden. Therefore, blood lead 
concentration is often used in epidemiologic and toxicological studies 
as an index of exposure and body burden for children.
    Lead is known for its ``broad array of deleterious effects on 
multiple organ systems via widely diverse mechanisms of action'' (Ref. 
22, p. 8-24 and section 8.4.1). This array of health effects includes 
effects on heme biosynthesis and related functions, neurological 
development and function,

[[Page 24852]]

reproduction and physical development, kidney function, cardiovascular 
function, and immune function. The weight of evidence varies across 
this array of effects and is comprehensively described in the EPA Air 
Quality Criteria for Lead (Criteria Document) (Ref. 22). There is also 
some evidence of lead carcinogenicity, primarily from animal studies, 
together with limited human evidence of suggestive associations (Ref. 
22, sections 5.6.2, 6.7, and 8.4.10). Lead has also been classified as 
a probable human carcinogen by the International Agency for Research on 
Cancer (inorganic lead compounds), based on limited evidence in humans 
and sufficient evidence in animals, and as reasonably anticipated to be 
a human carcinogen by the U.S. National Toxicology Program (lead and 
lead compounds) (Ref. 22, section 6.7.2). EPA considers lead a probable 
carcinogen based on the available animal data (https://www.epa.gov/iris/subst/0277.htm (Ref. 22, p. 6-195)).
    This discussion is focused on those effects most pertinent to 
ambient exposures, which, given the reductions in ambient lead levels 
over the past 30 years, are generally those associated with individual 
blood lead levels in children and adults in the range of 10 [mu]g/dL 
and lower. These key effects include neurological, hematological, and 
immune effects for children, and hematological, cardiovascular, and 
renal effects for adults (Ref. 22, Tables 8-5 and 8-6, pp. 8-60 to 8-
62). As evident from the discussions in chapters 5, 6, and 8 of the 
Criteria Document, ``neurotoxic effects in children and cardiovascular 
effects in adults are among those best substantiated as occurring at 
blood lead concentrations as low as 5 to 10 [mu]g/dL (or possibly 
lower); and these categories are currently clearly of greatest public 
health concern'' (Ref. 22, p. 8-60). At mean blood lead levels, in 
children, on the order of 10 [mu]g/dL, and somewhat lower, associations 
have been found with effects to the immune system, including altered 
macrophage activation, increased immunoglobulin E (IgE) levels and 
associated increased risk for autoimmunity and asthma (Ref. 22, 
sections 5.9, 6.8, and 8.4.6). A meta-analysis of numerous studies 
estimates that a doubling of blood-lead level (e.g., from 5 to 10 
[mu]g/dL) is associated with ~1.0 millimeter of mercury (mm Hg) 
increase in systolic blood pressure and ~0.6 mm Hg increase in 
diastolic pressure (Ref. 22, p. E-10). With respect to renal effects in 
adults, increased risk for nephrotoxicity was observed at the lowest 
lead exposure levels in epidemiological studies included in the 
Criteria Document (Ref. 22, p. 8-49). Nephrotic effects were reported 
among some adults with mean concurrent blood lead levels as low as 2 to 
4 [mu]g/dL. ``More specifically, the newly available general population 
studies have shown associations between blood Pb and indicators of 
renal function impairment at blood-Pb levels extending below 10 [mu]g/
dL, with nephrotic effects having been reported among some adults with 
mean concurrent blood-Pb levels as low as ~2 to 4 [mu]g/dL.'' (Ref. 22, 
p. 8-49).
    The toxicological and epidemiological information available 
``includes assessment of new evidence substantiating risks of 
deleterious effects on certain health endpoints being induced by 
distinctly lower than previously demonstrated lead exposures indexed by 
blood lead levels extending well below 10 [mu]g/dL in children and/or 
adults'' (Ref. 22, p. 8- 25). Some health effects associated with 
individual blood lead levels extend below 5 [mu]g/dL, and some studies 
have observed these effects at the lowest blood levels considered. With 
regard to population mean levels, the Criteria Document points to 
studies reporting ``lead effects on the intellectual attainment of 
preschool and school age children at population mean concurrent blood-
lead levels [BLLs] ranging down to as low as 2 to 8 [mu]g/dL'' (Ref. 
22, p. E-9).
    EPA notes that many studies over the past decade, in investigating 
effects at lower blood lead levels, have utilized the CDC advisory 
level or level of concern for individual children (10 [mu]g/dL). This 
level has variously been called an advisory level or level of concern. 
In addressing children's blood lead levels, CDC has stated, 
``[s]pecific strategies that target screening to high-risk children are 
essential to identify children with BLLs >= 10 [mu]g/dL'' (Ref. 1) as a 
benchmark for assessment, and this is reflected in the numerous 
references in the Criteria Document to 10 [mu]g/dL. Individual study 
conclusions stated with regard to effects observed below 10 [mu]g/dL 
are usually referring to individual blood lead levels. In fact, many 
such study groups have been restricted to individual blood lead levels 
below 10 [mu]g/dL or restricted to blood lead levels below levels that 
are lower than 10 [mu]g/dL (e.g., the blood lead levels must be below 8 
[mu]g/dL). EPA notes that the mean blood lead level for these groups 
will necessarily be lower than the blood lead level below which they 
are restricted, because the restricted blood lead level is the upper 
end of the blood lead level range of the study.
    Threshold levels, in terms of blood lead levels in individual 
children, for neurological effects cannot be discerned from the 
currently available studies (Ref. 22, pp. 8-60 to 8-63). The Criteria 
Document states, ``There is no level of lead exposure that can yet be 
identified, with confidence, as clearly not being associated with some 
risk of deleterious health effects'' (Ref. 22, p. 8-63). As discussed 
in the Criteria Document, ``a threshold for lead neurotoxic effects may 
exist at levels distinctly lower than the lowest exposures examined in 
these epidemiologic studies'' (Ref. 22, p. 8- 67). Physiological, 
behavioral and demographic factors contribute to increased risk of 
lead-related health effects. Population groups potentially at risk, 
sometimes also referred to as sensitive populations, include those with 
increased susceptibility (i.e., physiological factors contributing to a 
greater response for the same exposure), as well as those with greater 
vulnerability (i.e., those with increased exposure such as through 
exposure to higher media concentrations or resulting from behavior 
leading to increased contact with contaminated media), or those 
affected by socioeconomic factors, such as reduced access to health 
care or low socioeconomic status (Ref. 22).
    Children are at increased risk of lead-related health effects due 
to various factors that enhance their exposures (e.g., via the hand-to-
mouth activity that is prevalent in very young children, (Ref. 22, 
section 4.4.3)) and susceptibility. While children are considered to be 
at a period of maximum exposure around 18-27 months, recent 
epidemiologic studies have found other blood lead measurements, 
including concurrent blood lead levels or lifetime averages, to be 
stronger predictors of lead-associated effects than peak blood lead 
concentration (Ref. 22, pp. 6-60 and 6-61). The evidence ``supports the 
idea that lead exposure continues to be toxic to children as they reach 
school age, and [does] not lend support to the interpretation that all 
the damage is done by the time the child reaches 2 to 3 years of age'' 
(Ref. 22, section 6.2.12). The following physiological and demographic 
factors can further affect risk of lead-related effects in some 
children.
     Children with particular genetic polymorphisms (e.g., 
presence of the d-aminolevulinic acid dehydratase-2 [ALAD-2] allele) 
may have increased sensitivity to lead toxicity, which may be due to 
increased susceptibility to the same internal dose and/or to increased 
internal dose associated with same

[[Page 24853]]

exposure (Ref. 22, p. 8-71, sections 6.3.5, 6.4.7.3, and 6.3.6).
     Some children may have blood lead levels higher than those 
otherwise associated with a given lead exposure (Ref. 22, section 
8.5.3) as a result of nutritional status (e.g., iron deficiency, 
calcium intake), as well as genetic and other factors (Ref. 22, chapter 
4 and sections 3.4, 5.3.7, and 8.5.3).
     Situations of elevated exposure, such as residing near 
sources of ambient lead, as well as socioeconomic factors, such as 
reduced access to health care or low socioeconomic status can also 
contribute to increased blood lead levels and increased risk of 
associated health effects from air-related lead (Refs. 23, 24).
     Children in poverty and black, non-Hispanic children have 
notably higher blood lead levels than do economically well-off children 
and white children, in general (Ref. 25).
    2. Neurological effects in children. Among the wide variety of 
health endpoints associated with lead exposures, there is general 
consensus that the developing nervous system in children is among the, 
if not the, most sensitive. While blood lead levels in U.S. children 
have decreased notably since the late 1970s, newer studies have 
investigated and reported associations of effects on the 
neurodevelopment of children with these more recent blood lead levels 
(Ref. 22, chapter 6). Functional manifestations of lead neurotoxicity 
during childhood include neurophysiologic, motor, cognitive, and 
behavioral impacts. Numerous epidemiological studies have reported 
neurocognitive, neurobehavioral, neurophysiologic, and neuromotor 
function effects in children with blood lead levels below 10 [mu]g/dL 
(Ref. 22, sections 6.2 and 8.4). As discussed in the Criteria Document, 
``extensive experimental laboratory animal evidence has been generated 
that (a) substantiates well the plausibility of the epidemiologic 
findings observed in human children and adults and (b) expands our 
understanding of likely mechanisms underlying the neurotoxic effects'' 
(Ref. 22, p. 8-25; section 5.3).
    Cognitive effects associated with lead exposures that have been 
observed in epidemiological studies have included decrements in 
intelligence test results, such as the widely used IQ score, and in 
academic achievement as assessed by various standardized tests as well 
as by class ranking and graduation rates (Ref. 22, section 6.2.16 and 
pp. 8-29 to 8-30). As noted in the Criteria Document with regard to the 
latter, ``[a]ssociations between lead exposure and academic achievement 
observed in the studies noted in this section were significant even 
after adjusting for IQ, suggesting that lead-sensitive 
neuropsychological processing and learning factors not reflected by 
global intelligence indices might contribute to reduced performance on 
academic tasks'' (Ref. 22, pp. 8-29 to 8- 30). Further, neurological 
effects in general include behavioral effects, such as delinquent 
behavior (Ref. 22, sections 6.2.6 and 8.4.2.2), sensory effects, such 
as those related to hearing and vision (Ref. 22, sections 6.2.7 and 
8.4.2.3), and deficits in neuromotor function (Ref. 22, p. 8-36).
    With regard to potential implications of lead effects on IQ, the 
Criteria Document recognizes the ``critical'' distinction between 
population and individual risk, identifying issues regarding declines 
in IQ for an individual and for the population. The Criteria Document 
further states that a ``point estimate indicating a modest mean change 
on a health index at the individual level can have substantial 
implications at the population level'' (Ref. 22, p. 8-77). As an 
example, the Criteria Document states, ``although an increase of a few 
mm Hg in blood pressure might not be of concern for an individual's 
well-being, the same increase in the population mean might be 
associated with substantial increases in the percentages of individuals 
with values that are sufficiently extreme that they exceed the criteria 
used to diagnose hypertension'' (Ref. 22, p. 8-77). A downward shift in 
the mean IQ value is associated with both substantial decreases in 
percentages achieving very high scores and substantial increases in the 
percentage of individuals achieving very low scores (Ref. 22, p. 8-81). 
For example, for a population mean IQ of 100 (and standard deviation of 
15), 2.3% of the population would score above 130, but a shift of the 
population to a mean of 95 results in only 0.99% of the population 
scoring above 130 (Ref. 22, pp. 8-81 to 8-82). ``For an individual 
functioning in the low [IQ] range due to the influence of developmental 
risk factors other than lead, a lead-associated [IQ] decline of several 
points might be sufficient to drop that individual into the range 
associated with increased risk of educational, vocational, and social 
failure'' (Ref. 22, p. 8-77).
    Other cognitive effects observed in studies of children have 
included effects on attention, executive functions, language, memory, 
learning, and visuospatial processing (Ref. 22, sections 5.3.5, 6.2.5, 
and 8.4.2.1), with attention and executive function effects associated 
with lead exposures indexed by blood lead levels below 10 [mu]g/dL 
(Ref. 22, section 6.2.5 and pp. 8-30 to 8-31). The evidence for the 
role of lead in this suite of effects includes experimental animal 
findings (Ref. 22, section 8.4.2.1; p. 8-31), which provide strong 
biological plausibility of lead effects on learning ability, memory and 
attention (Ref. 22, section 5.3.5), as well as associated mechanistic 
findings.
    The persistence of such lead-induced effects is described in the 
Criteria Document (e.g., Ref. 22, sections 5.3.5, 6.2.11, and 8.5.2). 
The persistence or irreversibility of such effects can be the result of 
damage occurring without adequate repair offsets or of the persistence 
of lead in the body (Ref. 22, section 8.5.2). It is additionally 
important to note that there may be long-term consequences of such 
deficits over a lifetime. Poor academic skills and achievement can have 
``enduring and important effects on objective parameters of success in 
real life,'' as well as increased risk of antisocial and delinquent 
behavior (Ref. 22, section 6.2.16).
    Multiple epidemiologic studies of lead and child development have 
demonstrated inverse associations between blood lead concentrations and 
children's IQ and other cognitive-related outcomes at successively 
lower lead exposure levels over the past 30 years (Ref. 22, section 
6.2.13). For example, the overall weight of the available evidence, 
described in the Criteria Document, provides clear substantiation of 
neurocognitive decrements being associated in children with mean blood 
lead levels in the range of 5 to 10 [mu]g/dL, and some analyses 
indicate lead effects on intellectual attainment of children for which 
population mean blood lead levels in the analysis ranged from 2 to 8 
[mu]g/dL (Ref. 22, sections 6.2, 8.4.2, and 8.4.2.6). Thus, while blood 
lead levels in U.S. children have decreased notably since the late 
1970s, newer studies have investigated and reported associations of 
effects on the neurodevelopment of children with blood lead levels 
similar to the more recent, lower blood lead levels (Ref. 22, chapter 
6).
    Children in minority populations and children whose families are 
poor have an increased risk of exposure to harmful lead levels (Ref. 
25, at e376). Analysis of the National Health and Nutrition Examination 
Surveys (NHANES) data from 1988 through 2004 shows that the prevalence 
of blood lead levels equal to or exceeding 10 [micro]g/dL in children 
aged 1 to 5 years has decreased from 8.6% in 1988-1991 to 1.4% in 1999-
2004, which is an 84% decline (Ref. 25, at e377). However, the NHANES 
data from

[[Page 24854]]

1999-2004 indicates that non-Hispanic black children aged 1 to 5 years 
had higher percentages of blood lead levels equal to or exceeding 10 
[micro]g/dL (3.4%) than white children in the same age group (1.2%) 
(Ref. 25). In addition, among children aged 1 to 5 years over the same 
period, the geometric mean blood lead level was significantly higher 
for non-Hispanic blacks (2.8 [micro]g/dL), compared with Mexican 
Americans (1.9 [micro]g/dL) and non-Hispanic whites (1.7 [micro]g/dL) 
(Ref. 25, at e377). For children aged 1 to 5 years from families with 
low income, the geometric mean blood lead level was 2.4 [micro]g/dL 
(Ref. 25, at e377). Further, the incidences of blood-lead levels 
greater than 10 ug/dL and greater than or equal to 5 ug/dL were higher 
for non-hispanic blacks (14% and 3.4%, respectively) than for Mexican 
Americans (4.7% and 1.2%, respectively) and non-Hispanic whites (4.4% 
and 1.2%, respectively) (Ref. 25). The ``analysis indicates that 
residence in older housing, poverty, age, and being non-Hispanic black 
are still major risk factors for higher lead levels'' (Ref. 25, at 
e376).
    3. Adult health effects. As previously noted, the adult health 
effects of lead exposure include negative impacts on renal and 
cardiovascular function. While cardiovascular effects in adults are 
well substantiated as occurring at blood lead levels as low as 5 to 10 
[mu]g/dL (or possibly lower), newly-demonstrated renal system effects 
among general population groups are also emerging as low-level lead 
exposure effects of concern (Ref. 22, p. 8-60).
    Most studies in general adult and patient populations published 
during the past two decades have observed associations between ``Pb 
dose and worse renal function.'' (Ref. 22, p. 6-112) The cumulative 
effect of higher blood lead levels from past exposure may be a factor 
in the nephrotoxicity observed at current blood lead levels. However, 
one study found associations between blood lead and concurrent serum 
creatinine in participants whose peak blood lead levels were equal to 
or less than 10 [mu]g/dL (Ref. 22, p. 6-112). ``The threshold for lead-
related nephrotoxicity cannot be determined based on current data, but 
associations with clinically-relevant renal outcomes have been observed 
in populations with mean blood lead levels as low as 2.2 [mu]g/dL'' 
(Ref. 22, p. 6-112). In addition, the available data are not sufficient 
to determine whether the observed nephrotoxicity is related more to 
such current blood lead levels, higher levels from past exposures, or 
both (Ref. 22, p. 8-49). Some adult populations are at an even greater 
risk for adverse health effects as a result of lead exposure. ``The 
influence of an individual's health status on susceptibility to lead 
toxicity has been demonstrated most clearly for renal outcomes.'' 
``Individuals with diabetes, hypertension, and chronic renal 
insufficiency are at increased risk of Pb-associated declines in renal 
function, and indications of altered kidney function have been reported 
at blood Pb levels ranging somewhat below 5 [mu]g/dL (Lin et al., 2001, 
2003; Muntner et al., 2003; Tsaih et al., 2004).'' (Ref. 22 p. 8-72).
    Positive associations between lead exposure and increased blood 
pressure have been observed in numerous studies. Epidemiologic studies 
that have examined the effects of blood lead levels on blood pressure 
have generally found positive associations, even after controlling for 
confounding factors such as tobacco smoking, exercise, body weight, 
alcohol consumption, and socioeconomic status (Ref. 22, p. 8-45). 
Recent meta-analyses of these studies have reported robust, 
statistically-significant, though small effect-size, associations 
between blood-Pb concentrations and blood pressure. For example, the 
meta-analysis of Nawrot et al. (2002) indicated that a doubling of 
blood lead corresponded to a 1 mm Hg increase in systolic blood 
pressure. Although this magnitude of increase is not clinically 
meaningful for an individual, a population shift of 1 mm Hg is 
important (Ref 22, p. 8-45). The majority of the more recent studies 
employing bone lead level have also found a strong association between 
long-term lead exposure and arterial pressure. ``Since the residence 
time of Pb in blood is relatively short but very long in bone, the 
latter observations have provided compelling evidence for the positive 
relationship between Pb exposure and a subsequent rise in arterial 
pressure in human adults.'' (Ref 22, p. 8-45)
    Studies also demonstrate a relationship between increased lead 
exposure and other adverse cardiovascular outcomes, including increased 
incidence of hypertension and cardiovascular morbidity and mortality 
(Ref. 22, p. 6-154). ``Lead interference in calcium-dependent 
processes, including ionic transport systems and signaling pathways 
important in vascular reactivity may only represent the first step in 
the cascade of Pb-induced physiological events that culminates in 
cardiovascular disease. Lead alteration of endothelial cell response to 
vascular damage, inducement of smooth muscle cell hyperplasia, 
alteration of hormonal and transmitter systems regulating vascular 
reactivity, and its clear role as promoter of oxidative stress suggest 
mechanisms that could explain the Pb-associated increase in blood 
pressure, hypertension, and cardiovascular disease noted in this 
section'' (Ref. 22, p. 6-153).
    Current research does not definitively indicate whether health 
impacts observed later in life are the result of current lead exposure 
or exposure which occurred during early childhood or at some other time 
in the past. The following excerpts from the Criteria Document 
illustrate the uncertainties surrounding this issue:
     ``It could be that damage occurred during a circumscribed 
period when the critical substrate was undergoing rapid development, 
but that the high correlation between serial blood Pb levels impeded 
identification of the special significance of exposure at that time.'' 
(Ref. 22, p. 8-73).
     ``While some observations in children as old as 
adolescence indicate that exposure biomarkers measured concurrently are 
the strongest predictors of late outcomes, the interpretation of these 
observations with regard to critical windows of vulnerability remains 
uncertain'' (Ref. 22, p. 8-74).
    4. Renovations in residential settings and elevated blood lead 
levels. EPA's Wisconsin Childhood Blood-Lead Study, described more 
fully in Unit III.C.1.c. of the preamble to the 2006 Proposal, provides 
ample evidence of a link between renovation activities and elevated 
blood lead levels in resident children (Ref. 14). This peer-reviewed 
study concluded that general residential renovation and remodeling is 
associated with an increased risk of elevated blood lead levels in 
children and that specific renovation and remodeling activities are 
also associated with an increase in the risk of elevated blood lead 
levels in children. In particular, removing paint (using open flame 
torches, using heat guns, using chemical paint removers, and using wet 
scraping/sanding) and preparing surfaces by sanding or scraping 
significantly increased the risk of elevated blood lead levels.
    Three studies from New York support the findings of the Wisconsin 
Childhood Blood-Lead Study. In 1995, the New York State Department of 
Health assessed lead exposure among children resulting from home 
renovation and remodeling in 1993-1994. A review of the health 
department records of children with blood lead levels equal to or 
greater than 20 [mu]g/dL identified 320, or 6.9%, with elevated blood 
lead levels that were attributable to renovation and remodeling (Ref. 
26). An update to that study with data from environmental

[[Page 24855]]

investigations conducted during 2006-2007 in New York State (excluding 
New York City) identified renovation, repair, and painting activities 
as the probable source of lead exposure in 14% of 972 children with 
blood lead levels equal to or exceeding 20 [mu]g/dL (Ref. 27). The 
authors concluded that children living in housing undergoing 
renovation, repair, and painting that was built before 1978, and 
particularly before 1950, when concentrations of lead in paint were 
higher, are at high risk for elevated blood lead levels. The final 
study was a case-control study that assessed the association between 
elevated blood lead levels in children younger than 5 years and 
renovation or repair activities in homes in New York City (Ref. 28). 
EPA notes that the authors show that when dust and debris was reported 
(by respondents via telephone interviews) to be ``everywhere'' 
following a renovation, the children's blood lead levels were 
significantly higher than those of the children at homes that did not 
report remodeling work. On the other hand, when the respondent reported 
either ``no visible dust and debris'' or that ``dust and debris was 
limited to the work area,'' there was no statistically significant 
effect on blood lead levels relative to homes that did not report 
remodeling work. Although the study found only a weak and 
nonsignificant link between a report of any renovation activity and the 
likelihood that a resident child had an elevated blood-lead level, the 
link to the likelihood of an elevated blood-lead level was 
statistically significant for surface preparation by sanding and for 
renovation work that spreads dust and debris beyond the work area. The 
researchers noted the consistency of their results with EPA's Wisconsin 
Childhood Blood-Lead Study (Ref. 28, at 509).

III. Renovations in Public and Commercial Buildings

    In many respects, EPA's approach to determining whether and how to 
regulate exterior renovations on public and commercial buildings and 
whether and how to regulate interior renovations in public and 
commercial buildings will be similar to the approach taken towards 
renovation activities in and on target housing and child-occupied 
facilities. Although the statutory directive under TSCA section 
402(c)(3) is the same for all of these buildings, each type of building 
may present a different level of exposure to occupants. In this ANPRM, 
EPA is taking comment on the many considerations it must take into 
account when revising the regulations issued under TSCA section 402(a) 
to apply to those renovations that create lead-based paint hazards in 
public and commercial buildings.
    An important consideration in determining how to regulate 
renovations on the exteriors of public and commercial buildings is that 
these renovations can create lead-based paint hazards on and in target 
housing and child-occupied facilities. Lead dust can travel in the 
environment and has been shown to be readily tracked into homes and 
other buildings. In fact, as discussed in Unit III.B.1. a substantial 
proportion of interior dust is due to track-in activities.

A. Definitions of ``Public Building'' and ``Commercial Building''

    While the term ``target housing'' is defined in TSCA section 401, 
TSCA Title IV does not provide definitions for the terms ``public 
building'' and ``commercial building.'' The issue of the buildings that 
could and should be covered by these terms was raised, but not 
conclusively resolved, in the rulemaking to establish the existing 
Lead-based Paint Activities Regulations.
    As discussed previously, EPA promulgated the final Lead-based Paint 
Activities Regulations under TSCA section 402(a) in 1996 (Ref. 4). 
These regulations cover lead-based paint inspections, lead hazard 
screens, risk assessments, and abatements. The regulations include 
training and certification requirements for individuals and firms, 
accreditation requirements for lead-based paint training providers, and 
work practice standards designed in accordance with the statutory 
directive to ensure that lead-based paint activities are conducted 
safely, reliably and effectively. As initially proposed in 1994, one 
set of requirements for the training and certification of contractors 
and the accreditation of training programs, as well as specific work 
practice standards would have applied to lead-based paint activities 
conducted in target housing and public buildings (Ref. 29). The 1994 
proposal would have defined public buildings to include all buildings 
generally open to the public or occupied or visited by children, such 
as stores, museums, airports, offices, restaurants, hospitals, and 
government buildings, as well as schools and day-care centers. In the 
final rule, EPA decided to focus on buildings frequented by children 
and, thus, established a subset of the buildings EPA had intended to 
define as public. This subset is called ``child-occupied facilities'' 
and it is delineated terms of the frequency and duration of visits by 
particular children (Ref. 4).
    EPA continues to believe that it is important to emphasize the 
deleterious effects of lead exposure on young children, a sub-
population that has long been identified as being particularly 
susceptible to the adverse effects of lead. However, it is also 
important to address exposures for other sensitive sub-populations, 
such as women who are pregnant or who may become pregnant in the 
future. In addition, as discussed in Unit II.D. of this preamble, a 
growing body of scientific literature documents lead's adverse effects 
on older children and adults at lower levels of exposure than 
previously documented. As a result, EPA does not believe that the 
options considered in this rulemaking should be limited to those 
buildings or situations where young children are likely to be exposed. 
EPA intends to evaluate all of the available information on hazards, 
exposures, and risk to determine which renovations TSCA requires EPA to 
regulate and how TSCA requires EPA to regulate them.
    While TSCA Title IV does not define ``public building'' or 
``commercial building,'' a definition of ``public and commercial 
building'' was provided in TSCA Title II. TSCA Title II addresses the 
management of asbestos-containing building materials in school 
buildings and the training and accreditation (or certification) of 
persons who perform asbestos inspections or design or conduct asbestos 
abatement in public or commercial buildings. Because the primary focus 
of TSCA Title II is primary and secondary schools, and ensuring that 
asbestos-containing building materials in such schools are properly 
managed, primary and secondary schools are specifically excluded from 
the definition of the term ``public and commercial building'' in TSCA 
section 202. However, the rest of the definition signals Congress's 
intention for EPA to interpret the term broadly, because a public and 
commercial building is defined as ``any building'' other than a school 
building or a ``residential apartment building'' of fewer than 10 
units. EPA's regulatory definition of ``public and commercial 
building'' at 40 CFR part 763, Subpart E, Appendix C, Asbestos Model 
Accreditation Plan, provides examples of the types of buildings 
covered, including industrial and office buildings, government-owned 
buildings, colleges, museums, airports, hospitals, churches, 
preschools, stores, warehouses and factories. Notwithstanding the 
differences in focus between TSCA Title II and Title

[[Page 24856]]

IV, EPA believes that a similar broad approach to interpreting ``public 
building'' and ``commercial building'' is warranted in this rulemaking. 
Of course, EPA must still determine which renovations in which 
buildings create lead-based paint hazards.
    One other factor must be considered in interpreting the terms 
``public building'' and ``commercial building.'' In 1978, the CPSC 
banned the use of paint containing more than 0.06% lead by weight on 
toys, furniture, and interior and exterior surfaces in housing and 
other buildings and structures used by consumers (Ref. 30). However, 
this ban specifically exempted ``[i]ndustrial (and commercial) building 
and equipment maintenance coatings, including traffic and safety 
marking coatings.'' It is likely that Congress was thinking of this 
ban, and the exemption, when it limited rulemaking authority in TSCA 
section 402(c)(3) to public buildings built before 1978, but applied no 
such limitation to commercial buildings.
    With this in mind, EPA requests comment, information and data from 
the public on the types of buildings that should be considered ``public 
buildings'' or ``commercial buildings.'' Specifically, EPA asks 
commenters to consider the following questions:
    1. What types of buildings should be considered to be public 
buildings? What types should be considered to be commercial buildings? 
Should outbuildings and structures on the property be included in 
either category as they are in respect to target housing? Why?
    2. What types of building classifications should be considered? 
Should the criteria for classifying buildings include the presence of 
young children, pregnant women, or population density? Is it possible 
to categorize buildings based on the contractors and the workforce 
renovating them (i.e., do different contractors perform renovations in 
different types of public and commercial buildings, or do such work 
differently)? Is it possible to classify public and commercial 
buildings using building codes, zoning, or other characteristics? 
Should various classifications of buildings be treated differently with 
regard to required work practices, cleaning methods, and reoccupancy 
criteria?
    3. Some public or commercial buildings are mixed-use buildings, 
with residences, schools and/or child care facilities in the buildings. 
If portions of the buildings are residences that are target housing 
(i.e., the building was constructed before 1978 and the residences are 
not otherwise exempt), how should such buildings, or particular 
portions of them, be addressed in this rulemaking?
    4. Every four years, the Department of Energy (DOE) collects 
information on the stock of commercial buildings in the United States, 
their energy-related building characteristics, and their energy 
consumption and expenditures. For the purposes of this survey, the 
Commercial Buildings Energy Consumption Survey (CBECS), commercial 
buildings include all buildings in which at least half of the floor 
space is used for a purpose that is not residential, industrial, or 
agricultural. This survey includes building types that might not 
traditionally be considered commercial, such as schools, correctional 
institutions, and buildings used for religious worship. More 
information on the CBECS can be found at https://www.eia.doe.gov/emeu/cbecs/. DOE also collects data every four years on buildings used for 
manufacturing activities. The Manufacturing Energy Consumption Survey 
(MECS) collects data on buildings used by the manufacturing sector, 
defined by NAICS codes 31 to 33. The MECS data does not include 
information on building vintage. More information on MECS can be found 
at https://www.eia.doe.gov/emeu/mecs/contents.html. What other 
information is available on the ages, types, sizes, and other 
characteri