PROGRAM ANNOUNCEMENT (PA) TITLE:  THE FETAL BASIS OF ADULT DISEASE:  ROLE OF THE 
ENVIRONMENT

PAR NUMBER: PAR-02-105 (see replacement PAR-03-121)

RELEASE DATE:  May 2, 2002

Letter of Intent Receipt Dates: July 10, 2002, 2003, 2004

Application Receipt Dates: August 12, 2002, 2003, 2004 

This Program Announcement expires on August 13, 2004, unless reissued.

PARTICIPATING INSTITUTES AND CENTERS (ICs)

National Institute of Environmental Health Sciences (NIEHS) 
 (http://www.niehs.nih.gov)
 
THIS PA CONTAINS THE FOLLOWING INFORMATION

o Purpose of this PA
o Research Objectives
o Mechanism of Support 
o Eligible Institutions
o Funds Available
o Individuals Eligible to Become Principal Investigators
o Where to Send Inquiries
o Letter of Intent
o Submitting an Application
o Peer Review Process
o Review Criteria
o Award Criteria
o Required Federal Citations

PURPOSE OF THIS PA
  
It is recognized that between two-percent and five-percent of all live-born 
infants have a major developmental defect. Approximately 40-percent of these 
defects are thought to be due to the effect(s) of an adverse exposure of a 
genetically pre-disposed fetus to intra-uterine environmental factors. 
Exposure to environmental agents during development can result in death, 
structural malformation, and/or functional alteration of the embryo/fetus. 
These toxicant-induced pathogenic responses are most likely the result of 
altered gene expression associated with altered cell production and cell 
differentiation involved in the establishment of cell lineages leading to the 
structural and functional character of the tissues, organs, and systems that 
arise from these lineages.
 
The NIEHS has a significant program that addresses the role of developmental 
exposures on structural malformations i.e., classical birth defects. The new 
high-throughput functional-genomic, metabonomic, proteomic, and bioinformatic 
technologies now offer for the first time the opportunity to pursue an 
understanding of the role of in utero exposures to environmental agents in 
causing functional changes in organs and tissues that result in increased 
susceptibility to diseases later in life.

The purpose of this program announcement with a set aside of funds and a 
Special Emphasis Panel review by the NIH Center for Scientific Review is to 
stimulate research in an important and emerging area of developmental 
toxicology: the effect of in utero exposures that cause permanent functional 
changes that are not overtly, grossly teratogenic and that result in 
increased susceptibility to disease/dysfunction later in the life span. It is 
becoming increasingly apparent that there is an environmental component to 
nearly every disease. In some cases the environmental trigger is an exposure 
experienced in the adult environment. However, it is now clear that in many 
cases the fetus is more sensitive to the same environmental insults and that 
the effect of exposures during development may have a far more detrimental 
effect on the etiopathology of the disease, both for the fetus as well as the 
adult later in life.

RESEARCH OBJECTIVES

The underlying scientific hypothesis behind the fetal basis of adult diseases 
has been developed by epidemiology studies and emphasized by Dr. David Barker 
in the United Kingdom. This hypothesis, named the Barker Hypothesis, proposed 
that prenatal origins of health and disease is one of the most important 
issues that affects our lives and that of our children. Dr. Barker has shown 
that during development fetuses respond to severe malnutrition by favoring 
the metabolic demands of the growing brain/CNS and heart at the expense of 
other tissues. The growing brain/CNS and heart tissue may not, however, 
escape entirely unscathed. The long-term consequences of this response are 
that the fetus is protected from death, is live-born, but is more prone to 
diseases later in life. 

The Barker Hypothesis studies concentrated on grossly altered nutrition as 
the source of the stress during development. These studies showed via 
epidemiology studies that low birth weight, small for gestation age, frank 
intra-uterine growth retardation (IUGR) or clinically abnormal thinness at 
birth strongly predicts the subsequent occurrence of hypertension, 
hyperlipidemia, insulin resistance, type 2 diabetes, ischemic heart disease, 
breast cancer or prostate cancer in adult life. Fetuses that are clinically 
malnourished during the first trimester of development are three times more 
likely to be obese as adults. Evidence has been presented in human 
populations that gross, heavy exposure to PM10 air pollution containing 
carcinogenic PAHs can be correlated with increased IUGR with a peak impact in 
the earlier portion of the first trimester - a most vulnerable period of the 
cell lineage expansion, differentiation, and cell interactions events of 
organogenesis and first growth. 

The concept of fetal programming of structural-functional formations during 
development has been proposed to explain these findings and the resultant 
research area is referred to as Fetal Basis of Adult Disease (FeBAD) 
research. Programming is the term used to describe lifelong changes in 
function that follow a particular event in an earlier period of the life 
span. While epidemiology studies have identified the phenomenon of metabolic 
programming, little is known about the mechanism(s) by which fetal insults 
lead to altered programming and to disease later in life. In addition, 
emphasis thus far has been on alterations in nutrition during development 
with virtually no focus on the role that exposures to environmental agents, 
such as air or water pollution, either alone or in combination with 
qualitative alterations in macro- or micro-nutrition (i.e. soy protein, 
phytoestrogens, isoflavones or other chemicals in herbal supplements or 
dietary sources), might have on this phenomenon.

There is, however, evidence that some environmental agents, especially those 
with endocrine agonist or antagonist activity, may alter developmental 
programming via alteration in gene expression or gene imprinting that do not 
result in malformations but in functional deficits that do not become 
apparent until later in life.

In the reproductive tract, the classic example of this phenomenon in the 
environmental area is the diethylstilbestrol (DES) story. In humans, in utero 
exposure to DES leads to an increase in vaginal adenocarcinoma around the 
time of puberty. In mice, neonatal DES exposure leads to an increase in 
uterine adenocarcinoma in adulthood. While the direct connection has not been 
made between in utero programming changes due to DES and later life disease, 
it is known that DES (in the animal studies) results in altered gene 
expression in the uterus that is irreversible without any noticeable gross 
alterations in uterine morphology. Other examples in the reproductive area 
include developmental exposures of the monkey to androgens that lead to 
polycystic ovary syndrome-like effects in the adult, data (still considered 
controversial) showing that environmental estrogens, such as DES, 
methoxychlor and bisphenol A, cause alterations in gene expression in the rat 
prostate that are irreversible and are correlated with increased prostate 
cancer, and data showing a link between in utero exposure to dioxin and 
endometriosis later in life in primates and rodents.  

Cardiopulmonary diseases in postnatal life have also been linked to prenatal 
exposure. The most well known example is the association between low birth 
weight (which is associated with poor maternal nutrition and perhaps 
corticosteroid exposure) and cardiovascular disease (e.g., myocardial 
infarcts) and predictors of future cardiovascular disease, such as 
hypertension and atherosclerosis, and complex metabolic disease, such as 
diabetes. In addition, studies have shown that maternal smoking is associated 
with deficits in lung function and with asthma symptoms in the offspring.  
Data indicate that these associations are independent of smoking status after 
birth.

Some forms of neurodegenerative disease may have their origins in in utero 
exposures. For example, there is preliminary evidence that a bacterial 
stimulus (endotoxin) can produce cytokines that impair the development of the 
mesencephalic dopaminergic systems during pregnancy. This attenuation of the 
dopamine neurons during fetal development leaves the offspring with fewer 
dopaminergic neurons at birth and at possible increased risk for Parkinson's 
disease in later life. In a similar vein, there is preliminary evidence that 
exposure to environmental neurotoxins during dopaminergic development 
enhances the susceptibility to accelerated dopaminergic cell death during 
aging via the common molecular mechanism(s) of the alteration of 
stress-activated signal transduction pathways, expression of differentiation 
transcription factors, survival factors or phenotype marker proteins in the 
nigral dopaminergic neurons. Similarly there is evidence that in utero 
exposure to polycyclic biphenols (PCBs) leads to altered thyroid function and 
subsequent learning disabilities later in life. In all instances data are 
needed to show that the in utero exposures actually lead to an altered 
programming at the molecular level and that the disease/dysfunction is a 
direct result, albeit, temporally discordant in its onset and/or progression, 
of that altered programming.  

Based on the epidemiology data that support the Barker Hypothesis and the 
preliminary data showing alterations in gene expression and imprinting due to 
in utero exposures to some environmental agents, we propose that exposure to 
certain environmental chemicals as well as altered nutrition, or in 
combination with altered nutrition, will in some situations, not lead to 
easily identifiable structural malformations, but instead to alterations in 
developmental programming expressed as a permanently altered gland, organ or 
system potential. These states of altered potential would be a result of 
changes in gene expression, due to altered imprinting, and the underlining 
methylation-related protein-DNA relationships associated with chromatin 
remodeling. These effects may occur in a time specific (i.e. vulnerable 
window) and tissue specific manner and such alterations may be irreversible. 
The end-result is an animal that is sensitized such that it will be more 
susceptible to diseases later in life. The environmental insult could act via 
a one hit or two/three hit scenario. That is, there could be an in utero 
exposure that would lead by itself to pathophysiology later in life or there 
could be in utero exposure combined with a neonatal exposure (same or 
different compound(s) or adult exposure that would trigger the 
pathophysiology. The pathophysiology or functional change that results from 
the exposures/insult could lead to: a) the occurrence of a disease that 
otherwise would not have happened, b) an increase in risk for a disease that 
would normally be of lower prevalence, or c) either an earlier onset of a 
disease that would normally have occurred or an exacerbation of the disease.  
Finally, the pathophysiology could have a variable latent period from onset 
in the neonatal period, to early childhood, to pubertal, to early adulthood 
to late adulthood depending on the toxicant, time of exposure and 
tissue/organ affected and potentially transgenerational effects.

Research Approaches Relevant to this PA

The very nature of the problem mandates that the studies related to this 
initiative, at some time, involve whole animal developmental exposures with 
analysis of the fetus, embryo and pups, and well as later life 
disease/dysfunction incidence. These analyses can be done using transgenics, 
model organisms, or rodent models. Research proposed under this initiative 
must use environmentally relevant doses, dose response curves and the 
examination of the relationship between the molecular mechanism proposed and 
the disease/dysfunction studied. Human studies (clinical or epidemiology) are 
not responsive. However, it would be acceptable to propose studies to examine 
gene expression using human cells/tissues and as a prelude to future 
epidemiology studies. 

This initiative also requires the use of the new technologies of gene 
expression profiling, and epigenetics (methylation, imprinting and chromatin 
remodeling). The use of these technologies allows assessment of in utero 
exposure to environmental agents. A critical component of applications to 
this Program Announcement is the development of a direct correlation and 
eventually a cause and effect relationship between the alterations in gene 
expression during development (either increased, decreased or inappropriate 
timing) to alterations in signal transduction pathways and alterations in 
growth factors and cytokines and hormones that lead to a specific disease or 
dysfunction that occurs later in life.  

Another critical part of this initiative is the collaboration of 
developmental biologists/toxicologists with scientists studying the onset and 
exacerbation of adult onset diseases. All applications must show expertise in 
both developmental biology/toxicology and disease pathophysiology. In 
addition, a specific disease must be the focus of the application with 
emphasis on the role of in utero exposure and changes in gene expression in 
the fetus to the onset or severity of the disease.

This initiative will focus on only the three areas that have the most 
preliminary data and, thus, show the most promise of success: the 
reproductive tract, the pulmonocardiovascular system, and the brain/nervous 
system. 

The diseases of interest to NIEHS with respect to this initiative include 
reproductive/hormonal (fertility, endometriosis, fibroids, premature 
menopause, polycyclic ovary syndrome, prostate/ovary/breast cancer) 
cardiopulmonary (heart disease, atherosclerosis, hypertension, chronic 
obstructive pulmonary disease, adult asthma) and brain/CNS (neurodegenerative 
diseases - Parkinson's, Alzheimer). It may be possible to submit applications 
to this initiative with an emphasis on other diseases as long as they are 
related to one or more of the above noted emphasis areas. It should be noted 
that these are all adult onset diseases. Thus this initiative has a focus on 
diseases that have a long latency. Diseases of childhood or puberty or 
diseases of other tissues and organ systems are not responsive to this 
specific announcement. 

Applicants to this program must link in utero and/or neonatal exposures 
during critical windows of development to changes in gene expression that are 
tissue specific (reproductive, cardiopulmonary and brain) and irreversible. 
These changes in gene expression will then need to be measured in the adult 
and correlated with the diseases/dysfunction studied with or without 
additional adult exposures.

Applicants may study any environmental agent/chemical/stressor to which there 
is human exposure and the potential for in utero exposure. This includes any 
endocrine active chemicals and in addition, organic solvents, particulate 
matter, pesticides, nutritional supplements, phytochemicals and metals. 
Nutrition alone cannot be used as an in utero exposure alone but can be 
studied in conjunction with another exposure. Exposure to the environmental 
agent must be in utero but may also be neonatal and/or adult.

MECHANISM OF SUPPORT 

This PAR will use the NIH exploratory/developmental (R21) award mechanism.  
The R21 grant award mechanism supports innovative, high-risk/high-impact 
research requiring preliminary testing or development; exploration of the use 
of approaches and concepts new to a particular substantive area; research and 
development of data upon which significant future research may be built. 
Applications will be considered high-impact if they demonstrate the potential 
for groundbreaking, precedent setting significance, and high-risk because 
they either lack sufficient preliminary date to ensure their feasibility, or 
involve the use of a new model system or technique. As an applicant you will 
be solely responsible for planning, directing, and executing the proposed 
project.  

This PAR uses just-in-time concepts. It also uses the modular budgeting 
format. (see http://grants.nih.gov/grants/funding/modular/modular.htm). 
Specifically, if you are submitting an application with direct costs in each 
year of $250,000 or less, use the modular format.

ELIGIBLE INSTITUTIONS 

You may submit (an) application(s) if your institution has any of the 
following characteristics: 
o For-profit or non-profit organizations 
o Public or private institutions, such as universities, colleges, hospitals,                                 
and laboratories 
o Units of State and local governments
o Eligible agencies of the Federal government  
o Domestic or foreign

FUNDS AVAILABLE

The NIEHS intends to commit approximately $2 million in FY 2003, 2004 and 
2005 to fund new grants in response to this PAR. An applicant for an R21 
grant may request a project period of up to three years and a budget for 
total direct costs, including third party facilities and administrative 
costs, not to exceed $100,000 per year. Because the nature and scope of the 
proposed research will vary from application to application, it is 
anticipated that the size and duration of each award will also vary. Although 
the financial plans of the NIEHS provide support for this program, awards 
pursuant to this PAR are contingent upon the availability of funds and the 
receipt of a sufficient number of meritorious applications. 

INDIVIDUALS ELIGIBLE TO BECOME PRINCIPAL INVESTIGATORS

Any individual with the skills, knowledge, and resources necessary to carry 
out the proposed research is invited to work with their institution to 
develop an application for support. Individuals from underrepresented racial 
and ethnic groups as well as individuals with disabilities are always 
encouraged to apply for NIH programs.

WHERE TO SEND INQUIRIES

We encourage your inquiries concerning this PAR and welcome the opportunity 
to answer questions from potential applicants. Inquiries may fall into two 
areas: scientific/research, and financial or grants management issues:

o Direct your questions about scientific/research issues related to the 
reproductive/endocrine area to:

Jerry Heindel, Ph.D.
Scientific Program Administrator
Organs and Systems Toxicology Branch
Division of Extramural Research and Training
National Institute of Environmental Health Sciences
P.O. Box 12233 (EC-23)
Research Triangle Park, NC 27709
Telephone: 919-541-0781
FAX:  919-541-5064
Email: heindelj@niehs.nih.gov

o Direct your questions about scientific/research issues related to the 
cardiopulmonary area to:

J. Patrick Mastin, Ph.D.
Scientific Program Administrator
Organs and Systems Toxicology Branch
Division of Extramural Research and Training
National Institute of Environmental Health Sciences
P.O. Box 12233  (EC-23)
Research Triangle Park, NC 27709
Telephone: 919-541-3289
FAX: 919-541-5064
Email: mastin@niehs.nih.gov

Direct your questions about scientific/research issues related to the 
neurodegenerative area to:

Annette Kirshner, Ph.D.
Scientific Program Administrator
Organs and Systems Toxicology Branch
Division of Extramural Research and Training
National Institute of Environmental Health Sciences
P.O. Box 12233 (EC-23)
Research Triangle Park, NC 27709
Telephone: 919 541-0484
FAX: 919-541-5064
Email: kirshner@niehs.nih.gov

o Direct your questions about financial or grants management matters to:

Ms. Lerlita Garcia
Grants Management Specialist
Grants Management Branch
Division of Extramural Research and Training
National Institute of Environmental Health Sciences
P.O. Box 12233 (EC-22)
Research Triangle Park, NC 27709
Telephone: 919-316-4638
FAX: 919-541-2860
Email: garcia@niehs.nih.gov

Although not participating in this PA, the National Institute on Drug
Abuse (NIDA) is interested in funding research aimed at understanding the 
physiological and neurobiological consequences of in utero exposure to drugs 
of abuse, including inhalants (e.g. Toluene) that may be abused by pregnant 
women. NIDA is also interested in understanding the neurobiological 
consequences of in utero exposure of environmental chemicals that may confer 
risk or vulnerability to substance abuse disorder later in life. For more 
information on NIDA's pre-clinical in utero exposure program, please contact 
Dr. Pushpa Thadani at 301-443-6300, email: pt24e@nih.gov

LETTER OF INTENT
 
Prospective applicants are asked to submit a letter of intent that includes 
the following information:

o Descriptive title of the proposed research
o Name, address, and telephone number of the Principal Investigator
o Names of other key personnel 
o Participating institutions
o Number and title of this PA

Although a letter of intent is not required, is not binding, and does not 
enter into the review of a subsequent application, the information that it 
contains allows NIEHS staff to estimate the potential review workload and 
plan the review.
 
The letter of intent is to be sent by the date listed at the beginning of 
this document. The letter of intent should be sent to:

Ethel Jackson D.D.S.
Chief, Scientific Review Branch
Division of Extramural Research and Training
National Institute of Environmental Health Sciences
P.O. Box 12233, EC-30
(79 T.W. Alexander Drive, 4401 Bldg, 3rd Floor) express mail
Research Triangle Park, NC 27709
Telephone:  919-541-7846
FAX: 919-541-2503 
Email: jackson4@niehs.nih.gov

SUBMITTING AN APPLICATION

Applications must be prepared using the PHS 398 research grant application 
instructions and forms (rev. 5/2001). The PHS 398 is available at 
http://grants.nih.gov/grants/funding/phs398/phs398.html in an interactive 
format. For further assistance contact GrantsInfo, Telephone (301) 710-0267, 
Email: GrantsInfo@nih.gov.

Applicants should note that R21 applications have a page limitation of 15 
pages for the Research Plan. 

APPLICATION RECEIPT DATES

Applications submitted in response to this PA will be accepted on August 12, 
of 2002, 2003 and 2004.

SPECIFIC INSTRUCTIONS FOR MODULAR GRANT APPLICATIONS

Applications requesting up to $250,000 per year in direct costs must be 
submitted in a modular grant format. The modular grant format simplifies the 
preparation of the budget in these applications by limiting the level of 
budgetary detail. Applicants request direct costs in $25,000 modules.  
Section C of the research grant application instructions for the PHS 398 
(rev. 5/2001) at http://grants.nih.gov/grants/funding/phs398/phs398.html 
includes step-by-step guidance for preparing modular grants. Additional 
information on modular grants is available at 
http://grants.nih.gov/grants/funding/modular/modular.htm.

SENDING AN APPLICATION TO THE NIH

Submit a signed, typewritten original of the application, including the 
Checklist, and four signed, photocopies, in one package to:
 
Center for Scientific Review
National Institutes Of Health
6701 Rockledge Drive, Room 1040, MSC 7710
Bethesda, MD  20892-7710
Bethesda, MD  20817 (for express/courier service)
 
At the time of submission, one additional copy of the application must be 
sent to:

Ethel Jackson D.D.S.
Chief, Scientific Review Branch
Division of Extramural Research and Training
National Institute of Environmental Health Sciences
P.O. Box 12233 (EC-30)
(79 T.W. Alexander Drive, 4401 Bldg, 3rd floor) express mail
Research Triangle Park, NC 27709
Telephone: 919-541-7846
FAX: 919-541-2503 
Email: jackson4@niehs.nih.gov

APPLICATION PROCESSING

Applications must be received by or mailed before the receipt dates described 
above. The CSR will not accept any application in response to this PA that is 
essentially the same as one currently pending initial review unless the 
applicant withdraws the pending application. The CSR will not accept any 
application that is essentially the same as one already reviewed. This does 
not preclude the submission of a substantial revision of an application 
already reviewed, but such application must include an Introduction 
addressing the previous critique.

PEER REVIEW PROCESS
 
Upon receipt, applications will be reviewed for completeness by the CSR and 
responsiveness by the NIEHS. Incomplete and/or non-responsive applications 
will be returned to the applicant without further consideration.

Applications that are complete and responsive to the PA will be evaluated for 
scientific and technical merit by an appropriate peer-review Special Emphasis 
Panel convened by the CSR in accordance with the review criteria stated 
below. As part of the initial merit review, all applications will:

o Receive a written critique.
o Undergo a process in which only those applications deemed to have the 
highest scientific merit, generally the top half of the applications under 
review, will be discussed and assigned a priority score.
o Receive a second level review by the NIEHS National Advisory Council.
	
REVIEW CRITERIA

The goals of NIH-supported research are to advance our understanding of 
biological systems, improve the control of disease, and enhance health. In 
the written comments, reviewers will be asked to discuss the following 
aspects of your application in order to judge the likelihood that the 
proposed research will have a substantial impact on the pursuit of these 
goals: 

o Significance 
o Approach 
o Innovation
o Investigator
o Environment
  
The scientific review group will address and consider each of these criteria 
in assigning your application's overall score, weighting them as appropriate 
for each application. Your application does not need to be strong in all 
categories to be judged likely to have major scientific impact and thus 
deserve a high priority score. For example, you may propose to carry out 
important work that by its nature is not innovative but is essential to move 
a field forward.

(1) SIGNIFICANCE: Does your study address an important problem? If the aims 
of your application are achieved, how do they advance scientific knowledge?  
What will be the effect of these studies on the concepts or methods that 
drive this field?

(2) APPROACH: Are the conceptual framework, design, methods, and analyses 
adequately developed, well integrated, and appropriate to the aims of the 
project? Do you acknowledge potential problem areas and consider alternative 
tactics?

(3) INNOVATION: Does your project employ novel concepts, approaches or 
methods? Are the aims original and innovative? Does your project challenge 
existing paradigms or develop new methodologies or technologies?

(4) INVESTIGATOR: Are you appropriately trained and well suited to carry out 
this work? Is the work proposed appropriate to your experience level as the 
principal investigator and to that of other researchers (if any)?

(5) ENVIRONMENT: Does the scientific environment in which your work will be 
done contribute to the probability of success? Do the proposed experiments 
take advantage of unique features of the scientific environment or employ 
useful collaborative arrangements? Is there evidence of institutional 
support?
	
For R21 applications, the above stated criteria will be reviewed but it will 
be noted that the R21 is a developmental/exploratory grant mechanism that is 
used for high risk/high impact projects to generate preliminary data to 
develop novel hypotheses. Therefore, review standards for preliminary data 
and past performance are not applicable for this mechanism.

RECEIPT AND REVIEW SCHEDULE

Letter of Intent Receipt Date:    July 10, 2002, 2003, 2004
Application Receipt Date:         August 12, 2002, 2003, 2004
Peer Review Date:                 November 2002, 2003, 2004
Council Review:                   February 2003, 2004, 2005
Earliest Anticipated Start Date:  April 2003, 2004, 2005

AWARD CRITERIA

Applications submitted in response to a PA will compete for available funds 
with all other recommended applications. The following will be considered in 
making funding decisions:  

o Scientific merit of the proposed project as determined by peer review.
o Availability of funds. 
o Relevance to program priorities.

REQUIRED FEDERAL CITATIONS
 
PUBLIC ACCESS TO RESEARCH DATA THROUGH THE FREEDOM OF INFORMATION ACT

The Office of Management and Budget (OMB) Circular A-110 has been revised to 
provide public access to research data through the Freedom of Information Act 
(FOIA) under some circumstances. Data that are (1) first produced in a 
project that is supported in whole or in part with Federal funds and (2) 
cited publicly and officially by a Federal agency in support of an action 
that has the force and effect of law (i.e., a regulation) may be accessed 
through FOIA. It is important for applicants to understand the basic scope of 
this amendment. NIH has provided guidance at 
http://grants.nih.gov/grants/policy/a110/a110_guidance_dec1999.htm.

Applicants may wish to place data collected under this PA in a public 
archive, which can provide protections for the data and manage the 
distribution for an indefinite period of time. If so, the application should 
include a description of the archiving plan in the study design and include 
information about this in the budget justification section of the 
application. In addition, applicants should think about how to structure 
informed consent statements and other human subjects procedures given the 
potential for wider use of data collected under this award.

URLs IN NIH GRANT APPLICATIONS OR APPENDICES

All applications and proposals for NIH funding must be self-contained within 
specified page limitations. Unless otherwise specified in an NIH 
solicitation, Internet addresses (URLs) should not be used to provide 
information necessary to the review because reviewers are under no obligation 
to view the Internet sites. Furthermore, we caution reviewers that their 
anonymity may be compromised when they directly access an Internet site.

HEALTHY PEOPLE 2010

The Public Health Service (PHS) is committed to achieving the health 
promotion and disease prevention objectives of "Healthy People 2010," a PHS-
led national activity for setting priority areas. This PA is related to one 
or more of the priority areas. Potential applicants may obtain a copy of 
"Healthy People 2010" at http://www.health.gov/healthypeople.

AUTHORITY AND REGULATIONS

This program is described in the Catalog of Federal Domestic Assistance No. 
93.3113 and 93.114, and is not subject to the intergovernmental review 
requirements of Executive Order 12372 or Health Systems Agency review.  
Awards are made under authorization of Sections 301 and 405 of the Public 
Health Service Act as amended (42 USC 241 and 284) and administered under NIH 
grants policies described at http://grants.nih.gov/grants/policy/policy.htm 
and under Federal Regulations 42 CFR 52 and 45 CFR Parts 74 and 92.
 
The PHS strongly encourages all grant recipients to provide a smoke-free 
workplace and discourage the use of all tobacco products. In addition, Public 
Law 103-227, the Pro-Children Act of 1994, prohibits smoking in certain 
facilities (or in some cases, any portion of a facility) in which regular or 
routine education, library, day care, health care, or early childhood 
development services are provided to children. This is consistent with the 
PHS mission to protect and advance the physical and mental health of the 
American people.

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