Welcome to the first issue of the new Environmental Health Perspectives:
it looks a lot different from the original journal, but the tradition of
dedication to good science remains unchanged. We have published 100 volumes
of EHP and this, volume 101, is a new beginning. We have changed
formats and provided new ones to accommodate the numerous varieties and
forms that scientific information can take. We want to publish the very
best environmental health research and at the same time provide a forum
for discussion and dissemination of information about what is going on in
the environment.
We want our readers to contribute to this enterprise by submitting research
manuscripts, writing letters, and sending us news. Your involvement is particularly
important because we believe that many environmental problems have arisen
today because of inadequate communications in the past. Traditionally, laboratory
researchers have tended to communicate primarily with each other, and the
dissemination of information to the public has been slow and haphazard.
It is clear that enhanced communications could contribute to the avoidance
of environmental crises through both increased understanding of the underlying
science and the identification of potential problems before they become
overwhelming, expensive, and perhaps irreversible.
This is the age of information, and we want EHP to be a focal
point, a forum, and a node through which environmental health issues are
identified, examined, and resolved. In view of these ambitions it is appropriate
that the date on the cover of our first issue be April 22, 1993, the 23rd
Anniversary of Earth Day. We are pleased to contribute to the celebration
of Earth Day 1993 by the inauguration of our revised journal dedicated to
the health of the environment. Our cover is a symbol of our focus, the planet
earth. Our cover provides a perspective of our planet reminding us that
the earth is finite in its scope, finite in its resources, and finite in
its ability to sustain life. Let us work together to make our planet a good
place to live; after all, it is the only home we have.
Gary E. R. Hook and George W. Lucier
Editors-in-Chief
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Opportunities in Environmental Health Science Research
The National Institute of Environmental Health Sciences and the National
Toxicology Program have important roles in preventing human disease and
containing the spiraling health and regulatory costs of the nation. The
coalescence of toxicological testing with basic and mechanistic research
brings the full range of scientific inquiry to bear on studies of the environment
and human disease. The explosion of new knowledge and technology over the
past 25 years provides the NIEHS/NTP with the tools necessary to hasten
the understanding of the interactions between the environment and individual
genetic susceptibility. This new knowledge can be applied to advance the
fields of environmental medicine, public health, environmental protection,
and risk assessment.
Environmental agents to which humans are exposed from conception to death
can have significant health effects. The contribution of the environment
to human disease and dysfunction is unknown, in part because environmentally
related effects involve complex interactions between environment and genetic
constitution over the course of many years. The interplay among the environment,
genes, and time in the etiology or progression of human diseases and dysfunctions
significantly complicates population-based environmental studies and makes
it difficult to establish causal relationships.
The NIEHS/NTP has always operated on the principle that the Institute's
research programs should be responsive and relevant to the needs of Americans
without sacrificing the quality of research excellence or inhibiting innovation.
The past 18 months has been marked by extensive review and strategic planning
to make certain that cutting-edge technologies are used to address a broad
spectrum of human health problems related to the environment. In addition
to the input of various advisory panels, meetings were held with many representatives
from Congress, Executive Branch agencies, environmental and labor groups,
private and public health care practitioners, industry groups, academic
researchers, and concerned citizens to understand their perceptions of the
role and potential of NIEHS/NTP to address their needs and concerns. Based
on these discussions and reviews, NIEHS/NTP has established new research
priorities that emphasize two critical areas of science: basic biology and
the environment and molecular prevention/intervention. Additionally, the
toxicological testing program will be expanded to include testing a larger
number of environmental agents and the development of a more experimental,
hypothesis-driven research component [see Olden (1) for a more extensive
discussion of the toxicological testing program].
New and expanded research into environmental influences on human health
must be carried out if we are to understand the full range of biological
processes and disease states of clinical importance. Therefore, consideration
of environmental agents as causes of human diseases must be accorded a high
priority in establishing the nation's health research agenda. To understand
environmentally associated human diseases, we need a better knowledge of
how chemical messages that originate outside the cell can modulate cell
function by switching genes on and off or by modulating signal transduction
pathways. In addition to understanding the nature of the molecular/cellular
interactions with environmental agents, we must relate the molecular or
cellular effects to the health status of the human organism.
Numerous environmental agents have been identified that interact with
and damage DNA; this may represent an important mechanism underlying many
human diseases and dysfunctions. Because genes and the proteins they encode
are responsible for all cellular function, control, communication, and regulation,
the interactions of environmental agents with genes and gene products can
lead to disruption of critical biological functions. However, susceptibility
of biological systems to environmental perturbation is likely to be highly
variable because the genetic make-up of each individual is different. The
ability of electrophilic chemicals to damage DNA and cause mutations has
been demonstrated for many chemicals, yet there are chemical teratogens
and carcinogens that show no propensity for interacting with or altering
DNA. Several of these chemicals have been shown to interact with receptor
proteins and perturb signal transduction systems involved in cellular growth
and differentiation. This phenomenon and other hypotheses for the mechanisms
by which environmental agents can be involved in the disease process will
be investigated by NIEHS/ NTP.
Thus, NIEHS has assigned high priority to identifying critical genes
and gene products involved in the environmental contribution to impairing
biological events that result in human disease and disability. Such genes
include oncogenes and tumor-suppressor genes, genes responsible for programmed
cell death, cell differentiation, and DNA repair, and genes responsible
for differences in individual susceptibility. Issues such as polymorphism
in drug-metabolizing and DNA repair enzymes and the role of gender and age
in enhancing or protecting against effects of environmental exposures have
also been assigned high priority. For example, the development of biomarkers
that can quantify individual exposure, the effect of that exposure, and
the likelihood of susceptibility to that exposure would greatly improve
our ability to prevent adverse health effects from exposure to environmental
factors. The mechanistic data generated from such studies can be used to
improve human risk assessment and to design prevention and intervention
strategies with improved efficacy.
Historically, prevention efforts in environmental public health have
been dominated by behavioral, engineering, and regulatory approaches aimed
at eliminating exposure to toxic substances. Although these efforts are
entirely appropriate and necessary as humane and cost-effective interventions,
the elimination of exposure to many ubiquitous environmental hazards may
take decades to achieve, even if the resources and trained workforce were
immediately available. Thus, there is a need to develop new molecular approaches
to prevention and intervention based on knowledge of the mechanisms of disease
etiology.
Human health and disease are outgrowths of molecular events. Understanding
the basic biology of the molecular event offers considerable promise for
preventing disease. With increased opportunities for elucidating the role
of the environment in the etiology of human disease, we should soon be able
to modify or manipulate both gene products and environmental exposures or
effects to prevent disease or to intervene in their progression before they
become debilitating. Possibilities include the design of receptor blockers
to intercept adverse effects of receptor-mediated environmental toxicant
action, development of molecules that could "turn off" activated
oncogenes before they lead to neoplastic disease, identification of molecules
that could "turn on" tumor-suppressor genes or DNA repair mechanisms
to block disease progression, and development of antimetabolites to block
the generation of active toxicants in biological systems.
Molecular prevention and intervention offer real savings both in terms
of human suffering and in containing health costs associated with treatment
of end-stage disease and rehabilitation. Research areas to be emphasized
include development of biomarkers of exposure, effect, and susceptibility,
development of a better understanding of growth regulation, and development
of animal models to replicate both early and late events in disease pathogenesis.
Kenneth Olden
Director, National Institute
of Environmental Health Sciences
I thank Dan C. VanderMeer, director of the NIEHS Office of Program
Planning and Evaluation, for assistance in preparing this editorial.
Reference
1. Olden K. Environmental health science research and human
risk assessment. Regul Toxicol Pharmacol 17 (in press).
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Last Update: August 26, 1998
