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ENVIRONMENTAL EPIDEMIOLOGY RESEARCH CORE
Research Core Director: Roy E. Shore, Ph.D., Dr.P.H.

The focus of the Environmental Epidemiology Research Core is to gain new understanding of the impact of environmental factors upon human health and of the joint effects of environmental and host susceptibility factors. Identification of environmental determinants or co-factors in disease can lead to interventions that will reduce the burden of disease for exposed populations. It is clear that a range of susceptibilities to toxic exposures exists in the population, so that identification of the most susceptible, whether due to genetic predisposition, age, ethnic variation or other co-acting exposures, will help ensure the protection of vulnerable members of our society. To address these issues, the epidemiologic portfolio includes studies of the etiology of health disorders related to a number of environmental agents. The studies also seek to identify subsets of persons who are at risk of disease by using biological markers of exposure, biological damage or susceptibility to disease. A number of studies are being conducted by the Environmental Epidemiology Research Core in collaboration with members of other disciplines�toxicology, molecular biology, genomics, proteomics, health physics, pathology and clinical medicine�with the aim of elucidating the roles of environmental risk factors and their joint action with genetic or biochemical factors in disease etiology. The ongoing studies have a variety of disease endpoints, such as various cancers and non-malignant respiratory disease. They examine a variety of environmental exposures, including ionizing radiation, heavy metals, pesticides, asbestos, cigarette smoke, dietary factors, and medications

HUMAN EXPOSURE AND HEALTH EFFECTS RESEARCH CORE
Research Core Director: Morton Lippmann, Ph.D.

This Research Core is focused on defining the relationships between human exposure to ambient and occupational air pollution and their health effects, with an emphasis on the physical and chemical components of exposure atmospheres and their specific influences on health-related indices. Our advances in exposure assessment include the development of a new technique for determining the number concentration of ultrafine acidic droplet aerosols and improved characterization of carbonaceous fine particles and their spatial variation within urban areas and in the regional northeastern U.S. background aerosol. With the support provided by the Facility Cores, we have also developed technologies and procedures to characterize the temporal day-to-day variations in ambient aerosol composition over extended periods of time in order to correlate such changes with the daily variations in health-related responses being observed in mice exposed to concentrated ambient air particulate matter (CAPs) in studies being carried out in collaboration with the Systemic Toxicology Research Core. In terms of the characterization of health effects in human populations, we are extending our capabilities beyond studies that rely on non-specific mass concentrations of PM10 and/or PM2.5 to associations between mortality and morbidity and specific source-related pollution signatures for both acute and cumulative health effects. We are applying these new approaches to populations of particular concern, including asthmatic children in the South Bronx region of New York City and to residents of Lower Manhattan and Brooklyn who were acutely exposed to dust and smoke following the collapse of the World Trade Center (WTC) buildings on September 11, 2001. This involves utilization of air samples that we were able to collect at the NYU Downtown Hospital (5 blocks east of the WTC) on a daily basis beginning on September 14, 2001, and (in a collaborative study with the New Jersey NIEHS Center) on satellite imaging and meterological modelling of the fine plume exposures and their effects on hospital admissions for residents of Brooklyn in the days following September 11, 2001. Other notable strengths of the Core faculty include respiratory tract dosimetry and the modelling and analysis of temporal and spatial variations of air pollution exposure and other environmental variables that can influence or confound associations between measures of ambient air pollution and population based data on mortality and morbidity.

SYSTEMIC TOXICOLOGY RESEARCH CORE
Research Core Director: Terry Gordon, Ph.D.

The broad goal of the Systemic Toxicology Research Core is to obtain an understanding of responses resulting from exposure to environmental chemicals, the mechanisms underlying these effects, and the relationship between such effects and the pathogenesis of human disease. An important aspect of many studies within the Core is the evaluation of exposure factors, which modulate biological responses. While high concentrations of toxicants in occupational settings are clearly associated with overt disease, the role of exposure to lower ambient concentrations in the exacerbation of preexisting disease states, or in the induction of new ones, is less clear. Many projects within the Core are, thus, characterized by the use of relatively low levels of exposure, so as to better model the ambient situation and to avoid the need to extrapolate toxicology information from very high experimental exposure levels A critical factor in the ability to develop experimental atmospheres appropriate to "real" human exposure situations is the availability of specific Facility Cores within the Center. The research approaches within the Core are quite broad, extending from molecular to cellular to whole animal levels. While most studies employ experimental animals, human exposure studies have been performed in collaboration with other Research Cores within the Center. The problems of environmental health effects are complex, and their study clearly requires interdisciplinary assessments. The ability to examine effects of pollutant chemical exposure at multiple investigatory levels and using both in vivo and in vitro exposure methodologies allows for the development of an integrated, mechanistic evaluation of toxicant action and disease pathogenesis. Almost all studies within the Core are multidisciplinary in nature and cross traditional discipline boundaries, both within this Research Core and between Systemic Toxicology and other Research Cores in the Center. This is clearly reflected by the extent of research collaborations within individual projects and associated with publications. Current and recent research projects within the Core examine environmental influences upon the respiratory, immune, and cardiovascular systems. Studies involving the respiratory system make up the largest component of the research portfolio, and inhalation provides the major route of exposure for the projects within the Core. This has been a traditional focus of the Core, and is consistent with the long history of the Department of Environmental Medicine in the area of inhalation toxicology and its reputation for outstanding research accomplishments in this field over the past 50 years.

MOLECULAR TOXICOLOGY AND CARCINOGENESIS RESEARCH CORE
Research Core Director: Toby Rossman, Ph.D.

A primary goal of this Core is to elucidate the effects of environmental agents on structure and function at the cellular and gene expression levels and on DNA and other macromolecules, including factors involved in transcriptional control, and to identify mechanisms conferring resistance to environmental agents. A major focus of this Core is the etiology of cancer. A significant proportion of human cancers are attributable to environmental (including lifestyle) factors and to genetic susceptibility to those factors. Thus, it is important to gain a better understanding of the basic mechanisms underlying the environmental origins of human cancer as well as genetic factors affecting susceptibility to environmental agents. We believe that this information is crucial for designing better strategies for human cancer prevention and treatment. A central hypothesis guiding this research is that mutations and/or gene silencing lead to the loss of homeostatic regulatory mechanisms resulting in the development of cancer. These genetic changes may be the result of direct interactions with DNA of exogenous carcinogens or endogenous carcinogenic substances, such as reactive oxygen species or other stresses including effects on signaling pathways that promote the formation of mutations or changes in methylation status. The physiologic and genetic cellular factors may greatly affect not only the susceptibility of the cell�s genome or specific genes to DNA damaging agents, but also how the damage is processed. The cell may repair the damage with differing efficiency depending on the nature of the damage itself and on environmental agents that can influence the efficiency of DNA repair. A major area of research pertains to interventions that can inhibit or prevent the development of cancer and other toxicant-induced effects. While this Core is particularly strong in studies on inorganic compounds, such as arsenic, nickel, chromium and cadmium, the research of this Core is not limited to these compounds. The molecular toxicological effects of metals and other agents are studied by examining their interactions with DNA and with proteins that have structural, regulatory or enzymatic activities (such as metabolic enzymes, DNA repair proteins, and signaling proteins). The biochemistry of metal-mediated active oxygen species and the biological effects that result from such reactive radicals is of great interest to several members of this Core. Another factor governing the extent to which cellular DNA is damaged by exogenous carcinogens are the toxifying and detoxifying enzymes of the endoplasmic reticulum, which metabolize xenobiotics. The inducibility of such enzymes and the coding regions of the genes that encode for them show genetic variation which may influence susceptibility to cancer. Information about genetic variation may enable us to develop biomarkers to monitor the exposure to environmental carcinogens and develop effective measures for cancer prevention. Other areas of interest include signal transduction changes by environmental agents and the effects of estrogen-like compounds on gene expression.