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Record Count: 13
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header (Title, Principal Investigator, Institution, City, ST, Award Code, or
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DESCRIPTION (provided by applicant): Air quality intervention in developing countries is a new phenomenon. Delhi, the Capital of India, has witnessed a series of air quality interventions in recent years, which provides a natural experimental setting to evaluate the health effects of change in air quality in response to these interventions. Two overarching goals of this application are: (a) to evaluate the feasibility of satellite remote sensing to estimate daily air quality at different geographic scales, particularly for developing countries, which lack adequate coverage of air pollution monitoring, and (b) to assess the burden of mortality alleviated in response to these interventions in Delhi by differencing the cause-specific mortality with reference to air pollution in pre- (2000-02) and post-regulation (2004-06) periods. The spatially detailed air pollution data are unavailable for the study area. Nevertheless, an air pollution field campaign data collected during July-December 2003 at 113 sites in Delhi and its surroundings will be used to develop an empirical relation between ground measurements at these sites and satellite based aerosol optical depth (AOD). Exploiting this empirical relationship, the daily AOD will be used to predict daily estimates of airborne particles =2.5¿m, = 10¿m in aerodynamic diameter (PM2.5 and PM10, respectively) and PM10-2.5, after controlling for meteorological conditions at a spatial resolution = 5km. Although AOD can be computed using the data from various sensors, we will use data from Moderate Resolution Radiospectrometer (MODIS), onboard Terra and Aqua satellites, because these two satellites together capture both peak and off-peak estimates of air quality. Satellite data missing due to cloud cover will be filled using multiple imputation techniques within a Bayesian framework. An empirical relationship between the personal exposure of 4000 subjects (interviewed from January-April 2004) and their ambient exposure will be established. This relationship, in turn, will be used to predict the personal exposure for all cases of mortality for the entire study period. A Bayesian hierarchical model will be employed to examine cause- specific morality with reference to estimated personal exposure and potential confounders at different spatial-temporal scales. To evaluate the impact of air quality interventions on morality we propose differencing mortality and personal exposure association for infants, age cohorts with relatively stable migration pattern (30 to 40 years) and different age-sex groups across time, i.e. pre and post regulation time windows, and across Delhi and Kanpur in both pre- and post-regulation periods. PUBLIC HEALTH RELEVANCE: The findings of this research will advance our understanding of the health benefits of air quality interventions in developing countries, which in turn will be useful for enforcing the similar regulations in other cities of developing countries to protect human health.
DESCRIPTION (provided by applicant): Alexandrium tamarense is a unicellular dinoflagellate protist that causes harmful algal blooms (HABs) and paralytic shellfish poisoning through the production of saxitoxins. Very little is known about the factors that influence the formation of HABs, their recent spread to new areas, and the genes involved in toxin production. Our work also shows that dinoflagellates are outstanding models for understanding endosymbiosis (organelle genesis) and horizontal gene transfer because of their unparalleled ability to host different plastid endosymbionts and to accumulate genes through horizontal gene transfer. Here we propose to generate a significant genomics resource for Alexandrium to accelerate research on the biology and control of HABs and on nuclear genome evolution in dinoflagellates. Our specific aims are to use a highly efficient gene discovery strategy to generate a comprehensive expressed sequence tag (EST) unigene set for Alexandrium. Phylogenomic and detailed phylogenetic analysis of the different sequences in the Alexandrium unigene set will result in trees that help elucidate the contribution of horizontal gene transfer from endosymbionts and other sources to dinoflagellate nuclear genome evolution. We will also use massively parallel signature sequencing analysis to create a transcriptome tag database for Alexandrium cells grown in different culture conditions that affect nutrient physiology, cell and life cycle stages, and toxin production. This work will help us identify target genes involved in these functions and will form the basis for future microarray analyses. This proposal is an integrated, collaborative effort that relies on expertise in molecular evolution, EST processing, and phylogenomics (Bhattacharya, Scares), high quality cDNA library construction (Scares), and expertise in the ecology and physiology of Alexandrium (Anderson). The results of this study will result in a valuable molecular resource for scientists working to understand the ecology and toxicity of HAB species like Alexandrium and will provide the first comprehensive genomics resource for these fascinating protists.
DESCRIPTION (provided by applicant)
Environmental health sciences has evolved from studies that link a single exposure with a disease, to a new understanding of complex mechanisms by which agents in the environment interact at the molecular level to induce disease in individuals who are susceptible by virtue of age, genetics, nutrition, underlying disease or concurrent exposures. While methods of characterizing exposure and disease have improved, challenges remain when there are multiple exposures and the pathogenesis involves complex genetic and host factors. This is particularly apparent among rural populations with a multiplicity of chemical and biological exposures. This application is to continue funding of the Iowa Environmental Health Sciences Research Center (EHSRC) which has as its overarching theme, research and outreach on the adverse health effects of environmental contaminants among rural and agricultural populations. The EHSRC is at the forefront of research on environmental health problems such as rural asthma and other environmental lung diseases, bioaerosol-induced inflammation, innate immune responses to inhaled microorganisms, mechanisms of oxidative stress, and pesticide metabolism. The Center's focus on the rural environment provides the opportunity to conduct innovative mechanistic and population-based research and to translate that research to prevention and treatment through public health initiatives and clinical advancements. Junior scientists are trained to characterize biological response mechanisms and elucidate gene-environment interactions underlying environmental disease. The interdisciplinary research is organized around three Research Clusters: Inflammation & Innate Immunity, Oxidative Stress & Metabolism, and Environmental Lung Disease. A new initiative is the formation of an Environmental Genomics Research Cluster. Three Facility Cores provide cutting edge services and equipment: Integrative Health Sciences Facility, Pulmonary Toxicology Facility, and Environmental Modeling & Exposure Assessment Facility. An Administrative Core manages a highly effective Pilot Grant Program, Career Development Program, and Community Outreach & Education Core. Center goals are: 1) To coordinate and nurture innovative interdisciplinary EHS research with a focus on reducing adverse health effects of environmental contaminants, especially among rural populations; 2) To promote and enhance multi-disciplinary collaborations among basic scientists and physician researchers; 3) To recruit investigators from within and outside EHS by providing support for Research Clusters and dedicated Facility Cores; 4) To provide mentoring, research resources, and salary support to stellar junior investigators to develop their research careers in EHS; and 5) To provide outreach and education to translate research findings to improve the health and environment of rural people.
BACKGROUND
The Environmental Health Science Research Center (EHSRC) is located in the upper Midwest at the University of Iowa. With its main activities focused in the Schools of Medicine and Public Health, the Center has concentrated on environmental health problems located primarily in Iowa and neighboring areas, although wider collaborations nationally and internationally have been features since the early beginnings of this Center.
The EHSRC has been funded by the NIEHS since 1993. During that time it has had two Directors, Dr. James Merchant (1993-2003) and Dr. Peter Thorne (2003-present). The primary areas of research focus have been in areas of respiratory biology and airborne environmental exposures, environmental epidemiology and health surveys in relation to environmental exposures, exposure assessment, and the control of environmental exposures, primarily through engineering methods. An occupational medicine component was dropped in 2003.
During the previous review, concerns in several areas of the Center were noted that resulted in only three years of funding. Significant changes in the Center's structure have occurred in over the past years, partly in response to the concerns of the previous review and from input from NIEHS staff.
The structure of the Center's Research and Facility Cores since 2003 is well described in the application. The changes in structure were decided and implemented by the Director based on input from the Internal Advisory Committee and the External Advisory Committee. The most significant changes were a greater focus on environmental lung diseases and dropping the former Environmental Assessment and Control Core and the Exposure Assessment Facility. These latter components have been included in a new Iowa Superfund Program funded by the US EPA. The former Exposure Assessment Facility has been replaced by an Environmental Modeling and Exposure Assessment Facility that focuses on airborne exposures. In addition, elements of the Clinical Sciences Facility, with components of the Laboratory for Radiologic Imaging and the Asthma Center, were combined to form the Integrative Health Sciences Facility Core. The Inhalation Toxicology Facility was renamed the Pulmonary Toxicology Core. Reallocation of resources from five to three facility cores has provided three well funded cores that are responsive to the revised vision of the center.
Over the same period, the Research Cores underwent some consolidation and restructuring also. Elements of the Environmental Epidemiology Core and Health Registry Facility were refocused and combined with other components to create the areas of pulmonary health outcomes research and the new Environmental Lung Disease Research Cluster. The basic science components were defined from several previous areas to create an Inflammation and Innate Immunity Cluster and an Oxidative Stress and Metabolism Cluster in order to take advantage of areas of growing expertise at the University of Iowa that complemented the new focus of the Center.
The resulting redefinition of the EHSRC, in terms of its core research and facilities, now demonstrates a more focused and clearer vision, with better defined goals and objectives.
ESSENTIAL CHARACTERISTICS
Strategic Vision and Impact on Environmental Health
Crisp Terms/Key Words: rural health, clinical research, pollution related respiratory disorder, health science research support, environmental health, biomedical facility, air pollution, agriculture
DESCRIPTION (provided by applicant)
The Superfund basic research program at the University of Iowa (ISBRP) is a joint endeavor involving basic, mechanistic and applied projects in biomedical and non-biomedical research areas. The program's overall theme is the consequences of atmospheric sources and exposures to semi-volatile Polychlorinated Biphenyls (PCBs), and it deals with volatilization, transport and exposure of lower halogenated PCBs, especially those PCBs that are associated with contaminated waters, former industrial sites, other atmospheric sources, and the consequences of exposure to them. We plan to identify routes of exposure with an eye to preventing or limiting exposure and ameliorating the effects. The ISBRP brings together 15 scientists, representing 5 departments in 4 colleges. Working together, they will measure sources, transport and environmental exposure of PCBs (project #4 and #6); their distribution, metabolism and toxicity in animals and humans (project #1, #2 and #3); and novel methods of phytoremediation (project #5). Studies include a community-based participatory research project-an assessment of exposures to citizens who live or work in the vicinity of sources of lower chlorinated PCBs in the Chicago Metropolitan area. We enjoy the cooperation of citizen groups in Chicago, where many ethnic-minority citizens are living below the poverty line near deindustrialized sites. Our research projects and overall efficiency are supported by seven cores- Administration, Synthesis, Analytical, Inhalation Toxicology, Training, Research Translation and Community Outreach -through which program and project administrators will oversee coordination, information transfer, design and analysis of experiments, and assessment of research. The assessment process culminates in an annual meeting of our 8-member External Advisory Committee. The Synthesis Core will synthesize all compounds/mixtures to be studied while the Analytical Core provides critical compositional information from metabolism to movement. Community Outreach and Research Translation Cores will transmit research findings to a variety of stakeholders and involve those stakeholders in research activities. A Training Core and the research projects provide for the training of more than 20 students and postdoctoral scholars. Overall this multidisciplinary program brings abroad range of experience and expertise to bear on problems associated with Superfund chemicals that are critical to the Midwest and the nation.
Acetylcholinesterase inhibiting pesticides (i.e., organophosphate (OP) and carbamate pesticides) are widely used in the US and worldwide. Long-term neurological and neurobehavioral health effects of exposure to these pesticides are not well characterized. The investigators propose an epidemiological investigation of associations between long-term organophosphate and carbamate pesticide exposure and neurological and neurobehavioral health outcomes among approximately 700 pesticide applicators in Iowa and North Carolina (350 per state). Study participants will be recruited from among pesticide applicators currently enrolled in the Agricultural Health Study (AHS), a federally funded cohort study of licensed pesticide applicators from Iowa and North Carolina. Detailed information about individual exposure to a wide range of pesticides is available from the AHS. Applicators have been observed to experience wide variation in cumulative pesticide exposure making them suitable for investigation of health effects. Neurological and neurobehavioral health outcomes will be assessed with a battery of validated neurobehavioral tests that have been used successfully in previous investigations of neurotoxicant exposed individuals. The Primary Aim of the proposed investigation is to examine associations between cumulative lifetime exposure to the sum of all OP and carbamate pesticides and performance on selected measures of peripheral and central neurological function while controlling for effects of known covariates. A Secondary Aim of the proposal is to examine the effect of polymorphisms of paraoxonase, cytochromes P450, and glutathione-S-transferases (potential genetic modifiers of OP pesticide effect) on the association between exposure to OP pesticides and neurological and neuropsychological measures.
DESCRIPTION (provided by applicant): Exposure to environmental chemicals is a risk factor for Parkinson's Disease (PD). Specifically, pesticides used in agriculture, such as the organochlorine dieldrin, are associated with PD incidence; however, the link between exposure and disease is not known, and the underlying mechanisms remain to be determined. A potential pathway involves oxidative stress. Dieldrin, which is associated with PD incidence, has been shown to induce this injurious condition. However, it is not known how general oxidative stress, resulting from environmental exposure, can translate into specific dopaminergic toxicity. A proposed mechanism to account for this involves 3,4-dihydroxyphenylacetaldehyde (DOPAL), a dopamine (DA) derived neurotoxin. DA is metabolized to the toxic intermediate, DOPAL, which is oxidized via mitochondrial aldehyde dehydrogenase (mALDH) to 3,4-dihydroxyphenyl acetic acid (DOPAC) using the cofactor NAD. Aldehydes generated via oxidative stress, e.g., 4-hydroxynonenal (4HNE), are potent inhibitors of mALDH; therefore, cellular stress resulting from environmental agents may inhibit DOPAL metabolism yielding high levels of the DA-derived aldehyde. Furthermore, impairment of complex I, responsible for generation of mitochondrial NAD, has been observed for pesticides, and such an insult would also decrease the ability of mALDH to metabolize DOPAL. Preliminary data presented in this application demonstrate that both the oxidative stress product 4HNE and dieldrin yield inhibition of mitochondrial metabolism of DOPAL; furthermore, the DA-derived aldehyde is highly reactive toward proteins. Based on previous studies and preliminary data presented in this application, it is hypothesized that the organochlorine dieldrin inhibits cellular metabolism of DOPAL, yielding aberrant levels of this endogenous aldehyde neurotoxin and subsequent protein modification. To test the hypothesis, three specific aims will be completed. Specific Aim 1 will examine the ability of dieldrin to impair DOPAL metabolism in dopaminergic cells and elucidate the mechanism of inhibition. Specific Aim 2 will demonstrate protein adduction by the DA-derived aldehyde in cells treated with dieldrin. Specific Aim 3 will determine the extent of protein modification by DOPAL in vivo in a mouse model of chronic dieldrin dosing. The work proposed in this application is significant and innovative and will serve as a foundation for future research aimed at determining the role of environmetal exposure in PD pathogenesis.
DESCRIPTION (provided by applicant): Environmental exposure to high concentrations of manganese (Mn) results in adverse neurological deficits commonly referred to as Manganism. Manganese neurotoxicity is a significant toxicological problem resulting from the use of Mn as a gasoline additive, and its use in welding rods, pesticides, pharmaceutical preparations, alloy manufacturing, and in dry cell battery production, for instance. Mn predominantly accumulates in the basal ganglia structures including the globus pallidus and striatum area, but the cellular mechanisms underlying the neurotoxic effect of Mn in these target neurons are yet to be established. Recently, we have identified that protein kinase C-delta (PKCd), a member of the novel PKC isoform family, is a key pro-apoptotic kinase that is highly expressed in the basal ganglia, including striatal neurons, and serves as a key substrate for caspase-3. We also found that PKCd is proteolytically cleaved into regulatory and catalytic subunits by caspase-3 following Mn treatment to persistently increase its kinase activity, which further contributes to Mn-induced apoptosis in cell lines. Therefore, we propose to extend these preliminary findings to primary neuronal cultures obtained from striatum and mesencephalon and animal models by studying the following specific aims: i) To determine whether proteolytically cleaved PKCd by caspase-3 translocates to the nucleus in order to initiate key nuclear apoptotic events such as histone 2B, STAT1 and lamin B phosphorylation and DNA- PK inactivation, ii) To examine whether Mn exposure in an animal model induces caspase-3 dependent PKCd proteolytic activation, PKCd nuclear translocation, DNA-PK inactivation, and histone 2B, STAT1 and lamin B phosphorylation and finally, apoptotic cell death, and iii) To further confirm the involvement of PKCd in Mn-induced neurotoxicity by comparing the behavioral deficits, neurotransmitter depletion and neuronal degeneration in naive PKCd (+/+) and PKCd (-/-) animals. These specific aims will be delineated using cellular, molecular, and neurochemical approaches in relevant cell culture and animal models of Mn neurotoxicity. Collectively, experimental results of the proposed systematic studies will define the biochemical mechanisms underlying the apoptotic cell death process in Mn toxicity, and this knowledge will advance the development of interventional strategies for Mn neurotoxicity in humans.
DESCRIPTION (provided by applicant)
The response of the lungs in patients with significant exposure to asbestos is characterized by a prolonged, intense inflammatory response that often results in pulmonary fibrosis. The release of TNF-? by alveolar macrophages plays an integral role in the inflammatory response that occurs in the lungs of patients with asbestosis. A characteristic feature of the alveolar macrophages is that they spontaneously release TNF-? and they resemble monocytes. Data from the investigators show that monocytes produce a significant amount of TNF-? when stimulated in vitro with asbestos. In contrast to most stimuli, our novel data demonstrates that the p38 MAP kinase is a positive regulator and the ERK MAP kinase is a negative regulator of TNF-? production in response to asbestos stimulation. However, limited data is available on the upstream signaling pathways linking asbestos with TNF-? expression. The GTPase Rac1 is an upstream second messenger that plays an important role in inflammation. In this regard, our novel data also show that TNF-? production is augmented in monocytes over expressing Rac1, and Rac1 null mice are protected from developing pulmonary fibrosis after exposure to asbestos. The investigators hypothesize that Rac1 plays a pivotal role in differentially modulating MAP kinase activation and that this differential activation is critical for TNF-? gene expression in human monocytes stimulated with asbestos. In addition to our in vitro model, we will explore this in alveolar macrophages obtained from asbestosis patients and in an animal model of asbestosis. In Aim 1 we will focus most of our studies on the mechanism(s) by which Rac1 differentially modulates MAP kinase pathways. These studies will also determine if p38 inhibits expression of the ERK kinase by activating a dual specificity phosphatase. The use of wild-type and Rac1 null mice in a murine model of asbestosis will provide biological relevance. In Aim 2, we will first determine if Rac1 modulates TATA-binding protein (TBP) phosphorylation, which is essential for TNF-? gene expression. Since Rac1 has differential effects on MAP kinase activation, we will determine if an increase in p38 and a decrease in ERK activity are necessary for optimal TNF-? production. The investigators will also compare alveolar macrophages from asbestosis patients to normal subjects in regard to Rac1, p38, and ERK activity. The exposure of wild-type and Rac1 null mice to asbestos to determine the effect on the development of interstitial fibrosis will provide additional biological relevance.
DESCRIPTION (provided by applicant): Project Summary/Abstract: H2O2 is the most important ROS involved in cell signaling in the lung. PMA has been used to study H2O2-mediated signaling, but asbestosis is a good model to explore the role of H2O2 in cell signaling because asbestos is biologically relevant and is known to induce high levels of H2O2. The release of TNF-alpha by alveolar macrophages in asbestosis patients is critical in the development of the disease; however, the mechanism linking H2O2 generation to TNF-alpha production is not known. Another feature of asbestosis is that alveolar macrophages from patients resemble monocytes. Our data show that monocytes produce TNF-alpha when stimulated, in vitro, with asbestos unlike alveolar macrophages. Thus, human monocytes provide a good model to explore TNF-alpha gene expression, as it relates to H2O2 generation. In this regard, our preliminary data show that H2O2 is necessary for optimal production of TNF-alpha in monocytes and that the source of H2O2 is primarily from Cu,Zn-SOD. Our preliminary data also demonstrate that Cu,Zn-SOD is highly expressed in alveolar macrophages obtained from patients with asbestosis. Since our data shows that alveolar macrophages from asbestosis patients have a high level p38 MAP kinase activity and absent ERK activity and that H2O2 activates p38 and inhibits ERK, we hypothesize that H2O2 plays a pivotal role in differentially modulating MAP kinase activity, and Cu,Zn-SOD enhances differential MAP kinase activation and TNF-alpha production in human monocytes. We will use PMA in the initial studies to understand the role of H2O2 in cell signaling in addition to performing studies using asbestos, which is more biologically relevant. In Aim 1 we will determine if Cu,Zn-SOD-induced H2O2 modulates MAP kinase activation. Since MAP kinase activity is often controlled by phosphatases, we will investigate if H2O2 is oxidizing a phosphatase, MKP-1, and inducing expression of PP2A, which results in p38 activation and ERK inactivation, respectively. The comparison of H2O2 generation and MAP activation in wild-type and Cu,Zn- SOD KO mice will provide biological relevance. In Aim 2 we will determine if Cu,Zn-SOD-induced H2O2 increases TNF-alpha production in monocytes and if optimal TNF-alpha expression depends on differential MAP kinase activity. We will compare MAP kinase and Cu,Zn-SOD activity and H2O2 generation in alveolar macrophages obtained from asbestosis patients to normal macrophages. Additional biological relevance will be provided by investigating the development of interstitial fibrosis in wild-type and Cu,Zn- SOD KO mice. Project Narrative: Exposure to asbestos and other environmental agents, such as diesel exhaust and particulate matter, increase hydrogen peroxide generation in the lung. The goal of the project is to understand the mechanisms by which hydrogen peroxide causes lung injury and fibrosis. Although the studies in this proposal relate to asbestosis, they will also apply to other inflammatory and fibrotic lung diseases.
DESCRIPTION (provided by applicant):
The immediate objective of this Mentored Research Scientist Award is to allow Dr. Hans-Joachim Lehmler to make a successful transition to an independent investigator in the field of environmental toxicology. In the research component of this award, Dr. Lehmler will test the working hypothesis is that chiral environmental contaminants such as PCB 84 are enantioselectively metabolized by cytochrome P450, resulting in a selective enrichment of one enantiomer of PCB 84 in certain tissues. Alternatively, the enrichment of one PCB 84 enantiomer resulting from differential transport of PCB enantiomers by plasma proteins will be investigated. The specific aims are (1) to determine the enantioselectivity of the in vitro metabolism of PCB 84, (2) to study the binding of both PCB 84 enantiomers to mice and human serum proteins, and (3) to determine the distribution and disposition of PCB 84 enantiomers in female mice and the transfer of the enantiomers into the fetus and suckling offspring. This research component will be complemented by a vigorous career development plan which will include (1) formal training in biostatistics and the ethical conduct of research as part of the curriculum of the NIEHS training grant in the Department of Occupational and Environmental Health, (2) regular meetings with his mentors, collaborators and consultants, (3) participation in group meetings and departmental seminars, (4) presenting results at scientific meetings such as the PCB Workshop and (5) publishing in peer reviewed journals. It is envisioned that the multidisciplinary team of mentors, collaborators and consultants plays an active role in both the research as well as the career development component of this award. The long term career goal is to establish Dr. Lehmler as an investigator with independent research status and funding.
DESCRIPTION (provided by applicant): IL- 1¿ and LPS stimulate related receptors (IL-1R1 and TLR-4, respectively) from the Toll-like receptor family. Each of these receptors play an important role in either initiating or propagating signaling events that promote inflammation following exposure to bacterial endotoxin. IL-1R1 and TLR-4 share many similar effectors (MyD88, IRAK, TRAF6), but also have unique effectors (TIRAP/Mal, TRAM, TRIP), that specify unique biological properties of each receptor pathway. However, both receptors can stimulate NF-KB in a redox-dependent manner that involves NADPH oxidases (Nox). Our laboratory has recently described a unique mechanism whereby NADPH oxidases spatially regulate the redox-dependent activation of receptors at the level of the endosome. Our data suggests that LPS, IL- 1¿, and TNFa all signal via this mechanism to activate NF-KB. The goal of this proposal is to further define how redox-active endosomes facilitate the IL- 1¿ and LPS signaling pathways. I propose to study these mechanisms in cell culture and mouse models through the use of high throughput proteomics and by focusing on how Toll-like receptors activate Nox2 in the endosomal compartment. In Aim1, IL- 1¿ will be used as the model system to test the hypotheses that Nox2 enters redox-active endosomes from the plasma membrane (as opposed to early endosome fusion), that endocytosis is caveolin-1 mediated, and that Rac1 is activated by one of four candidate GEFs: ¿-Pix, Sos, Vav1, or P-Rex1. Experiments will utilize siRNA, chemical inhibitors and dominant negative mutants to dissect these pathways. In Aim 2, proteomic analyses of redox-active endosomes will be performed using both 2D gel / MOLDI TOF experiments and the use of tandem mass spectrometry. These studies will identify effector proteins in-common and unique to redox-active endosomes harboring ligand activated Toll- like receptors. Identifying unique proteins in the LPS pathway is of particular interest, as this could lead to key therapeutic targets for the treatment of sepsis. Further proteomic work will include the use of floxed Rac1, MyD88 KO, and Nox2 KO mice to generate mechanistic pathways of LPS and IL- 1¿ redox signaling. Statement of Relevance: This study will investigate novel aspects of inflammation caused by a common bacterial toxin called LPS. Results of this research will also translate into practical knowledge for many other types of environmental injuries that involve inflammation and reactive oxygen species. Eventually, this research could allow for the development of medical treatments to attenuate inflammation caused by LPS and other diseases involving inflammation.
DESCRIPTION (provided by applicant)
A current NIEHS awardee, the HMTRI submits this $2,000,000 five-year application on behalf members of the Community College Consortium for Health and Safety Training (CCCHST) serving Department of Energy (DOE) environmental restoration and waste management sites across the United States. They include, BWXT Pantex, TX; Hanford Site, WA; INEEL,ID; Paducah Gaseous Diffusion Plant, KY; Portsmouth Site, OH; Oak Ridge Operations, TN; and Savannah River Site. SC. The five-year goal is to train a minimum 12,500 workers, technicians, and supervisors, through 75,000 contact hours of training, to protect themselves, their facilities, and their communities from exposure to hazardous materials encountered during hazardous waste site clean-up, in the transportation of hazardous materials, and in the response to releases of hazardous materials. Each year, 2,500 students will successfully complete 250 courses for a total 15,000 contact hours of training. Annually, an average 100courses will be delivered online. HMTRI will support the University of Tennessee in Knoxville, TN, and Amarillo Community College in Amarillo, Texas as subawardees delivering training at these sites. Aiken Technical College will train at the Savannah River Site but does not anticipate enough training to justify a subaward. The number of CCCHSTDOE providers may increase in future years as new members request participation. HMTRI will provide hazardous materials curriculum for worker training and will develop web-supported learning objects to complement existing curriculum. HMTRI will provide a 1-800 technical assistance line and a website linking all sites, instructors and students. HMTRI will provide centralized record keeping and quality control for the consortium, submitting to NIEHS the number of students trained at CCCHST-DOE sites and their demographic data, conducting site audits, reviewing student evaluations, acting upon the guidance of the advisory committee, and mediating the delivery of training with other NIEHS-supported consortia.
DESCRIPTION (provided by applicant)
Kirkwood Community College's HMTRI, a current NIEHS awardee, submits this application on behalf of the Community College Consortium for Health and Safety Training (CCCHST). CCCHST membership consists of community colleges partnered with business and industry, universities, and community-based organizations offering a consistent and quality response to the national training need for hazardous waste workers and emergency response personnel.
The goal of CCCHST-HWWTP is to make NIEHS-approved worker training nationally available through more than 100 partners offering hazardous materials instruction (Hazwoper and related 29CFR 1910.120 training) in nearly all states of the nation through a train-the-trainer model program. CCCHST instructors, prepared and supported by HMTRI, will train a minimum 100,000 students, workers, and supervisors in nearly all states of the nation to protect themselves and their communities from exposure to hazardous materials encountered during hazardous waste site cleanup, Brownfields redevelopment, transportation of hazardous materials, and response to spills and releases of hazardous materials. CCCHST members will collectively offer 1,000,000 contact hours of instruction over a 5-year period at the cost of $5,876,499.
The goal of CCCHST-HDPTP is to train a minimum of 10,000 workers and provide a total 30,000 contact hours of instruction in Hazmat Disaster Preparedness Awareness, Response and Recovery courses over a 5-year period at the cost of $1,383,080. The goal of CCCHST-BMWTP is to support three subawardees who will train and place 250 minority youth, ages 18-25, over a 5-year period for environmental jobs. The subawardees are Civic Works, Baltimore; St. Louis Community College, MO; and El Paso Community College, TX. Cost is $$2,281,138.
Since 1992, HMTRI has received NIEHS funding to provide management, instructor training and certification, curriculum, textbooks, instructional aids, quality control, evaluation, and promotion for the members of the CCCHST national consortium, and most lately, the development of distance-supported education.
Hazardous Waster Worker Training Program (HWWTP)
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