Intervention and


PIPER collects environmental data mimicking a 2-year old's activity and proximity to the ground or floor

Directors: Joshua Miller, PhD and Andrew Gow, PhD

Members: Elisa Bandera, MD; Brian Buckley, PhD; Joanna Burger, PhD; Cristine Delnevo, PhD, MPH, FAAHB; Mingzhu Fang, PhD; Donald Gerecke, PhD; Peter Gillies, PhD; Michael Gochfeld, MD, PhD; Marion Gordon, PhD; Andrew Gow, PhD; A.N. Kong, PhD; Debra Laskin, PhD;Jeffrey Laskin, PhD; Robert Laumbach, MD, MPH, CIH; Kenneth Reuhl, PhD; Dipak Sarkar, PhD; Sue Shapses, PhD; Nanjoo Suh, PhD; Clifford Weisel, PhD; Chung S. Yang, PhD; Helmut Zarbl, PhD; Liping Zhao, PhD; Wei-Xing Zong

The Intervention and Prevention Research Core incorporates knowledge developed from integrated exposure and mechanistic studies to develop and implement targeted interventions and prevention strategies. Core members translate their findings into actionable interventions to (1) reduce exposures in affected or at risk populations, (2) modify high risk behaviors, and (3) develop chemopreventive agents to mitigate the development and progression of disease.

Members investigate:

  • Dietary constituents and environmental cancer: Chemoprevention of environmental cancer is a major research focus of investigators within this core. Collaborative studies led by C.S. Yang demonstrated cancer preventive activities of g-tocopherol, d-tocopherol and their mixtures in animal models for colon (C.S. Yang), lung (A. Gow), mammary (N. Suh) and prostate (A. Kong, C.S. Yang) carcinogenesis. D. Sarkar found that combining opiate antagonists and agonists persistently activates NK cells, contributing to the suppression of tumor growth. These studies suggested a new chemoprevention strategy using the endogenous opioid peptide, ß-endorphin.
  • Inflammatory cells and mediators as targets for intervention: Several models are being used to understand the nature and contribution of inflammatory cells accumulating in toxicant-exposed tissues to pathogenic processes. Using rodent and human models of air pollution exposure (e.g., ozone, PM, WTC dust), D. Laskin, J. Laskin, A. Gow and S. Hussain identified distinct subpopulations of activated lung macrophages. Studies in transgenic and chimeric mice showed that these subpopulations release different inflammatory mediators to regulate injury and repair, suggesting novel targets for targeted intervention.
  • Translational/human intervention studies: Using the Integrated Health Sciences Facility Core, H. Kipen, M. Fang, and H. Zarbl conduct an occupationally-based randomized trial to assess the ability of methylselenocysteine to mitigate the increased risk of breast and prostate cancer due to disruption of circadian rhythm during shift work, a probable human carcinogen Type 2A (IARC). C.S. Yang, in collaborative studies with the Cancer Institute of New Jersey (CINJ), completed a phase 0 intervention trial in prostate cancer patients. Randomized groups were administered a placebo or a mixture of tocopherols prior to prostatectomy. The blood and prostate levels of the g -T, d -T isomers and their degradation products were significantly increased by tocopherol supplements. J. Miller’s studies on the effects of folate and vitamin B12 supplementation showed that the differential metabolism of B12 by the microbiome is a determinant of cancer promotion.
  • Exposure guided interventions: CEED members use data obtained from personal and mechanized monitors to model exposures in order to develop and assess the efficacy of engineering controls and specific mitigation/cleanup strategies. For example, S. Shalat developed a Pre-toddler Inhalation Particulate Environmental Robot (PIPER) to guide interventions for reducing exposure of pre-toddlers to bacterial endotoxin in the home, with the goal of reducing childhood incidence of asthma. This approach is also used in collaboration with the Community Engagement Core to monitor efficacy of remediation in communities (i.e., chromium in Jersey City, NJ).

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