20
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Using Nutrition for Intervention and Prevention against Environmental Chemical Toxicity and Associated Diseases

      article-commentary

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Nutrition and lifestyle are well-defined modulators of chronic diseases. Poor dietary habits (such as high intake of processed foods rich in fat and low intake of fruits and vegetables), as well as a sedentary lifestyle clearly contribute to today’s compromised quality of life in the United States. It is becoming increasingly clear that nutrition can modulate the toxicity of environmental pollutants.

          Objectives

          Our goal in this commentary is to discuss the recommendation that nutrition should be considered a necessary variable in the study of human disease associated with exposure to environmental pollutants.

          Discussion

          Certain diets can contribute to compromised health by being a source of exposure to environmental toxic pollutants. Many of these pollutants are fat soluble, and thus fatty foods often contain higher levels of persistent organics than does vegetable matter. Nutrition can dictate the lipid milieu, oxidative stress, and antioxidant status within cells. The modulation of these parameters by an individual’s nutritional status may have profound affects on biological processes, and in turn influence the effects of environmental pollutants to cause disease or dysfunction. For example, potential adverse health effects associated with exposure to polychlorinated biphenyls may increase as a result of ingestion of certain dietary fats, whereas ingestion of fruits and vegetables, rich in antioxidant and anti-inflammatory nutrients or bioactive compounds, may provide protection.

          Conclusions

          We recommend that future directions in environmental health research explore this nutritional paradigm that incorporates a consideration of the relationships between nutrition and lifestyle, exposure to environmental toxicants, and disease. Nutritional interventions may provide the most sensible means to develop primary prevention strategies of diseases associated with many environmental toxic insults.

          Related collections

          Most cited references26

          • Record: found
          • Abstract: found
          • Article: not found

          Potential Role of Ultrafine Particles in Associations between Airborne Particle Mass and Cardiovascular Health

          Numerous epidemiologic time-series studies have shown generally consistent associations of cardiovascular hospital admissions and mortality with outdoor air pollution, particularly mass concentrations of particulate matter (PM) ≤2.5 or ≤10 μm in diameter (PM2.5, PM10). Panel studies with repeated measures have supported the time-series results showing associations between PM and risk of cardiac ischemia and arrhythmias, increased blood pressure, decreased heart rate variability, and increased circulating markers of inflammation and thrombosis. The causal components driving the PM associations remain to be identified. Epidemiologic data using pollutant gases and particle characteristics such as particle number concentration and elemental carbon have provided indirect evidence that products of fossil fuel combustion are important. Ultrafine particles < 0.1 μm (UFPs) dominate particle number concentrations and surface area and are therefore capable of carrying large concentrations of adsorbed or condensed toxic air pollutants. It is likely that redox-active components in UFPs from fossil fuel combustion reach cardiovascular target sites. High UFP exposures may lead to systemic inflammation through oxidative stress responses to reactive oxygen species and thereby promote the progression of atherosclerosis and precipitate acute cardiovascular responses ranging from increased blood pressure to myocardial infarction. The next steps in epidemiologic research are to identify more clearly the putative PM casual components and size fractions linked to their sources. To advance this, we discuss in a companion article (Sioutas C, Delfino RJ, Singh M. 2005. Environ Health Perspect 113:947–955) the need for and methods of UFP exposure assessment.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Dioxin: a review of its environmental effects and its aryl hydrocarbon receptor biology.

            A highly persistent trace environmental contaminant and one of the most potent toxicants known is dioxin (2,3,7,8-tetrachlorodibenzo-para-dioxin or TCDD). TCDD induces a broad spectrum of biological responses, including induction of cytochrome P-450 1A1 (CYP1A1), disruption of normal hormone signaling pathways, reproductive and developmental defects, immunotoxicity, liver damage, wasting syndrome, and cancer. Its classification was upgraded from "possible human carcinogen" (group 2B) to "human carcinogen" (group 1) by the International Agency for Research on Cancer (IARC) in 1997. Exposure to TCDD may also cause changes in sex ratio, and tumor promotion in other animals. Because of the growing public and scientific concern, toxicological studies have been initiated to analyze the short- and long-term effects of dioxin. TCDD brings about a wide variety of toxic and biochemical effects via aryl hydrocarbon receptor (AhR)-mediated signaling pathways. Essential steps in this adaptive mechanism include AhR binding of ligand in the cytoplasm of cells associated with two molecules of chaperone heatshock protein (Hsp90) and AhR interactive protein, translocation of the receptor to the nucleus, dimerization with the Ah receptor nuclear translocator, and binding of this heterodimeric transcription factor (present in CYP1A) to dioxin-responsive elements upstream of promoters that regulate the expression of genes involved in xenobiotic metabolism.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Effects of aryl hydrocarbon receptor signaling on the modulation of TH1/TH2 balance.

              An orally active antiallergic agent, M50367, skews the Th1/Th2 balance toward Th1 dominance by suppressing naive Th cell differentiation into Th2 cells in vitro. Administration results in the suppression of IgE synthesis and peritoneal eosinophilia in vivo. In this report, we determined that M50354 (an active metabolite of M50367) was a ligand for the aryl hydrocarbon receptor (AhR); the immunological effects of this compound on in vitro Th1/Th2 differentiation from naive Th cells and Th1/Th2 balance in vivo were manifested through binding to AhR. These effects were completely abolished in AhR-deficient mice. AhR expression in the naive Th cell was significantly up-regulated by costimulation of TCR and CD28. Suppression of naive Th cell differentiation into Th2 cells via binding of M50354 to AhR was associated with inhibition of GATA-3 expression in Th cells. In addition, forced expression of a constitutively active form of AhR or activation of AhR by the addition of representative ligands suppressed naive Th cell differentiation into Th2 cells. Based on these results, we conclude that AhR functions as a modulator of the in vivo Th1/Th2 balance through activation in naive Th cells.
                Bookmark

                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                April 2007
                16 January 2007
                : 115
                : 4
                : 493-495
                Affiliations
                [1 ] Molecular and Cell Nutrition Laboratory, College of Agriculture, University of Kentucky, Lexington, Kentucky, USA
                [2 ] Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
                [3 ] Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio, USA
                [4 ] Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA
                [5 ] Department of Medicine, Division of Gastroenterology/Hepatology, University of Louisville, Louisville, Kentucky, USA
                [6 ] National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, USA
                [7 ] Department of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, New York, USA
                [8 ] Lipid Chemistry & Molecular Biology Laboratory, Department of Food Science, Purdue University, West Lafayette, Indiana, USA
                [9 ] Center for Risk and Integrated Sciences, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA
                Author notes
                Address correspondence to B. Hennig, Molecular and Cell Nutrition Laboratory, College of Agriculture, University of Kentucky, Rm. 591, Wethington Health Sciences Building, 900 S. Limestone, Lexington, KY 40536-0200 USA. Telephone: (859) 323-4933, ext. 81387 or ext. 81343. Fax: (859) 257-1811. E-mail: bhennig@ 123456uky.edu

                R.J.J. is a consultant for GlaxoSmithKline. The remaining authors declare they have no competing financial interests.

                Article
                ehp0115-000493
                10.1289/ehp.9549
                1852675
                17450213
                48ab7669-1c20-4558-a357-e7eabf5b924a
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI
                History
                : 26 July 2006
                : 16 January 2007
                Categories
                Commentaries & Reviews
                Commentary

                Public health
                disease,antioxidants,nutrition,prevention,pollutants,environmental toxicants,diet
                Public health
                disease, antioxidants, nutrition, prevention, pollutants, environmental toxicants, diet

                Comments

                Comment on this article