Exposures to Airborne Particulate Matter and Adverse Perinatal Outcomes: A Biologically Plausible Mechanistic Framework for Exploring Potential Effect Modification by Nutrition
Objectives: The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review...
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Published in | Environmental health perspectives Vol. 114; no. 11; pp. 1636 - 1642 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
National Institute of Environmental Health Sciences. National Institutes of Health. Department of Health, Education and Welfare
01.11.2006
National Institute of Environmental Health Sciences |
Subjects | |
Online Access | Get full text |
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Abstract | Objectives: The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. Methods: We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. Conclusions: Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts. |
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AbstractList | OBJECTIVES: The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. METHODS: We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. CONCLUSIONS: Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts. The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts. Objectives: The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LEW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. METHODS: We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. CONCLUSIONS: Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts. An interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology is presented. Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of particulate matter (PM) on low birth weight (LBW), preterm delivery (PTD), and intrauterine growth retardation (IUGR) may manifest through the cardiovascular mechanism of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biological responses and adverse birth outcomes may be derived from both PM and non-PM sources. The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts. |
Audience | Academic |
Author | Krishnakumar, Ambika Misra, Dawn P. Kannan, Srimathi Dvonch, J. Timothy |
AuthorAffiliation | 2 Department of Health Behavior and Health Education, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA 1 Department of Environmental Health Sciences, Human Nutrition Program, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA 3 Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA 4 Department of Child and Family Studies, Syracuse University, College of Human Studies and Health Professions, Syracuse, New York, USA |
AuthorAffiliation_xml | – name: 2 Department of Health Behavior and Health Education, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA – name: 3 Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA – name: 1 Department of Environmental Health Sciences, Human Nutrition Program, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA – name: 4 Department of Child and Family Studies, Syracuse University, College of Human Studies and Health Professions, Syracuse, New York, USA |
Author_xml | – sequence: 1 givenname: Srimathi surname: Kannan fullname: Kannan, Srimathi – sequence: 2 givenname: Dawn P. surname: Misra fullname: Misra, Dawn P. – sequence: 3 givenname: J. Timothy surname: Dvonch fullname: Dvonch, J. Timothy – sequence: 4 givenname: Ambika surname: Krishnakumar fullname: Krishnakumar, Ambika |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17107846$$D View this record in MEDLINE/PubMed |
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Snippet | Objectives: The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may... The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the... An interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and... OBJECTIVES: The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may... |
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SubjectTerms | Academic conferences Air Pollutants - toxicity Air pollution Commentaries & Reviews Diet Dose response relationship Effect Modifier, Epidemiologic Environmental Exposure - adverse effects Environmental health Environmental policy Facsimiles Female Hormesis Humans Infants (Premature) International conferences Internet Particulate Matter - toxicity Pregnancy Pregnancy Outcome Prenatal Nutritional Physiological Phenomena Public health Review |
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Title | Exposures to Airborne Particulate Matter and Adverse Perinatal Outcomes: A Biologically Plausible Mechanistic Framework for Exploring Potential Effect Modification by Nutrition |
URI | https://www.jstor.org/stable/4091790 https://www.ncbi.nlm.nih.gov/pubmed/17107846 https://www.proquest.com/docview/222662190/abstract/ https://search.proquest.com/docview/14798103 https://search.proquest.com/docview/20392355 https://search.proquest.com/docview/21179774 https://search.proquest.com/docview/36334904 https://pubmed.ncbi.nlm.nih.gov/PMC1665414 |
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