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 inEnvironmental health perspectives Vol. 114; no. 11; pp. 1636 - 1642
Main Authors Kannan, Srimathi, Misra, Dawn P., Dvonch, J. Timothy, Krishnakumar, Ambika
Format Journal Article
LanguageEnglish
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
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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.
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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  doi: 10.1161/01.CIR.0000052939.59093.45
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  doi: 10.1093/aje/154.12.1113
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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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StartPage 1636
SubjectTerms Academic conferences
Air Pollutants - toxicity
Air pollution
Commentaries & Reviews
Diet
Dose response relationship
Effect Modifier, Epidemiologic
Email
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
Volume 114
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