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      Exposures to Airborne Particulate Matter and Adverse Perinatal Outcomes: A Biologically Plausible Mechanistic Framework for Exploring Potential Effect Modification by Nutrition

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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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          Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

          C. Pope, Richard Burnett, George Thurston … (2004)
          Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.
          Article 0 comments Cited 596 times – based on 0 reviews     Review now
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            Fine particulate air pollution and mortality in 20 U.S. cities, 1987-1994.

            Jonathan M. Samet, Francesca Dominici, Frank C Curriero … (2000)
            Air pollution in cities has been linked to increased rates of mortality and morbidity in developed and developing countries. Although these findings have helped lead to a tightening of air-quality standards, their validity with respect to public health has been questioned. We assessed the effects of five major outdoor-air pollutants on daily mortality rates in 20 of the largest cities and metropolitan areas in the United States from 1987 to 1994. The pollutants were particulate matter that is less than 10 microm in aerodynamic diameter (PM10), ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide. We used a two-stage analytic approach that pooled data from multiple locations. After taking into account potential confounding by other pollutants, we found consistent evidence that the level of PM10 is associated with the rate of death from all causes and from cardiovascular and respiratory illnesses. The estimated increase in the relative rate of death from all causes was 0.51 percent (95 percent posterior interval, 0.07 to 0.93 percent) for each increase in the PM10 level of 10 microg per cubic meter. The estimated increase in the relative rate of death from cardiovascular and respiratory causes was 0.68 percent (95 percent posterior interval, 0.20 to 1.16 percent) for each increase in the PM10 level of 10 microg per cubic meter. There was weaker evidence that increases in ozone levels increased the relative rates of death during the summer, when ozone levels are highest, but not during the winter. Levels of the other pollutants were not significantly related to the mortality rate. There is consistent evidence that the levels of fine particulate matter in the air are associated with the risk of death from all causes and from cardiovascular and respiratory illnesses. These findings strengthen the rationale for controlling the levels of respirable particles in outdoor air.
            Article 0 comments Cited 412 times – based on 0 reviews     Review now
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              Application of a new statistical method to derive dietary patterns in nutritional epidemiology.

              Kurt Hoffmann, Matthias B. Schulze, Anja Schienkiewitz … (2004)
              Because foods are consumed in combination, it is difficult in observational studies to separate the effects of single foods on the development of diseases. A possible way to examine the combined effect of food intakes is to derive dietary patterns by using appropriate statistical methods. The objective of this study was to apply a new statistical method, reduced rank regression (RRR), that is more flexible and powerful than the classic principal component analysis. RRR can be used efficiently in nutritional epidemiology by choosing disease-specific response variables and determining combinations of food intake that explain as much response variation as possible. The authors applied RRR to extract dietary patterns from 49 food groups, specifying four diabetes-related nutrients and nutrient ratios as responses. Data were derived from a nested German case-control study within the European Prospective Investigation into Cancer and Nutrition-Potsdam study consisting of 193 cases with incident type 2 diabetes identified until 2001 and 385 controls. The four factors extracted by RRR explained 93.1% of response variation, whereas the first four factors obtained by principal component analysis accounted for only 41.9%. In contrast to principal component analysis and other methods, the new RRR method extracted a significant risk factor for diabetes.
              Article 0 comments Cited 218 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Environ Health Perspect
                Title: Environmental Health Perspectives
                Publisher: National Institute of Environmental Health Sciences
                ISSN (Print): 0091-6765
                Publication date (Print): November 2006
                Publication date (Electronic): 17 August 2006
                Volume: 114
                Issue: 11
                Pages: 1636-1642
                Affiliations
                [1 ] Department of Environmental Health Sciences, Human Nutrition Program, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA
                [2 ] Department of Health Behavior and Health Education, 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
                Author notes
                Address correspondence to S. Kannan, Department of Environmental Health Sciences, Human Nutrition Program, University of Michigan, Room 6338, SPH-I (Tower), School of Public Health, Ann Arbor, MI 48109-2029 USA. Telephone: (734) 936-1629. Fax: (734) 763-8095. E-mail: kannans@ 123456umich.edu

                The authors declare they have no competing financial interests.

                Article
                Publisher ID: ehp0114-001636
                DOI: 10.1289/ehp.9081
                PMC ID: 1665414
                PubMed ID: 17107846
                SO-VID: cb16d2cd-e49c-4ac7-8c88-54181d606ab9
                Copyright © 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
                Date received : 9 February 2006
                Date accepted : 16 August 2006
                Categories
                Subject: Commentaries & Reviews

                ScienceOpen disciplines: Public health
                Keywords: birth outcomes,biomarkers,cardiovascular disease,particulate matter,nutrition,air pollution
                Data availability:
                ScienceOpen disciplines: Public health
                Keywords: birth outcomes, biomarkers, cardiovascular disease, particulate matter, nutrition, air pollution

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