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      Improved Air Quality and Attenuated Lung Function Decline: Modification by Obesity in the SAPALDIA Cohort

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          Abstract

          Background: Air pollution and obesity are hypothesized to contribute to accelerated decline in lung function with age through their inflammatory properties.

          Objective: We investigated whether the previously reported association between improved air quality and lung health in the population-based SAPALDIA cohort is modified by obesity.

          Methods: We used adjusted mixed-model analyses to estimate the association of average body mass index (BMI) and changes in particulate matter with aerodynamic diameter ≤ 10 µm (PM 10; ΔPM 10) with lung function decline over a 10-year follow-up period.

          Results: Lung function data and complete information were available for 4,664 participants. Age-related declines in lung function among participants with high average BMI were more rapid for FVC (forced vital capacity), but slower for FEV 1/FVC (forced expiratory volume in 1 sec/FVC) and FEF 25–75 (forced expiratory flow at 25–75%) than declines among those with low or normal average BMI. Improved air quality was associated with attenuated reductions in FEV 1/FVC, FEF 25–75, and FEF 25–75/FVC over time among low- and normal-BMI participants, but not overweight or obese participants. The attenuation was most pronounced for ΔFEF 25–75/FVC (30% and 22% attenuation in association with a 10-μg/m 3 decrease in PM 10 among low- and normal-weight participants, respectively.)

          Conclusion: Our results point to the importance of considering health effects of air pollution exposure and obesity in parallel. Further research must address the mechanisms underlying the observed interaction.

          Citation: Schikowski T, Schaffner E, Meier F, Phuleria HC, Vierkötter A, Schindler C, Kriemler S, Zemp E, Krämer U, Bridevaux P-O, Rochat T, Schwartz J, Künzli N, Probst-Hensch N. 2013. Improved air quality and attenuated lung function decline: modification by obesity in the SAPALDIA cohort. Environ Health Perspect 121:1034–1039; http://dx.doi.org/10.1289/ehp.1206145

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          Lung function testing: selection of reference values and interpretative strategies. American Thoracic Society.

          Psychiatric Association American, Society for Reproductive Medicine American, S Waqqas (1991)
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            Physiology of obesity and effects on lung function.

            Cheryl M Salome, Gregory G King, Norbert Berend (2010)
            In obese people, the presence of adipose tissue around the rib cage and abdomen and in the visceral cavity loads the chest wall and reduces functional residual capacity (FRC). The reduction in FRC and in expiratory reserve volume is detectable, even at a modest increase in weight. However, obesity has little direct effect on airway caliber. Spirometric variables decrease in proportion to lung volumes, but are rarely below the normal range, even in the extremely obese, while reductions in expiratory flows and increases in airway resistance are largely normalized by adjusting for lung volumes. Nevertheless, the reduction in FRC has consequences for other aspects of lung function. A low FRC increases the risk of both expiratory flow limitation and airway closure. Marked reductions in expiratory reserve volume may lead to abnormalities in ventilation distribution, with closure of airways in the dependent zones of the lung and ventilation perfusion inequalities. Greater airway closure during tidal breathing is associated with lower arterial oxygen saturation in some subjects, even though lung CO-diffusing capacity is normal or increased in the obese. Bronchoconstriction has the potential to enhance the effects of obesity on airway closure and thus on ventilation distribution. Thus obesity has effects on lung function that can reduce respiratory well-being, even in the absence of specific respiratory disease, and may also exaggerate the effects of existing airway disease.
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              Systemic inflammation and comorbidity in COPD: a result of 'overspill' of inflammatory mediators from the lungs? Review of the evidence.

              Robert A Stockley, Nicola J Sinden (2010)
              Chronic obstructive pulmonary disease (COPD) is characterised by an inflammatory response by the lungs to inhaled substances such as cigarette smoking and air pollutants. In addition to the pulmonary features of COPD, several systemic effects have been recognised even after controlling for common aetiological factors such as smoking or steroid use. These include skeletal muscle dysfunction, cardiovascular disease, osteoporosis and diabetes. Individuals with COPD have significantly raised levels of several circulating inflammatory markers indicating the presence of systemic inflammation. This raises the issue of cause and effect. The role of tumour necrosis factor α in COPD is thought to be central to both lung and systemic inflammation and has been implicated in skeletal muscle dysfunction, osteoporosis and type 2 diabetes. It has been hypothesised that inflammation in the lung results in 'overspill' into the circulation causing systemic inflammation. There is supportive evidence that protein movement can occur from the lung surface to the systemic circulation. Evidence from inhaled substances such as air pollutants and cigarette smoke has demonstrated a temporal link between the inflammatory process in the lung and systemic inflammation. Also, studies have shown alterations in circulating inflammatory cells in patients with COPD compared with controls which may reflect the effects of inflammatory mediators (derived from the lung) on circulating cells or the bone marrow. This paper considers the concept of 'overspill' in depth, reviews the current evidence and highlights problems in generating direct evidence to support or refute this concept.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Environ Health Perspect
                Journal ID (publisher-id): EHP
                Title: Environmental Health Perspectives
                Publisher: National Institute of Environmental Health Sciences
                ISSN (Print): 0091-6765
                ISSN (Electronic): 1552-9924
                Publication date (Electronic): 02 July 2013
                Publication date (Print): September 2013
                Volume: 121
                Issue: 9
                Pages: 1034-1039
                Affiliations
                [1 ]Swiss Tropical and Public Health Institute, Basel, Switzerland
                [2 ]University of Basel, Basel, Switzerland
                [3 ]Department of Epidemiology, Leibnitz Institut for Environmental Medicine at the Heinrich-Heine University (IUF), Düsseldorf, Germany
                [4 ]Division of Pulmonary Medicine, University Hospitals of Geneva, Geneva, Switzerland
                [5 ]Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
                Author notes
                Address correspondence to T. Schikowski, Swiss Tropical and Public Health Institute, Socinstrasse 57, 4051 Basel, Switzerland. Telephone: 41 61 284 83 97. E-mail: tamara.schikowski@ 123456unibas.ch
                Article
                Publisher ID: ehp.1206145
                DOI: 10.1289/ehp.1206145
                PMC ID: 3764076
                PubMed ID: 23820868
                SO-VID: 03604978-1c7f-465f-9f72-ad4ffa71ae8e
                Copyright statement: Copyright @ 2013
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, properly cited.

                History
                Date received : 16 October 2012
                Date accepted : 27 June 2013
                Date: 02 July 2013
                Date: 01 September 2013
                Categories
                Subject: Research

                ScienceOpen disciplines: Public health
                Data availability:
                ScienceOpen disciplines: Public health

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