Chronic exposure to outdoor air pollution and lung function in adults

Forbes, Lindsay; Kapetanakis, Venediktos; Rudnicka, Alicja R.; Cook, Derek G; Bush, Tony; Stedman, John; Whincup, Peter H.; Strachan, David P.; Anderson, Hugh

doi:10.1136/thx.2008.109389

Cited by 104 publications

(76 citation statements)

References 29 publications

(15 reference statements)

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“…COPD pathogenetic mechanisms are constantly revisited and now include some novel aspects, e.g. shifts in lung microflora (Sze et al 2012), autoimmune component of the disease (Cosio et al 2002) and other than cigarette smoke environmental risk factors, that include indoor and outdoor air pollution, dust and fumes (Forbes et al 2009;Hopkinson and Polkey 2015). Scientific community still lacks a holistic understanding of COPD development and only several mechanisms are well described and generally recognized, i.e.…”

Section: Introductionmentioning

confidence: 99%

Native matrix-based human lung alveolar tissue model in vitro: studies of the reparatory actions of mesenchymal stem cells

et al. 2016

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Studies of lung diseases in vitro often rely on flat, plastic-based monocultures, due to short lifespan of primary cells, complicated anatomy, lack of explants, etc. We hereby present a native 3D model with cues for repopulating epithelial cells. Abilities of mesenchymal stem cells (MSC) to modulate bacterial lipopolysaccharide (LPS) and cigarette smoke-induced injury to pulmonary epithelium were tested in our model. Post-mortem human lung tissue was sliced, cut and decellularized. Resulting matrix pads were reseeded with pulmonary epithelium (A549 line). Markers of the layer integrity and certain secreted proteins in the presence of cigarette smoke extract (CSE) and LPS were assessed via Western blot, ELISA and RT-PCR assays. In parallel, the effects of MSC paracrine factors on exposed epithelial cells were also investigated at gene and protein levels. When cultured on native 3D matrix, A549 cells obtain dual, type I-and II-like morphology. Exposure to CSE and LPS leads to downregulation of several epithelial proteins and suppressed proliferation rate. MSC medium added to the model restores proliferation rate and some of the epithelial proteins, i.e. e-cadherin and beta-catenin. CSE also increases secretion of proinflammatory cytokines by epithelial cells and upregulates transcription factor NFjB. Some of these effects might be counteracted by MSC in our model. We introduce repopulated decellularized lung matrix that highly resembles in vivo situation and is convenient for studies of disease pathogenesis, cytotoxicology and for exploring therapeutic strategies in the human lung context in vitro. MSC paracrine products have produced protecting effects in our model.

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Section: Introductionmentioning

confidence: 99%

Native matrix-based human lung alveolar tissue model in vitro: studies of the reparatory actions of mesenchymal stem cells

et al. 2016

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“…The relationship between measures of lung function (forced expiratory volume in 1 second (FEV1) and FEV1 as a percentage of forced vital capacity (FVC)) and long-term exposure was examined in four representative cross-sectional surveys of the English population aged 16 years in and 2001(Forbes et al, 2009). Year-specific estimates were pooled, using fixed effect meta-analysis.…”

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confidence: 99%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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This document presents answers to 24 questions relevant to reviewing European policies on air pollution and to addressing health aspects of these policies. The answers were developed by a large group of scientists engaged in the WHO project "Review of evidence on health aspects of air pollution -REVIHAAP". The experts reviewed and discussed the newly accumulated scientific evidence on the adverse effects on health of air pollution, formulating science-based answers to the 24 questions. Extensive rationales for the answers, including the list of key references, are provided. The review concludes that a considerable amount of new scientific information on the adverse effects on health of particulate matter, ozone and nitrogen dioxide, observed at levels commonly present in Europe, has been published in recent years. This new evidence supports the scientific conclusions of the WHO air quality guidelines, last updated in 2005, and indicates that the effects in some cases occur at air pollution concentrations lower than those serving to establish these guidelines. It also provides scientific arguments for taking decisive actions to improve air quality and reduce the burden of disease associated with air pollution in Europe.This publication arises from the project REVIHAAP and has been co-funded by the European Union. Keywords AIR POLLUTANTS AIR POLLUTION -ADVERSE EFFECTS ENVIRONMENT AND PUBLIC HEALTH EVIDENCE BASED PRACTICE GUIDELINES HEALTH POLICYAddress requests about publications of the WHO Regional Office for Europe to: Publications WHO Regional Office for Europe Scherfigsvej 8 DK-2100 Copenhagen Ø, Denmark Alternatively, complete an online request form for documentation, health information, or for permission to quote or translate, on the Regional Office web site (http://www.euro.who.int/pubrequest). © World Health Organization 2013All rights reserved. The Regional Office for Europe of the World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full.The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate borderlines for which there may not yet be full agreement.The mention of specific companies or of certain manufacturers products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either express or implied. ...

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“…Thus, exposure to air pollution appears to reduce the %FEV 1 to a greater extent than does a history of smoking. In this connection, exposure to SO 2 , NO 2 , and PM 10 was significantly correlated with a decrease in FEV 1 (Schikowski et al 2005;Forbes et al 2009). Furthermore, despite the improvement in the air pollution, the lung function did not recover in officially acknowledged victims of pollution-related illness ).…”

Section: Discussionmentioning

confidence: 93%

“…Some reports have indicated that smoking with pollution is more significantly correlated with decreased FVC compared to non-smoking with pollution (Qian et al 2005;Forbes et al 2009). Our findings suggest a negative influence of the synergistic effect of smoking after air pollution exposure on the %FVC.…”

Section: Discussionmentioning

confidence: 99%

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Smoking Aggravates the Impaired Pulmonary Function of Officially Acknowledged Female Victims of Air Pollution of 40 Years Ago

Nishinakagawa

Senjyu

Tanaka

et al. 2014

Tohoku J. Exp. Med.

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Air pollution due to industrial waste and tobacco smoke is detrimental to pulmonary function. However, the combined effects of air pollution and smoking on pulmonary function have not been investigated. We examined the combined effect of air pollution of 40 years ago and concurrent smoking on the pulmonary function of officially acknowledged female victims in Japan, because females are more susceptible to the adverse effects of both irritants than males. The subjects comprised 655 female victims living in one of two areas with air pollution of 40 years ago and 572 females living in an area without air pollution. All victims have been prescribed standard respiratory medications. Pulmonary function was measured in 2000 for air-pollution groups (130 smokers and 525 non-smokers; mean age, 68.4 years) and during the period of 2004 to 2013 for non-air-pollution groups (113 smokers and 459 non-smokers; mean age, 69.0 years). The smokers included both current smokers and ex-smokers. The victims with a history of smoking had significantly lower forced expiratory volume in 1 second (FEV 1 % predicted) (mean, 74%) and significantly lower FEV 1 /forced vital capacity (FVC) (mean, 70%) than the other groups (P < 0.001). Thus, smoking aggravates the pulmonary function in officially acknowledged female victims, despite the improved air pollution and the continuous medical care provided by the government. In conclusion, exposure to air pollution of 40 years ago and cigarette smoking are associated with reduced pulmonary function. These results highlight the importance of measures aimed at smoking cessation and limiting air pollution.

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Chronic exposure to outdoor air pollution and lung function in adults

Cited by 104 publications

References 29 publications

Native matrix-based human lung alveolar tissue model in vitro: studies of the reparatory actions of mesenchymal stem cells

Native matrix-based human lung alveolar tissue model in vitro: studies of the reparatory actions of mesenchymal stem cells

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Smoking Aggravates the Impaired Pulmonary Function of Officially Acknowledged Female Victims of Air Pollution of 40 Years Ago

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