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      Use of cleaner-burning biomass stoves and airway macrophage black carbon in Malawian women

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          Abstract

          Exposure to particulate matter (PM) from burning of biomass for cooking is associated with adverse health effects. It is unknown whether or not cleaner burning biomass-fuelled cookstoves reduce the amount of PM inhaled by women compared with traditional open fires.

          We sought to assess whether airway macrophage black carbon (AMBC) - a marker of inhaled dose of carbonaceous PM from biomass and fossil fuel combustion - is lower in Malawian women using a cleaner burning biomass-fuelled cookstove compared with those using open fires for cooking. AMBC was assessed in induced sputum samples using image analysis and personal exposure to carbon monoxide (CO) and PM were measured using Aprovecho Indoor Air Pollution meters. A fossil-fuel exposed group of UK women was also studied.

          Induced sputum samples were obtained from 57 women from which AMBC was determined in 31. Median AMBC was 6.87 μm 2 (IQR 4.47–18.5) and 4.37 μm 2 (IQR 2.57–7.38) in the open fire ( n = 11) and cleaner burning cookstove groups ( n = 20), respectively ( p = 0.028). There was no difference in personal exposure to CO and PM between the two groups. UK women ( n = 5) had lower AMBC (median 0.89 μm 2, IQR 0.56–1.13) compared with both Malawi women using traditional cookstoves ( p < 0.001) and those using cleaner cookstoves ( p = 0.022).

          We conclude that use of a cleaner burning biomass-fuelled cookstove reduces inhaled PM dose in a way that is not necessarily reflected by personal exposure monitoring.

          Graphical abstract

          Highlights

          • Sputum induction to assess airway macrophage black carbon is feasible in the field.

          • Airway macrophage black carbon represents a way to assess internal dose of particulate matter exposure.

          • Cleaner burning biomass-fuelled cookstoves reduce inhaled PM dose.

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          Most cited references12

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          Air pollution and airway disease.

          Epidemiological and toxicological research continues to support a link between urban air pollution and an increased incidence and/or severity of airway disease. Detrimental effects of ozone (O(3)), nitrogen dioxide (NO(2)) and particulate matter (PM), as well as traffic-related pollution as a whole, on respiratory symptoms and function are well documented. Not only do we have strong epidemiological evidence of a relationship between air pollution and exacerbation of asthma and respiratory morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD), but recent studies, particularly in urban areas, have suggested a role for pollutants in the development of both asthma and COPD. Similarly, while prevalence and severity of atopic conditions appear to be more common in urban compared with rural communities, evidence is emerging that traffic-related pollutants may contribute to the development of allergy. Furthermore, numerous epidemiological and experimental studies suggest an association between exposure to NO(2) , O(3) , PM and combustion products of biomass fuels and an increased susceptibility to and morbidity from respiratory infection. Given the considerable contribution that traffic emissions make to urban air pollution researchers have sought to characterize the relative toxicity of traffic-related PM pollutants. Recent advances in mechanisms implicated in the association of air pollutants and airway disease include epigenetic alteration of genes by combustion-related pollutants and how polymorphisms in genes involved in antioxidant pathways and airway inflammation can modify responses to air pollution exposures. Other interesting epidemiological observations related to increased host susceptibility include a possible link between chronic PM exposure during childhood and vulnerability to COPD in adulthood, and that infants subjected to higher prenatal levels of air pollution may be at greater risk of developing respiratory conditions. While the characterization of pollutant components and sources promise to guide pollution control strategies, the identification of susceptible subpopulations will be necessary if targeted therapy/prevention of pollution-induced respiratory diseases is to be developed. © 2011 Blackwell Publishing Ltd.
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            Respiratory effects of air pollution on children.

            A substantial proportion of the global burden of disease is directly or indirectly attributable to exposure to air pollution. Exposures occurring during the periods of organogenesis and rapid lung growth during fetal development and early post-natal life are especially damaging. In this State of the Art review, we discuss air toxicants impacting on children's respiratory health, routes of exposure with an emphasis on unique pathways relevant to young children, methods of exposure assessment and their limitations and the adverse health consequences of exposures. Finally, we point out gaps in knowledge and research needs in this area. A greater understanding of the adverse health consequences of exposure to air pollution in early life is required to encourage policy makers to reduce such exposures and improve human health.
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              Carbon in airway macrophages and lung function in children.

              Epidemiologic studies indirectly suggest that the inhalation of carbonaceous particulate matter impairs lung function in children. Using the carbon content of airway macrophages as a marker of individual exposure to particulate matter derived from fossil fuel, we sought direct evidence of this association. Airway macrophages were obtained from healthy children through sputum induction, and the area of airway macrophages occupied by carbon was measured. Lung function was measured with the use of spirometry. We modeled the exposure to primary particulate matter (PM) that is less than 10 mum in aerodynamic diameter (PM10) at or near each child's home address. Linear regression was used to evaluate associations between carbon content of alveolar macrophages and variables that may affect individual exposure. To determine whether lung function that is reduced for other reasons is associated with an increase in the carbon content of airway macrophages, we also studied children with severe asthma. We were able to assess the carbon content of airway macrophages in 64 of 114 healthy children (56 percent). Each increase in primary PM10 of 1.0 microg per cubic meter was associated with an increase of 0.10 microm2 (95 percent confidence interval, 0.01 to 0.18) in the carbon content of airway macrophages, and each increase of 1.0 microm2 in carbon content was associated with a reduction of 17 percent (95 percent confidence interval, 5.6 to 28.4 percent) in forced expiratory volume in one second, of 12.9 percent (95 percent confidence interval, 0.9 to 24.8 percent) in forced vital capacity, and of 34.7 percent (95 percent confidence interval, 11.3 to 58.1 percent) in the forced expiratory flow between 25 and 75 percent of the forced vital capacity. The carbon content of airway macrophages was lower in children with asthma than in healthy children. There is a dose-dependent inverse association between the carbon content of airway macrophages and lung function in children. We found no evidence that reduced lung function itself causes an increase in carbon content. Copyright 2006 Massachusetts Medical Society.
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                Author and article information

                Contributors
                Journal
                Sci Total Environ
                Sci. Total Environ
                The Science of the Total Environment
                Elsevier
                0048-9697
                1879-1026
                01 September 2018
                01 September 2018
                : 635
                : 405-411
                Affiliations
                [a ]Centre for Child Health, Blizard Institute, Queen Mary University of London, London, UK
                [b ]Division of Epidemiology and Biostatistics, School of Public Health, University of Cape Town, Cape Town, South Africa
                [c ]School of Public Health, University of California, Berkeley, Berkeley, USA
                [d ]School of Medicine, University of California, San Francisco, San Francisco, USA
                [e ]Liverpool School of Tropical Medicine, Liverpool, UK
                [f ]Malawi Liverpool Wellcome Trust Programme, Blantyre, Malawi
                Author notes
                [* ]Corresponding author at: Centre for Child Health, Blizard Institute, Queen Mary University of London, Newark Street, E1 2AT, London. j.grigg@ 123456qmul.ac.uk
                Article
                S0048-9697(18)31283-X
                10.1016/j.scitotenv.2018.04.125
                6024563
                29677666
                4e653e64-1abb-4fe6-b1fb-74a400f54cff
                © 2018 The Authors

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 9 November 2017
                : 7 April 2018
                : 8 April 2018
                Categories
                Article

                General environmental science
                macrophage black carbon,air pollution,cookstove,particulate matter

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