The American Thoracic Society has previously published statements on what constitutes an adverse effect on health of air pollution in 1985 and 2000. We set out to update and broaden these past ...statements that focused primarily on effects on the respiratory system. Since then, many studies have documented effects of air pollution on other organ systems, such as on the cardiovascular and central nervous systems. In addition, many new biomarkers of effects have been developed and applied in air pollution studies.This current report seeks to integrate the latest science into a general framework for interpreting the adversity of the human health effects of air pollution. Rather than trying to provide a catalogue of what is and what is not an adverse effect of air pollution, we propose a set of considerations that can be applied in forming judgments of the adversity of not only currently documented, but also emerging and future effects of air pollution on human health. These considerations are illustrated by the inclusion of examples for different types of health effects of air pollution.
Summary Background WHO estimates exposure to air pollution from cooking with solid fuels is associated with over 4 million premature deaths worldwide every year including half a million children ...under the age of 5 years from pneumonia. We hypothesised that replacing open fires with cleaner burning biomass-fuelled cookstoves would reduce pneumonia incidence in young children. Methods We did a community-level open cluster randomised controlled trial to compare the effects of a cleaner burning biomass-fuelled cookstove intervention to continuation of open fire cooking on pneumonia in children living in two rural districts, Chikhwawa and Karonga, of Malawi. Clusters were randomly allocated to intervention and control groups using a computer-generated randomisation schedule with stratification by site, distance from health centre, and size of cluster. Within clusters, households with a child under the age of 4·5 years were eligible. Intervention households received two biomass-fuelled cookstoves and a solar panel. The primary outcome was WHO Integrated Management of Childhood Illness (IMCI)-defined pneumonia episodes in children under 5 years of age. Efficacy and safety analyses were by intention to treat. The trial is registered with ISRCTN, number ISRCTN59448623. Findings We enrolled 10 750 children from 8626 households across 150 clusters between Dec 9, 2013, and Feb 28, 2016. 10 543 children from 8470 households contributed 15 991 child-years of follow-up data to the intention-to-treat analysis. The IMCI pneumonia incidence rate in the intervention group was 15·76 (95% CI 14·89–16·63) per 100 child-years and in the control group 15·58 (95% CI 14·72–16·45) per 100 child-years, with an intervention versus control incidence rate ratio (IRR) of 1·01 (95% CI 0·91–1·13; p=0·80). Cooking-related serious adverse events (burns) were seen in 19 children; nine in the intervention and ten (one death) in the control group (IRR 0·91 95% CI 0·37–2·23; p=0·83). Interpretation We found no evidence that an intervention comprising cleaner burning biomass-fuelled cookstoves reduced the risk of pneumonia in young children in rural Malawi. Effective strategies to reduce the adverse health effects of household air pollution are needed. Funding Medical Research Council, UK Department for International Development, and Wellcome Trust.
Inhaled particulate matter (PM) from combustion- and friction-sourced air pollution adversely affects organs distant from the lung. A putative mechanism for the remote effect of inhaled PM is that ...ultrafine, nano-sized fraction (<100 nm) translocates across the air-tissue barrier, directly interacting with phagocytic tissue cells. Although PM is reported in other tissues, whether it is phagocytosed by non-respiratory tissue resident cells is unclear.
Using the placenta as an accessible organ for phagocytic cells, we sought to seek evidence for air pollution-derived PM in tissue resident phagocytes. Macrophage-enriched placental cells (MEPCs) were isolated, and examined by light and electron microscopy. MEPC carbon was assessed by image analysis (mean μm2/1000 cells); particle composition and numbers were investigated using magnetic analyses and energy dispersive X-ray spectroscopy. MEPCs phagocytic capacity was assessed by culture with diesel exhaust PM in vitro.
Fifteen placentas were analysed. Black inclusions morphologically compatible with inhaled PM were identified within MEPCs from all samples (mean ± SEM carbon loading, 1000 MEPCs/participant of 0.004 ± 0.001 μm2). High resolution scanning/transmission electron microscopy revealed abundant nano-sized particle aggregates within MEPCs. MEPC PM was predominantly carbonaceous but also co-associated with a range of trace metals, indicative of high temperature (i.e. exogenous) generation. MEPCs contained readily-measurable amounts of iron-rich, ferrimagnetic particles, in concentrations/particle number concentrations ranging, respectively, from 8 to 50 ng/g and 10 to 60.107 magnetic particles/g (wet wt) MEPCs. Extracted MEPCs (n = 20/ placenta) were phagocytic for PM since all cells showed increased carbon area after culture with diesel PM in vitro (mean ± SEM increase 7.55 ± 1.26 μm2 carbon PM).
These findings demonstrate that inhaled, metal-bearing, air pollution-derived PM can not only translocate to distant organs, but is taken up by tissue resident phagocytes in vivo. The human placenta, and hence probably the fetus, thus appears to be a target for such particles.
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•Human placentas were used to investigate translocation of inhaled nanoparticles.•Carbon and metal-bearing nanoparticles were found in tissue phagocytes in vivo.•Size, shape and elemental composition of these exogenous particles were identified.•Tissue phagocytes uptake of diesel exhaust particles was demonstrated in vitro.
Exposure to air pollution has been associated with the loss of lung function in epidemiologic studies. In this study, exposures of individual children were assessed through the measurement of carbon ...in macrophages and were shown to be related to exposure to local pollution and to lung function.
Exposures of individual children were assessed through the measurement of carbon in macrophages and were shown to be related to exposure to local pollution and to lung function.
Black carbon is a major component of inhalable particulate matter (particulate matter <10 μm in aerodynamic diameter PM
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Black carbon consists of a carbon core enriched with trace metals and organic compounds, and it is thought to mediate many of the adverse health effects reported in epidemiologic studies to be associated with PM
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Children are especially vulnerable to the adverse effects of PM
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with the cumulative effects on the growth of lung function of particular concern. For example, Gauderman et al.
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studied air pollution data from . . .
Welders are more susceptible to pneumococcal pneumonia. The mechanisms are yet unclear. Pneumococci co-opt the platelet activating factor receptor (PAFR) to infect respiratory epithelial cells. We ...previously reported that exposure of respiratory cells to welding fumes (WF), upregulates PAFR-dependent pneumococcal infection. The signaling pathway for this response is unknown, however, in intestinal cells, hypoxia-inducible factor-1 α (HIF 1α) is reported to mediate PAFR-dependent infection. We sought to assess whether oxidative stress plays a role in susceptibility to pneumococcal infection via the platelet activating factor receptor. We also sought to evaluate the suitability of nasal epithelial PAFR expression in welders as a biomarker of susceptibility to infection. Finally, we investigated the generalisability of the effect of welding fumes on pneumococcal infection and growth using a variety of different welding fume samples. Nasal epithelial PAFR expression in welders and controls was analysed by flow cytometry. WF were collected using standard methodology. The effect of WF on respiratory cell reactive oxygen species production, HIF-1α expression, and pneumococcal infection was determined using flow cytometry, HIF-1α knockdown and overexpression, and pneumococcal infection assays. We found that nasal PAFR expression is significantly increased in welders compared with controls and that WF significantly increased reactive oxygen species production, HIF-1α and PAFR expression, and pneumococcal infection of respiratory cells. In unstimulated cells, HIF-1α knockdown decreased PAFR expression and HIF-1α overexpression increased PAFR expression. However, in knockdown cells pneumococcal infection was paradoxically increased and in overexpressing cells infection was unaffected. Nasal epithelial PAFR expression may be used as a biomarker of susceptibility to pneumococcal infection in order to target individuals, particularly those at high risk such as welders, for the pneumococcal vaccine. Expression of HIF-1α in unexposed respiratory cells inhibits basal pneumococcal infection via PAFR-independent mechanisms.
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Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
This European Respiratory Society statement provides a comprehensive overview on protracted bacterial bronchitis (PBB) in children. A task force of experts, consisting of clinicians from Europe and ...Australia who manage children with PBB determined the overall scope of this statement through consensus. Systematic reviews addressing key questions were undertaken, diagrams in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement constructed and findings of relevant studies summarised. The final content of this statement was agreed upon by all members.The current knowledge regarding PBB is presented, including the definition, microbiology data, known pathobiology, bronchoalveolar lavage findings and treatment strategies to manage these children. Evidence for the definition of PBB was sought specifically and presented. In addition, the task force identified several major clinical areas in PBB requiring further research, including collecting more prospective data to better identify the disease burden within the community, determining its natural history, a better understanding of the underlying disease mechanisms and how to optimise its treatment, with a particular requirement for randomised controlled trials to be conducted in primary care.
A third of the world's population uses solid fuel derived from plant material (biomass) or coal for cooking, heating, or lighting. These fuels are smoky, often used in an open fire or simple stove ...with incomplete combustion, and result in a large amount of household air pollution when smoke is poorly vented. Air pollution is the biggest environmental cause of death worldwide, with household air pollution accounting for about 3·5-4 million deaths every year. Women and children living in severe poverty have the greatest exposures to household air pollution. In this Commission, we review evidence for the association between household air pollution and respiratory infections, respiratory tract cancers, and chronic lung diseases. Respiratory infections (comprising both upper and lower respiratory tract infections with viruses, bacteria, and mycobacteria) have all been associated with exposure to household air pollution. Respiratory tract cancers, including both nasopharyngeal cancer and lung cancer, are strongly associated with pollution from coal burning and further data are needed about other solid fuels. Chronic lung diseases, including chronic obstructive pulmonary disease and bronchiectasis in women, are associated with solid fuel use for cooking, and the damaging effects of exposure to household air pollution in early life on lung development are yet to be fully described. We also review appropriate ways to measure exposure to household air pollution, as well as study design issues and potential effective interventions to prevent these disease burdens. Measurement of household air pollution needs individual, rather than fixed in place, monitoring because exposure varies by age, gender, location, and household role. Women and children are particularly susceptible to the toxic effects of pollution and are exposed to the highest concentrations. Interventions should target these high-risk groups and be of sufficient quality to make the air clean. To make clean energy available to all people is the long-term goal, with an intermediate solution being to make available energy that is clean enough to have a health impact.
...in Vietnam, a population-based survey found a 1.5-fold (95% confidence interval CI, 1.25-fold to 1.92-fold) increased risk for pneumonia in young children exposed to environmental tobacco smoke, ...with 28% of childhood pneumonia attributable to environmental tobacco smoke (3); more recently, a meta-analysis of 10 European birth cohorts found a 1.3-fold (95% CI, 1.02-fold to 1.65-fold) increase in risk for pneumonia in young children with long-term exposure to traffic-related nitrogen dioxide (per 10 mg/m3 NO2), and 1.8-fold (95% CI, 1.0-fold to 3.09-fold) increase for particulate matter less than 10 microns in aerodynamic diameter (per 10 mg/m3 PM10) (4). On one hand, we now have sufficient data on the adverse health effects of air pollution throughout the life course, so that healthcare professionals should advocate further immediate rapid reductions in fossil fuel emissions to protect population health. The study of Horne and colleagues (6) should therefore stimulate researchers to revisit RSV and pollutant interactions in vitro and, if possible, to model the effect of individual pollutants on the emerging area of the role of viral respiratory tract infection in increasing risk for clinically severe bacterial infections (11). ?
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