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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. 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. 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). 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. Medical Research Council, UK Department for International Development, and Wellcome Trust.

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.

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 10 ]) directly emitted from the combustion of fossil fuels. 1 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 10 . 2 Children are especially vulnerable to the adverse effects of PM 10 , 2 with the cumulative effects on the growth of lung function of particular concern. For example, Gauderman et al. 3 studied air pollution data from . . .

[...]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). ?

Many but not all studies suggest an association between air pollution exposure and infant mortality. We sought to investigate whether pollution exposure is differentially associated with all-cause neonatal or postneonatal mortality, or specific causes of infant mortality. We separately investigated the associations of exposure to particulate matter with aerodynamic diameter ≤ 10 μm (PM10), nitrogen dioxide (NO2), and sulphur dioxide (SO2) with all-cause infant, neonatal, and postneonatal mortality, and with specific causes of infant deaths in 7,984,366 live births between 2001 and 2012 in England and Wales. Overall, 51.3% of the live births were male, and there were 36,485 infant deaths (25,110 neonatal deaths and 11,375 postneonatal deaths). We adjusted for the following major confounders: deprivation, birthweight, maternal age, sex, and multiple birth. Adjusted odds ratios (95% CI; p-value) for infant deaths were significantly increased for NO2, PM10, and SO2 (1.066 [1.027, 1.107; p = 0.001], 1.044 [1.007, 1.082; p = 0.017], and 1.190 [1.146, 1.235; p < 0.001], respectively) when highest and lowest pollutant quintiles were compared; however, neonatal mortality was significantly associated with SO2 (1.207 [1.154, 1.262; p < 0.001]) but not significantly associated with NO2 and PM10 (1.044 [0.998, 1.092; p = 0.059] and 1.008 [0.966, 1.052; p = 0.702], respectively). Postneonatal mortality was significantly associated with all pollutants: NO2, 1.108 (1.038, 1.182; p < 0.001); PM10, 1.117 (1.050, 1.188; p < 0.001); and SO2, 1.147 (1.076, 1.224; p < 0.001). Whilst all were similarly associated with endocrine causes of infant deaths (NO2, 2.167 [1.539, 3.052; p < 0.001]; PM10, 1.433 [1.066, 1.926; p = 0.017]; and SO2, 1.558 [1.147, 2.116; p = 0.005]), they were differentially associated with other specific causes: NO2 and PM10 were associated with an increase in infant deaths from congenital malformations of the nervous (NO2, 1.525 [1.179, 1.974; p = 0.001]; PM10, 1.457 [1.150, 1.846; p = 0.002]) and gastrointestinal systems (NO2, 1.214 [1.006, 1.466; p = 0.043]; PM10, 1.312 [1.096, 1.571; p = 0.003]), and NO2 was also associated with deaths from malformations of the respiratory system (1.306 [1.019, 1.675; p = 0.035]). In contrast, SO2 was associated with an increase in infant deaths from perinatal causes (1.214 [1.156, 1.275; p < 0.001]) and from malformations of the circulatory system (1.172 [1.011, 1.358; p = 0.035]). A limitation of this study was that we were not able to study associations of air pollution exposure and infant mortality during the different trimesters of pregnancy. In addition, we were not able to control for all confounding factors such as maternal smoking. In this study, we found that NO2, PM10, and SO2 were differentially associated with all-cause mortality and with specific causes of infant, neonatal, and postneonatal mortality.

Background Asthma control is a major challenge particularly in low and middle-income countries where access to care is still poor. Asthma education is a cornerstone in self-management and achieving asthma symptom control. However, there is limited human resources to offer asthma education in low-resources settings. This study will investigate the feasibility, acceptability and effectiveness of community health worker (CHW)-led asthma education in improving asthma control among children and adolescents in Uganda. Methods The study will employ a cluster-randomized trial (CRT) study design. It will be conducted in 8 primary care health facilities (HFs) in Jinja region, Eastern Uganda. The HFs will be randomly assigned to the control and intervention arms in the ratio 1:1. The sample size will be 300 children (150 per arm), and asthma control, emergency care visits and hospitalizations will be assessed at baseline, month 1,3 and 6. Asthma education will be provided by CHWs known as Village Health Teams (VHTs) at each visit. Data on direct and indirect costs of asthma education will be collected prospectively. Focus Group Discussions (FGDs) will be conducted among VHTs and caregivers of participating children at the intervention sites to assess the feasibility and acceptability of the intervention. To estimate the mean difference in asthma control scores between the intervention and control arms, adjusted for baseline scores and facility-level clustering, we shall use a random-effects linear regression model and intention-to-treat analysis. The primary endpoint will be asthma control scores. Cost-effectiveness will be assessed by computing the Incremental Cost-Effectiveness Ratio. Thematic content analysis will be used to analyze data from the FGDs. Discussion It is anticipated that the study will provide evidence about the role of community health workers in supporting the care of patients with asthma and achieving symptom control, through providing health education. The data on feasibility, acceptability and cost-effectiveness will be critical in informing scale up plans. Trial registration number ISRCTN16018011. Date : 25/05/2024.

[...]the judgement provides us with a real-life example of what has been known for some time from epidemiological studies, that traffic-derived air pollution not only contributes to incident asthma but also triggers fatal asthma attacks. Since the link between air pollution and asthma has now been settled by legal judgement in the UK, the question is where next for air pollution research? The Royal College of Physicians/Royal College of Paediatrics and Child Health report ‘Every Breath We Take’, published in 2016, identified emerging epidemiological evidence for the effects of maternal inhalation of air pollutants on the developing fetus.2 For example, the ESCAPE (European Study of Cohorts for Air Pollution Effects) cohort study found an increased risk of low birth weight at term, both in terms of direct exposure levels and proximity to high-density traffic areas.3 The mechanistic question is how can PM and gaseous pollutants inhaled into the lung exert their adverse effects on distant organs? Evidence of this phenomenon was reported in 2019 by Bové et al, who found indirect evidence of carbonaceous PM in human placentas.4 We recently extended this observation by showing the presence of PM, with composition compatible to PM from fossil–fuel combustion, in placental phagocytes (figure 1).5 What remains unclear is whether the concentrations of PM observed in placental phagocytes (compared with airway cells) have the capacity to alter placental function, and further studies are needed to explore this in detail. Some interventions may have potential impacts that can be extrapolated from the short-term effects of exposure such as that demonstrated by the Oxford Street study with adult asthmatics, which clearly showed an acute negative impact on lung function on a highly polluted street.17 However, to date, there is minimal evidence to support this or that intervention, such as the use of air purifiers (with considerable costs at times), to reduce the migration of outdoor pollutants into the indoor environment and to improve respiratory health.18 Box 1 Advice that can be given to children with asthma to reduce personal exposure When there is a short-term increase in air pollution levels across the city, there is an increased risk of more asthma symptoms.

In an analysis of data from the National Health and Nutrition Examination Survey (NHANES), they found an association between higher AGE intake from meat and paediatric wheeze. [...]the 2020 UK Health Alliance on Climate Change report ‘All consuming; Building a healthier food system for people and the planet’ concludes that red meat consumption will need to be cut by half if the food system is to stay within sustainable environmental limits.5 Irrespective of the adverse health effects of AGEs, it may therefore now be time to advocate a diet with smaller amounts of higher-quality and more sustainable cooked meat. Increased advanced glycation end-product and meat consumption is associated with childhood wheeze: analysis of the National Health and Nutrition Examination Survey.

Background The Ultra-Low Emission Zone (ULEZ), introduced in Central London in April 2019, aims to enhance air quality and improve public health. The Children's Health in London and Luton (CHILL) study evaluates the impact of the ULEZ on children's health. This analysis focuses on the one-year impacts on the shift towards active travel to school. Methods CHILL is a prospective parallel cohort study of ethnically diverse children, aged 6–9 years attending 84 primary schools within or with catchment areas encompassing London’s ULEZ (intervention) and Luton (non-intervention area). Baseline (2018/19) and one-year follow-up (2019/20) data were collected at school visits from 1992 (58%) children who reported their mode of travel to school ‘today’ (day of assessment). Multilevel logistic regressions were performed to analyse associations between the introduction of the ULEZ and the likelihood of switching from inactive to active travel modes, and vice-versa. Interactions between intervention group status and pre-specified effect modifiers were also explored. Results Among children who took inactive modes at baseline, 42% of children in London and 20% of children in Luton switched to active modes. For children taking active modes at baseline, 5% of children in London and 21% of children in Luton switched to inactive modes. Relative to the children in Luton, children in London were more likely to have switched from inactive to active modes (OR 3.51, 95% CI 1.68–7.31). Children in the intervention group were also less likely to switch from active to inactive modes (OR 0.22, 0.12–0.41). Moderator analyses showed that children living further from school were more likely to switch from inactive to active modes (OR 5.20; 1.67–15.21) compared to those living closer (OR 1.54, 0.33-7.21). Conclusions Implementation of clean air zones can increase uptake of active travel to school and was particularly associated with more sustainable and active travel in children living further from school.