Pneumonia is a leading killer of children younger than 5 years despite high vaccination coverage, improved nutrition, and widespread implementation of the Integrated Management of Childhood Illnesses algorithm. Assessing the effect of interventions on childhood pneumonia is challenging because the choice of case definition and surveillance approach can affect the identification of pneumonia substantially. In anticipation of an intervention trial aimed to reduce childhood pneumonia by lowering household air pollution, we created a working group to provide recommendations regarding study design and implementation. We suggest to, first, select a standard case definition that combines acute (≤14 days) respiratory symptoms and signs and general danger signs with ancillary tests (such as chest imaging and pulse oximetry) to improve pneumonia identification; second, to prioritise active hospital-based pneumonia surveillance over passive case finding or home-based surveillance to reduce the risk of non-differential misclassification of pneumonia and, as a result, a reduced effect size in a randomised trial; and, lastly, to consider longitudinal follow-up of children younger than 1 year, as this age group has the highest incidence of severe pneumonia.
Approximately three billion individuals are exposed to household air pollution (HAP) from the burning of biomass fuels worldwide. Household air pollution is responsible for 2.9 million annual deaths and causes significant health, economic and social consequences, particularly in low- and middle-income countries. Although there is biological plausibility to draw an association between HAP exposure and respiratory diseases, existing evidence is either lacking or conflicting. We abstracted systematic reviews and meta-analyses for summaries available for common respiratory diseases in any age group and performed a literature search to complement these reviews with newly published studies. Based on the literature summarized in this review, HAP exposure has been associated with acute respiratory infections, tuberculosis, asthma, chronic obstructive pulmonary disease, pneumoconiosis, head and neck cancers, and lung cancer. No study, however, has established a causal link between HAP exposure and respiratory disease. Furthermore, few studies have controlled for tobacco smoke exposure and outdoor air pollution. More studies with consistent diagnostic criteria and exposure monitoring are needed to accurately document the association between household air pollution exposure and respiratory disease. Better environmental exposure monitoring is critical to better separate the contributions of household air pollution from that of other exposures, including ambient air pollution and tobacco smoking. Clinicians should be aware that patients with current or past HAP exposure are at increased risk for respiratory diseases or malignancies and may want to consider earlier screening in this population.
Rationale: Approximately 40% of people worldwide are exposed to household air pollution (HAP) from the burning of biomass fuels. Previous efforts to document health benefits of HAP mitigation have been stymied by an inability to lower emissions to target levels.Objectives: We sought to determine if a household air pollution intervention with liquefied petroleum gas (LPG) improved cardiopulmonary health outcomes in adult women living in a resource-poor setting in Peru.Methods: We conducted a randomized controlled field trial in 180 women aged 25-64 years living in rural Puno, Peru. Intervention women received an LPG stove, continuous fuel delivery for 1 year, education, and behavioral messaging, whereas control women were asked to continue their usual cooking practices. We assessed for stove use adherence using temperature loggers installed in both LPG and biomass stoves of intervention households. Measurements and Main Results:We measured blood pressure, peak expiratory flow (PEF), and respiratory symptoms using the St. George's Respiratory Questionnaire at baseline and at 3-4 visits after randomization. Intervention women used their LPG stove exclusively for 98% of days. We did not find differences in average postrandomization systolic blood pressure (interventioncontrol 0.7 mm Hg; 95% confidence interval, 22.1 to 3.4), diastolic blood pressure (0.3 mm Hg; 21.5 to 2.0), prebronchodilator peak expiratory flow/height 2 (0.14 L/s/m 2 ; 20.02 to 0.29), postbronchodilator peak expiratory flow/height 2 (0.11 L/s/m 2 ; 20.05 to 0.27), or St. George's Respiratory Questionnaire total score (21.4; 23.9 to 1.2) over 1 year in intention-to-treat analysis. There were no reported harms related to the intervention.Conclusions: We did not find evidence of a difference in blood pressure, lung function, or respiratory symptoms during the year-long intervention with LPG.Clinical trial registered with www.clinicaltrials.gov (NCT02994680).
Background In resource-limited settings, pneumonia diagnosis and management are based on thresholds for respiratory rate (RR) and oxyhaemoglobin saturation (SpO 2 ) recommended by WHO. However, as RR increases and SpO 2 decreases with elevation, these thresholds might not be applicable at all altitudes. We sought to determine upper thresholds for RR and lower thresholds for SpO 2 by age and altitude at four sites, with altitudes ranging from sea level to 4348 m. MethodsIn this cross-sectional study, we enrolled healthy children aged 0-23 months who lived within the study areas in India, Guatemala, Rwanda, and Peru. Participants were excluded if they had been born prematurely (<37 weeks gestation); had a congenital heart defect; had history in the past 2 weeks of overnight admission to a health facility, diagnosis of pneumonia, antibiotic use, or respiratory or gastrointestinal signs; history in the past 24 h of difficulty breathing, fast breathing, runny nose, or nasal congestion; and current runny nose, nasal congestion, fever, chest indrawing, or cyanosis. We measured RR either automatically with the Masimo Rad-97, manually, or both, and measured SpO 2 with the Rad-97. Trained staff measured RR in duplicate and SpO 2 in triplicate in children who had no respiratory symptoms or signs in the past 2 weeks. We estimated smooth percentiles for RR and SpO 2 that varied by age and site using generalised additive models for location, shape, and scale. We compared these data with WHO RR and SpO 2 thresholds for tachypnoea and hypoxaemia to determine agreement.
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