The Effects of Household Air Pollution (HAP) on Lung Function in Children: A Systematic Review.
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SUBMITTER: Aithal SS
PROVIDER: S-EPMC8623006 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Half of the world's population still relies on solid fuels to fulfill its energy needs for cooking and space heating, leading to high levels of household air pollution (HAP), adversely affecting human health and the environment. A cross-sectional cohort study was conducted to investigate any associations between: (1) HAP metrics (mass concentration of particulate matter of aerodynamic size less than 2.5 μm (PM2.5 ), lung-deposited surface area (LDSA) and carbon monoxide (CO)); (2) a range of household and socio-demographic characteristics; and (3) lung function for women and children exposed daily to biomass cookstove emissions, in rural southern India. HAP measurements were collected inside the kitchen of 96 households, and pulmonary function tests were performed for the women and child in each enrolled household. Detailed questionnaires captured household characteristics, health histories and various socio-demographic parameters. Simple linear and logistic regression analysis was performed to examine possible associations between the HAP metrics, lung function and all household/socio-demographic variables. Obstructive lung defects (forced vital capacity (FVC) ≥ lower limit of normal (LLN) and forced expiratory volume in 1 second (FEV1 )/FVC < LLN) were found in 8% of mothers and 9% of children, and restrictive defects (FVC < LLN and FEV1 /FVC ≥ LLN) were found in 17% of mothers and 15% of children. A positive association between LDSA, included for the first time in this type of epidemiological study, and lung function was observed, indicating LDSA is a superior metric compared to PM2.5 to assess effects of PM on lung function. HAP demonstrated a moderate association with subnormal lung function in children. The results emphasize the need to look beyond mass-based PM metrics to assess fully the association between HAP and lung function.
| S-EPMC10545302 | biostudies-literature
Project description:Background3 billion people worldwide rely on polluting fuels and technologies for domestic cooking and heating. We estimate the global, regional, and national health burden associated with exposure to household air pollution.MethodsFor the systematic review and meta-analysis, we systematically searched four databases for studies published from database inception to April 2, 2020, that evaluated the risk of adverse cardiorespiratory, paediatric, and maternal outcomes from exposure to household air pollution, compared with no exposure. We used a random-effects model to calculate disease-specific relative risk (RR) meta-estimates. Household air pollution exposure was defined as use of polluting fuels (coal, wood, charcoal, agricultural wastes, animal dung, or kerosene) for household cooking or heating. Temporal trends in mortality and disease burden associated with household air pollution, as measured by disability-adjusted life-years (DALYs), were estimated from 2000 to 2017 using exposure prevalence data from 183 of 193 UN member states. 95% CIs were estimated by propagating uncertainty from the RR meta-estimates, prevalence of household air pollution exposure, and disease-specific mortality and burden estimates using a simulation-based approach. This study is registered with PROSPERO, CRD42019125060.Findings476 studies (15·5 million participants) from 123 nations (99 [80%] of which were classified as low-income and middle-income) met the inclusion criteria. Household air pollution was positively associated with asthma (RR 1·23, 95% CI 1·11-1·36), acute respiratory infection in both adults (1·53, 1·22-1·93) and children (1·39, 1·29-1·49), chronic obstructive pulmonary disease (1·70, 1·47-1·97), lung cancer (1·69, 1·44-1·98), and tuberculosis (1·26, 1·08-1·48); cerebrovascular disease (1·09, 1·04-1·14) and ischaemic heart disease (1·10, 1·09-1·11); and low birthweight (1·36, 1·19-1·55) and stillbirth (1·22, 1·06-1·41); as well as with under-5 (1·25, 1·18-1·33), respiratory (1·19, 1·18-1·20), and cardiovascular (1·07, 1·04-1·11) mortality. Household air pollution was associated with 1·8 million (95% CI 1·1-2·7) deaths and 60·9 million (34·6-93·3) DALYs in 2017, with the burden overwhelmingly experienced in low-income and middle-income countries (LMICs; 60·8 million [34·6-92·9] DALYs) compared with high-income countries (0·09 million [0·01-0·40] DALYs). From 2000, mortality associated with household air pollution had reduced by 36% (95% CI 29-43) and disease burden by 30% (25-36), with the greatest reductions observed in higher-income nations.InterpretationThe burden of cardiorespiratory, paediatric, and maternal diseases associated with household air pollution has declined worldwide but remains high in the world's poorest regions. Urgent integrated health and energy strategies are needed to reduce the adverse health impact of household air pollution, especially in LMICs.FundingBritish Heart Foundation, Wellcome Trust.
| S-EPMC7564377 | biostudies-literature
Project description:Cooking with polluting and inefficient fuels and technologies is responsible for a large set of global harms, ranging from health and time losses among the billions of people who are energy poor, to environmental degradation at a regional and global scale. This paper presents a new decision-support model-the BAR-HAP Tool-that is aimed at guiding planning of policy interventions to accelerate transitions towards cleaner cooking fuels and technologies. The conceptual model behind BAR-HAP lies in a framework of costs and benefits that is holistic and comprehensive, allows consideration of multiple policy interventions (subsidies, financing, bans, and behavior change communication), and realistically accounts for partial adoption and use of improved cooking technology. It incorporates evidence from recent efforts to characterize the relevant set of parameters that determine those costs and benefits, including those related to intervention effectiveness. Practical aspects of the tool were modified based on feedback from a pilot testing workshop with multisectoral users in Nepal. To demonstrate the functionality of the BAR-HAP tool, we present illustrative calculations related to several cooking transitions in the context of Nepal. In accounting for the multifaceted nature of the issue of household air pollution, the BAR-HAP model is expected to facilitate cross-sector dialogue and problem-solving to address this major health, environment and development challenge.
| S-EPMC7822293 | biostudies-literature
Project description:IntroductionHousehold air pollution from solid fuel burning kills over 4 million people every year including half a million children from acute lower respiratory infections. Although biologically plausible, it is not clear whether household air pollution is also associated with acute lower respiratory infections in adults. We systematically reviewed the literature on household air pollution and acute lower respiratory infection in adults to identify knowledge gaps and research opportunities.MethodsTen bibliographic databases were searched to identify studies of household air pollution and adult acute lower respiratory infection. Data were extracted from eligible studies using standardised forms.ResultsFrom 4617 titles, 513 abstracts and 72 full-text articles were reviewed. Eight studies met the inclusion criteria of which 2 found a significant adjusted increased risk of acute lower respiratory infection, 2 identified a univariate association whilst 4 found no significant association. Study quality was generally limited. Heterogeneity in methods and findings precluded meta-analysis.DiscussionA systematic review of the literature found limited evidence for an association between household air pollution and risk of acute lower respiratory infection in adults. Additional research, with carefully defined exposure and outcome measures, is required to complete the risk profile caused by household air pollution in adults.Registration numberCRD42015028042.
| S-EPMC5132292 | biostudies-literature
Project description:BackgroundThere is evidence for adverse effects of outdoor air pollution on lung function of children. Quantitative summaries of the effects of air pollution on lung function, however, are lacking due to large differences among studies.ObjectivesWe aimed to study the association between residential exposure to air pollution and lung function in five European birth cohorts with a standardized exposure assessment following a common protocol.MethodsAs part of the European Study of Cohorts for Air Pollution Effects (ESCAPE) we analyzed data from birth cohort studies situated in Germany, Sweden, the Netherlands, and the United Kingdom that measured lung function at 6-8 years of age (n = 5,921). Annual average exposure to air pollution [nitrogen oxides (NO2, NOx), mass concentrations of particulate matter with diameters < 2.5, < 10, and 2.5-10 ?m (PM2.5, PM10, and PMcoarse), and PM2.5 absorbance] at the birth address and current address was estimated by land-use regression models. Associations of lung function with estimated air pollution levels and traffic indicators were estimated for each cohort using linear regression analysis, and then combined by random effects meta-analysis.ResultsEstimated levels of NO2, NOx, PM2.5 absorbance, and PM2.5 at the current address, but not at the birth address, were associated with small decreases in lung function. For example, changes in forced expiratory volume in 1 sec (FEV1) ranged from -0.86% (95% CI: -1.48, -0.24%) for a 20-?g/m3 increase in NOx to -1.77% (95% CI: -3.34, -0.18%) for a 5-?g/m3 increase in PM2.5.ConclusionsExposure to air pollution may result in reduced lung function in schoolchildren.
| S-EPMC3855518 | biostudies-literature
Project description:BackgroundAlthough ambient air pollution has been linked to reduced lung function in healthy children, longitudinal analyses of pollution effects in asthmatic patients are lacking.ObjectiveWe sought to investigate pollution effects in a longitudinal asthma study and effect modification by controller medications.MethodsWe examined associations of lung function and methacholine responsiveness (PC20) with ozone, carbon monoxide (CO), nitrogen dioxide, and sulfur dioxide concentrations in 1003 asthmatic children participating in a 4-year clinical trial. We further investigated whether budesonide and nedocromil modified pollution effects. Daily pollutant concentrations were linked to ZIP/postal code of residence. Linear mixed models tested associations of within-subject pollutant concentrations with FEV1 and forced vital capacity (FVC) percent predicted, FEV1/FVC ratio, and PC20, adjusting for seasonality and confounders.ResultsSame-day and 1-week average CO concentrations were negatively associated with postbronchodilator percent predicted FEV1 (change per interquartile range, -0.33 [95% CI, -0.49 to -0.16] and -0.41 [95% CI, -0.62 to -0.21], respectively) and FVC (-0.19 [95% CI, -0.25 to -0.07] and -0.25 [95% CI, -0.43 to -0.07], respectively). Longer-term 4-month CO averages were negatively associated with prebronchodilator percent predicted FEV1 and FVC (-0.36 [95% CI, -0.62 to -0.10] and -0.21 [95% CI, -0.42 to -0.01], respectively). Four-month averaged CO and ozone concentrations were negatively associated with FEV1/FVC ratio (P < .05). Increased 4-month average nitrogen dioxide concentrations were associated with reduced postbronchodilator FEV1 and FVC percent predicted. Long-term exposures to sulfur dioxide were associated with reduced PC20 (percent change per interquartile range, -6% [95% CI, -11% to -1.5%]). Treatment augmented the negative short-term CO effect on PC20.ConclusionsAir pollution adversely influences lung function and PC20 in asthmatic children. Treatment with controller medications might not protect but rather worsens the effects of CO on PC20. This clinical trial design evaluates modification of pollution effects by treatment without confounding by indication.
| S-EPMC4742428 | biostudies-literature
Project description:Over half of the world's population is exposed to household air pollution from the burning of solid fuels at home. Household air pollution from solid fuel use is a leading risk factor for global disease and remains a major public health problem, especially in low- and mid-income countries. This is a particularly serious problem in China, where many people in rural areas still use coal for household heating and cooking. This review focuses on several decades of research carried out in Xuanwei County, Yunnan Province, where household coal use is a major source of household air pollution and where studies have linked household air pollution exposure to high rates of lung cancer. We conducted a series of case-control and cohort studies in Xuanwei to characterize the lung cancer risk in this population and the factors associated with it. We found lung cancer risk to vary substantially between different coal types, with a higher risk associated with smoky (i.e., bituminous) coal use compared to smokeless (i.e., anthracite) coal use. The installation of a chimney in homes resulted in a substantial reduction in lung cancer incidence and mortality. Overall, our research underscores the need among existing coal users to improve ventilation, use the least toxic fuel, and eventually move toward the use of cleaner fuels, such as gas and electricity.
| S-EPMC4198749 | biostudies-literature
Project description:ImportanceBreastfeeding and exposure to ambient air pollutants have been found to be independently associated with respiratory health in children; however, previous studies have not examined the association of breastfeeding as a potential moderator of the association.ObjectiveTo assess associations of breastfeeding and air pollution with lung function in children.Design, setting, and participantsUsing a cross-sectional study design, children were recruited from 62 elementary and middle schools located in 7 Chinese cities from April 1, 2012, to October 31, 2013. Data analyses were conducted from November 1, 2018, to March 31, 2019.ExposuresLong-term concentrations of airborne particulate matter with a diameter of 1 μm or less (PM1), airborne particulate matter with a diameter of 2.5 μm or less (PM2.5), airborne particulate matter with a diameter of 10 μm or less (PM10), and nitrogen dioxide were estimated using a spatial statistical model matched to children's geocoded home addresses, and concentrations of PM10, sulfur dioxide, nitrogen dioxide, and ozone were measured by local air monitoring stations.Main outcomes and measuresBreastfeeding was defined as maternal report of having mainly breastfed for longer than 3 months. Lung function was measured using portable electronic spirometers. Using previously published predicted spirometric values for children in Northeast China as the reference, lung impairment was defined as forced vital capacity (FVC) less than 85%, forced expiratory volume in the first second of expiration less than 85%, peak expiratory flow less than 75%, or maximum midexpiratory flow less than 75%.ResultsParticipants included 6740 children (mean [SD] age, 11.6 [2.1] years; 3382 boys [50.2%]). There were 4751 children (70.5%) who were breastfed. Mean (SD) particulate matter concentrations ranged from 46.8 (6.5) μg/m3 for PM1 to 95.6 (9.8) μg/m3 for PM10. The prevalence of lung function impairment ranged from 6.8% for peak expiratory flow to 11.3% for FVC. After controlling for age, sex, and other covariates, 1-interquartile range greater concentration of pollutants was associated with higher adjusted odds ratios (AORs) for lung function impairment by FVC among children who were not breastfed compared with those who were (PM1: AOR, 2.71 [95% CI, 2.02-3.63] vs 1.20 [95% CI, 0.97-1.48]; PM2.5: AOR, 2.27 [95% CI, 1.79-2.88] vs 1.26 [95% CI, 1.04-1.51]; and PM10: AOR, 1.93 [95% CI, 1.58-2.37] vs 1.46 [95% CI, 1.23-1.73]). Younger age (<12 years) was associated with lower lung function impairment among the children who had been breastfed. In children from elementary schools, 1-interquartile range greater concentration of pollutants was associated with higher AORs for lung function impairment by FVC among children who had not been breastfed compared with those who had (PM1: AOR, 6.43 [95% CI, 3.97-10.44] vs 1.89 [95% CI, 1.28-2.80]; PM2.5: AOR, 3.83 [95% CI, 2.63-5.58] vs 1.50 [95% CI, 1.12-2.01]; and PM10: AOR, 2.61 [95% CI, 1.90-3.57] vs 1.52 [95% CI, 1.19-1.95]). Results from linear regression models also showed associations of air pollution with worse lung function among children who were not breastfed compared with their counterparts who were breastfed, especially for FVC (PM1: β, -240.46 [95% CI, -288.71 to -192.21] vs -38.21 [95% CI, -69.27 to -7.16] mL) and forced expiratory volume in the first second of expiration (PM1: β, -201.37 [95% CI, -242.08 to -160.65] vs -30.30 [95% CI, -57.66 to -2.94] mL).Conclusions and relevanceIn this study, breastfeeding was associated with lower risk of lung function impairment among children in China exposed to air pollution, particularly among younger children.
| S-EPMC6632134 | biostudies-literature
Project description:Young children are particularly vulnerable to otitis media (OM) which globally affects over 80% of children below the age of 3 years. Although there is convincing evidence for an association between environmental tobacco smoke exposure and OM in children, the relationship with ambient air pollution is not clear. We aimed to systematically review the literature on the relationship between ambient air pollution exposure and OM in children. A systematic search was performed in PubMed and EMBASE databases. Of 934 references identified, 24 articles were included. There is an increasing body of evidence supporting an association between higher ambient air pollution exposure and a higher risk of OM in children. While NO₂ showed the most consistent association with OM, other specific pollutants showed inconsistent associations. Studies were mainly conducted in high/middle income countries with limited evidence from low-income countries. Although there was a general consensus that higher air pollution exposure is associated with a greater prevalence of OM, the evidence for associations with specific pollutants is inconsistent. More well-designed studies on associations between specific air pollutants as risk factors for OM are warranted, especially in low income countries with high air pollution levels.
| S-EPMC5858326 | biostudies-literature
Project description:Background Previous studies have investigated the association of ambient air pollution with blood pressure (BP) in children and adolescents, however, the results are not consistent. We conducted a systematic review and meta-analysis to assess the relationship between short-term and long-term ambient air pollutant exposure with BP values among children and adolescents. Methods and Results We searched PubMed, Web of Science, and Embase before September 6, 2020. Two reviewers independently searched and selected studies, extracted data, and assessed study quality. The studies were divided into groups by composition of air pollutants (NO2, particulate matter (PM) with diameter ≤10 μm or ≤2.5 μm) and length of exposure. The beta regression coefficients (β) and their 95% CIs were calculated to evaluate the strength of the effect with each 10 μg/m3 increase in air pollutants. Out of 36 650 articles, 14 articles were included in this meta-analysis. The meta-analysis showed short-term exposure to PM with diameter ≤10 μm (β=0.267; 95% CI, 0.033‒0.501) was significantly associated with elevated systolic BP values. In addition, long-term exposure to PM with diameter ≤2.5 μm (β=1.809; 95% CI, 0.962‒2.655), PM with diameter ≤10 μm (β=0.526; 95% CI, 0.095‒0.958), and NO2 (β=0.754; 95% CI, 0.541‒0.968) were associated with systolic BP values and long-term exposure to PM with diameter ≤2.5 μm (β=0.931; 95% CI, 0.157‒1.705), and PM with diameter ≤10 μm (β=0.378; 95% CI, 0.022‒0.735) was associated with diastolic BP. Conclusions Our study indicates that both short-term and long-term exposure to some ambient air pollutants may increase BP values among children and adolescents.
| S-EPMC8200690 | biostudies-literature