Air Pollution and Suppression of Lung Function Growth: A Triumph for Epidemiology.
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ABSTRACT:
SUBMITTER: Grigg J
PROVIDER: S-EPMC7049926 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:RationaleGlutathione plays an important role in antioxidant and inflammatory processes in the lung. Alterations in glutathione metabolism are a central feature of several chronic lung diseases.ObjectivesTo determine whether sequence variation in genes in the glutathione synthesis pathway alters susceptibility to air pollution effects on lung function.MethodsIn this prospective study, 14,821 lung function measurements were taken on 2,106 children from 12 Southern California cities. Tagging single-nucleotide polymorphisms in glutathione metabolism pathway genes GSS, GSR, GCLM, and GCLC were genotyped by GoldenGate assay (Illumina, San Diego, CA). Mixed regression models were used to determine whether particular haplotypes were associated with FEV(1), maximal mid-expiratory flow rate, and FVC and whether any of the genetic associations varied with levels of exposure to air pollutants.Measurements and main resultsWe found that variation in the GSS locus was associated with differences in susceptibility of children for lung function growth deficits associated with NO(2), PM(10), PM(2.5), elemental carbon, organic carbon, and O(3). The negative effects of air pollutants were largely observed within participants who had a particular GSS haplotype. The effects ranged from -124.2 to -149.1 for FEV(1), from -92.9 to -126.7 for FVC, and from -193.9 to -277.9 for maximal mid-expiratory flow rate for all pollutants except O(3), which showed a larger decrease in lung function in children without this haplotype.ConclusionsVariation in GSS was associated with differences in susceptibility to adverse effects of pollutants on lung function growth.
| S-EPMC3040392 | biostudies-literature
Project description:BackgroundThe interrelationships between air pollution, lung function and the incidence of childhood asthma have yet to be established. A study was undertaken to determine whether lung function is associated with new onset asthma and whether this relationship varies by exposure to ambient air pollutants.MethodsA cohort of children aged 9-10 years without asthma or wheeze at study entry were identified from the Children's Health Study and followed for 8 years. The participants resided in 12 communities with a wide range of ambient air pollutants that were measured continuously. Spirometric testing was performed and a medical diagnosis of asthma was ascertained annually. Proportional hazard regression models were fitted to investigate the relationship between lung function at study entry and the subsequent development of asthma and to determine whether air pollutants modify these associations.ResultsThe level of airway flow was associated with new onset asthma. Over the 10th-90th percentile range of forced expiratory flow over the mid-range of expiration (FEF(25-75), 57.1%), the hazard ratio (HR) of new onset asthma was 0.50 (95% CI 0.35 to 0.71). This protective effect of better lung function was reduced in children exposed to higher levels of particulate matter with an aerodynamic diameter <2.5 microm (PM(2.5)). Over the 10th-90th percentile range of FEF(25-75), the HR of new onset asthma was 0.34 (95% CI 0.21 to 0.56) in communities with low PM(2.5) (<13.7 microg/m(3)) and 0.76 (95% CI 0.45 to 1.26) in communities with high PM(2.5) (> or = 13.7 microg/m(3)). A similar pattern was observed for forced expiratory volume in 1 s. Little variation in HR was observed for ozone.ConclusionExposure to high levels of PM(2.5) attenuates the protective effect of better lung function against new onset asthma.
| S-EPMC2117135 | 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:BackgroundThe association of long-term air pollution and lung function has not been studied across adult European multi-national populations before. The aim of this study was to determine the association between long-term urban background air pollution and lung function levels, as well as change in lung function among European adults.MethodsForced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and the ratio thereof (FEV1/FVC) were assessed at baseline and after 9 years of follow-up in adults from 21 European centres (followed-up sample 5610). Fine particles (PM(2.5)) were measured in 2000/2001 using central monitors.ResultsDespite sufficient statistical power no significant associations were found between city-specific annual mean PM(2.5) and average lung function levels. The findings also do not support an effect on change in lung function, albeit statistical power was insufficient to significantly detect such an association.ConclusionsThe inability to refuse the null hypothesis may reflect (i) no effect of urban air pollution on lung function or (ii) inherent biases due to the study design. Examples of the latter are lack of individual-level air quality assignment, not quantified within-city contrasts in traffic-related pollution, or the heterogeneity of the studied populations and their urban environments. Future studies on long-term effects of air pollution on lung function could increase statistical power and reduce potential misclassification and confounding by characterizing exposure on the level of individuals, capturing contrasts due to local sources, in particular traffic.
| S-EPMC2734069 | biostudies-literature
Project description:RationaleExposure to ambient air pollutants has been associated with increased lung cancer incidence and mortality, but due to the high case fatality rate, little is known about the impacts of air pollution exposures on survival after diagnosis. This study aimed to determine whether ambient air pollutant exposures are associated with the survival of patients with lung cancer.MethodsParticipants were 352 053 patients with newly diagnosed lung cancer during 1988-2009 in California, ascertained by the California Cancer Registry. Average residential ambient air pollutant concentrations were estimated for each participant's follow-up period. Cox proportional hazards models were used to estimate HRs relating air pollutant exposures to all-cause mortality overall and stratified by stage (localised only, regional and distant site) and histology (squamous cell carcinoma, adenocarcinoma, small cell carcinoma, large cell carcinoma and others) at diagnosis, adjusting for potential individual and area-level confounders.ResultsAdjusting for histology and other potential confounders, the HRs associated with 1 SD increases in NO2, O3, PM10, PM2.5 for patients with localised stage at diagnosis were 1.30 (95% CI 1.28 to 1.32), 1.04 (95% CI 1.02 to 1.05), 1.26 (95% CI 1.25 to 1.28) and 1.38 (95% CI 1.35 to 1.41), respectively. Adjusted HRs were smaller in later stages and varied by histological type within stage (p<0.01, except O3). The largest associations were for patients with early-stage non-small cell cancers, particularly adenocarcinomas.ConclusionsThese epidemiological findings support the hypothesis that air pollution exposures after lung cancer diagnosis shorten survival. Future studies should evaluate the impacts of exposure reduction.
| S-EPMC5400105 | biostudies-literature
Project description:BackgroundImpaired lung function is predictive of mortality and is a key component of chronic obstructive pulmonary disease. Lung function has a strong genetic component but is also affected by environmental factors such as increased exposure to air pollution, but the effect of their interactions is not well understood.ObjectivesTo identify interactions between genetic variants and air pollution measures which affect COPD risk and lung function. Additionally, to determine whether previously identified lung function genetic association signals showed evidence of interaction with air pollution, considering both individual effects and combined effects using a genetic risk score (GRS).MethodsWe conducted a genome-wide gene-air pollution interaction analysis of spirometry measures with three measures of air pollution at home address: particulate matter (PM2.5 & PM10) and nitrogen dioxide (NO2), in approximately 300,000 unrelated European individuals from UK Biobank. We explored air pollution interactions with previously identified lung function signals and determined their combined interaction effect using a GRS.ResultsWe identified seven new genome-wide interaction signals (P<5×10-8), and a further ten suggestive interaction signals (P<5×10-7). Additionally, we found statistical evidence of interaction for FEV1/FVC between PM2.5 and previously identified lung function signal, rs10841302, near AEBP2, suggesting increased susceptibility as copies of the G allele increased (but size of the impact was small - interaction beta: -0.363 percentage points, 95% CI: -0.523, -0.203 per 5 µg/m3). There was no observed interaction between air pollutants and the weighted GRS.DiscussionWe carried out the largest genome-wide gene-air pollution interaction study of lung function and identified potential effects of clinically relevant size and significance. We observed up to 440 ml lower lung function for certain genotypes when exposed to mean levels of outdoor air pollution, which is approximately equivalent to nine years of average normal loss of lung function in adults.
| S-EPMC8739564 | 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:Cohort studies in air pollution epidemiology aim to establish associations between health outcomes and air pollution exposures. Statistical analysis of such associations is complicated by the multivariate nature of the pollutant exposure data as well as the spatial misalignment that arises from the fact that exposure data are collected at regulatory monitoring network locations distinct from cohort locations. We present a novel clustering approach for addressing this challenge. Specifically, we present a method that uses geographic covariate information to cluster multi-pollutant observations and predict cluster membership at cohort locations. Our predictive k-means procedure identifies centers using a mixture model and is followed by multi-class spatial prediction. In simulations, we demonstrate that predictive k-means can reduce misclassification error by over 50% compared to ordinary k-means, with minimal loss in cluster representativeness. The improved prediction accuracy results in large gains of 30% or more in power for detecting effect modification by cluster in a simulated health analysis. In an analysis of the NIEHS Sister Study cohort using predictive k-means, we find that the association between systolic blood pressure (SBP) and long-term fine particulate matter (PM2.5) exposure varies significantly between different clusters of PM2.5 component profiles. Our cluster-based analysis shows that for subjects assigned to a cluster located in the Midwestern U.S., a 10 ?g/m3 difference in exposure is associated with 4.37 mmHg (95% CI, 2.38, 6.35) higher SBP.
| S-EPMC5448716 | biostudies-literature
Project description: Not available
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