Ambient particulate matter and lung function growth in Chinese children.
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ABSTRACT:
SUBMITTER: Roy A
PROVIDER: S-EPMC3985859 | biostudies-literature | 2012 May
REPOSITORIES: biostudies-literature
Publications
Ambient particulate matter and lung function growth in Chinese children.
Roy Ananya A Hu Wei W Wei Fusheng F Korn Leo L Chapman Robert S RS Zhang Junfeng Jim JJ
Epidemiology (Cambridge, Mass.) 20120501 3
<h4>Background</h4>Exposure to particulate matter (PM) has been associated with deficits in lung function growth among children in Western countries. However, few studies have explored this association in developing countries, where PM levels are often substantially higher.<h4>Methods</h4>Children (n = 3273) 6-12 years of age were recruited from 8 schools in 4 Chinese cities. The lung function parameters of forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) were measured ...[more]
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Project description:People generally spend more time indoors than outdoors resulting in a higher proportion of exposure to particulate matter (PM) occurring indoors. Consequently, indoor PM levels, in contrast to outdoor PM levels, may have a stronger relationship with lung function. To test this hypothesis, indoor and outdoor PM2.5 and fungal spore data were simultaneously collected from the homes of forty-four asthmatic children aged 10-16?years. An optical absorption technique was utilized on the collected PM2.5 mass to obtain concentrations of black carbon (BC) and ultraviolet light absorbing particulate matter, (UVPM; a marker of light absorbing PM2.5 emitted from smoldering organics). Enrolled children completed spirometry after environmental measurements were made. Given the high correlation between PM2.5, BC, and UVPM, principal component analysis was used to obtain uncorrelated summaries of the measured PM. Separate linear mixed-effect models were developed to estimate the association between principal components of the PM variables and spirometry values, as well as the uncorrelated original PM variables and spirometry values. A one-unit increase in the first principal component variable representing indoor PM (predominantly composed of UVPM and PM2.5) was associated with 4.1% decrease (99% CI?=?-6.9, -1.4) in FEV1/FVC ratio. 11.3??g/m3 increase in indoor UVPM was associated with 6.4% and 14.7% decrease (99% CI?=?-10.4, -2.4 and 99% CI?=?-26.3, -2.9, respectively) in percent predicted FEV1/FVC ratio and FEF25-75 respectively. Additionally, 17.7??g/m3 increase in indoor PM2.5 was associated with 6.1% and 12.9% decrease (99% CI?=?-10.2, -1.9 and 99% CI?=?-24.9, -1.0, respectively) in percent predicted FEV1/FVC ratio and FEF25-75, respectively. Outdoor PM, indoor BC, and indoor fungal spores were not significantly associated with lung function. The results indicate that indoor PM is more strongly associated with lung function in children with asthma as compared with outdoor PM.
| S-EPMC6392459 | biostudies-literature
Project description:BackgroundThe association between long-term exposure to ambient fine particulate matter with aerodynamic diameter ≤2.5μm (PM2.5) and lung function in young people remains uncertain, particularly in Asia, where air pollution is generally a serious problem.ObjectivesThis study investigated the association between long-term exposure to ambient PM2.5 and lung function in Taiwanese children, adolescents, and young adults.MethodsThis study comprised 24,544 participants 6-24 years of age, with 33,506 medical observations made between 2000 and 2014. We used a spatiotemporal model to estimate PM2.5 concentrations at participants' addresses. Spirometry parameters, i.e., forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and maximum midexpiratory flow (MMEF), were determined. A generalized linear mixed model was used to examine the associations between long-term exposure to ambient PM2.5 and lung function. The odds ratios (ORs) of poor lung function were also calculated after adjusting for a range of covariates.ResultsEvery 10-μg/m3 increase in the 2-y average PM2.5 concentration was associated with decreases of 2.22% [95% confidence interval (CI): -2.60, -1.85], 2.94 (95% CI: -3.36, -2.51), and 2.79% (95% CI: -3.15, -2.41) in the FVC, FEV1, and MMEF, respectively. Furthermore, it was associated with a 20% increase in the prevalence of poor lung function (OR: 1.20; 95% CI: 1.12, 1.29).ConclusionsTwo-year ambient PM2.5 concentrations were inversely associated with lung function and positively associated with the prevalence of poor lung function in children, adolescents, and young adults in Taiwan. https://doi.org/10.1289/EHP5220.
| S-EPMC6957275 | biostudies-literature
Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 µm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) –induced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naïve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Keywords: gene expression
2007-12-01 | GSE9465 | GEO
Project description:BackgroundEpidemiological observations have demonstrated that ambient fine particulate matter with dp < 2.5 μm (PM2.5) as the major factor responsible for the increasing incidence of lung cancer in never-smokers. However, there are very limited experimental data to support the association of PM2.5 with lung carcinogenesis and to compare PM2.5 with smoking carcinogens.MethodsTo study whether PM2.5 can contribute to lung tumorigenesis in a way similar to smoking carcinogen 4-methylnitrosamino-l-3-pyridyl-butanone (NNK) via 15-lipoxygenases (15-LOXs) reduction, normal lung epithelial cells and cancer cells were treated with NNK or PM2.5 and then epigenetically and post-translationally examined the cellular and molecular profiles of the cells. The data were verified in lung cancer samples and a mouse lung tumor model.ResultsWe found that similar to smoking carcinogen NNK, PM2.5 significantly enhanced cell proliferation, migration and invasion, but reduced the levels of 15-lipoxygenases-1 (15-LOX1) and 15-lipoxygenases-2 (15-LOX2), both of which were also obviously decreased in lung cancer tissues. 15-LOX1/15-LOX2 overexpression inhibited the oncogenic cell functions induced by PM2.5/NNK. The tumor formation and growth were significantly higher/faster in mice implanted with PM2.5- or NNK-treated NCI-H23 cells, accompanied with a reduction of 15-LOX1/15-LOX2. Moreover, 15-LOX1 expression was epigenetically regulated at methylation level by PM2.5/NNK, while both 15-LOX1 and 15-LOX2 could be significantly inhibited by a set of PM2.5/NNK-mediated microRNAs.ConclusionCollectively, PM2.5 can function as the smoking carcinogen NNK to induce lung tumorigenesis by inhibiting 15-LOX1/15-LOX2.
| S-EPMC6697918 | biostudies-literature
Project description:ImportanceOutdoor particulate matter 2.5 μm or less in diameter (PM2.5) is a ubiquitous environmental neurotoxicant that may affect the developing brain. Little is known about associations between PM2.5 and white matter connectivity.ObjectivesTo assess associations between annual residential PM2.5 exposure and white matter microstructure health in a US sample of children 9 to 10 years of age and to examine whether associations are specific to certain white matter pathways or vary across neuroimaging diffusion markers reflective of intracellular and extracellular microstructural processes.Design, setting, and participantsThis cross-sectional study, the Adolescent Brain and Cognitive Development (ABCD) Study, was composed of 21 study sites across the US and used baseline data collected from children 9 to 10 years of age from September 1, 2016, to October 15, 2018. Data analysis was performed from September 15, 2020, to June 30, 2021.ExposuresAnnual mean PM2.5 exposure estimated by ensemble-based models and assigned to the primary residential addresses at baseline.Main outcomes and measuresDiffusion-weighted imaging (DWI) and tractography were used to delineate white matter tracts. The biophysical modeling technique of restriction spectrum imaging (RSI) was implemented to examine total hindered diffusion and restricted isotropic and anisotropic intracellular diffusion in each tract. Hierarchical mixed-effects models with natural splines were used to analyze the associations between PM2.5 exposure and DWI.ResultsIn a study population of 7602 children (mean [SD] age, 119.1 [7.42] months; 3955 [52.0%] female; 160 [ 21.%] Asian, 1025 [13.5%] Black, 1616 [21.3%] Hispanic, 4025 [52.9%] White, and 774 [10.2%] other [identified by parents as American Indian/Native American or Alaska Native; Native Hawaiian, Guamanian, Samoan, other Pacific Islander; Asian Indian, Chinese, Filipino, Japanese, Korean, Vietnamese, or other Asian; or other race]), associations were seen between annual ambient PM2.5 and hemispheric differences in white matter microstructure. Hemisphere-stratified models revealed significant associations between PM2.5 exposure and restricted isotropic intracellular diffusion in the left cingulum, in the left superior longitudinal fasciculus, and bilaterally in the fornix and uncinate fasciculus. In tracts with strong positive associations, a PM2.5 increase from 8 to 12 μg/m3 was associated with increases of 2.16% (95% CI, 0.49%-3.84%) in the left cingulum, 1.95% (95% CI, 0.43%-3.47%) in the left uncinate, and 1.68% (95% CI, 0.01%-3.34%) in the right uncinate. Widespread negative associations were observed between PM2.5 and mean diffusivity.Conclusions and relevanceThe findings of this cross-sectional study suggest that annual mean PM2.5 exposure during childhood is associated with increased restricted isotropic diffusion and decreased mean diffusivity of specific white matter tracts, potentially reflecting differences in the composition of white matter microarchitecture.
| S-EPMC8662373 | biostudies-literature
Project description:BackgroundFetal growth restriction (FGR) is not only a major determinant of perinatal morbidity and mortality but also leads to adverse health effects in later life. Over the past decade, numerous studies have indicated that maternal exposure to ambient air pollution has been a risk factor for abnormal fetal growth in developed countries where PM2.5 levels are relatively low. However, studies in highly polluted regions, such as China, and studies that rely on assessments in utero are scarce.MethodsA total of 7965 women were selected from 11,441 women from the Shanghai Maternity and Infant Living Environment (SMILE) cohort who were pregnant between January 1, 2014, and April 30, 2015. From January 1, 2014, to April 30, 2015, weekly average PM2.5 values from 53 monitors were calculated and the inverse distance weighted (IDW) method was used to create a Shanghai pollution surface map according to the participants residential addresses. Individual exposure was the average PM2.5 value of every gestational week between the first gestational week and one week before the ultrasound measurement date (the range of measurements per participant was 1 to 10). Repeated fetal ultrasound measurements during gestational weeks 14~40 were selected. The estimated fetal weight (EFW) was calculated by biparietal diameter (BPD), abdominal circumference (AC), and femur length (FL) formulas. In total, 29,926 ultrasound measurements were analysed. Demographic variables, other pollutants (SO2, NO2, PM10 and O3) and relative humidity and temperature were controlled for potential confounding through generalized estimating equations (GEE).ResultsThe full model showed that with each 10 μg/m3 increase in PM2.5 exposure, the means (mm) of AC, BPD, FL decreased by 5.48 (- 9.06, - 1.91), 5.57 (- 6.66, - 4.47), and 5.47 (- 6.39, - 4.55), respectively; the mean EFW decreased by 14.49 (- 16.05, - 13.49) grams by Hadlock's third formula and 13.56 (- 14.71, - 12.50) grams by Shepard's formula with each 10 μg/m3 increase in PM2.5 exposure.ConclusionsA negative correlation existed between maternal PM2.5 exposure during pregnancy and fetal growth indicators, which may increase the risk of fetal growth restriction.
| S-EPMC6524254 | biostudies-literature
Project description:Air pollution exposure during pregnancy has been associated with impaired fetal growth and postnatal weight gain, but few studies have examined the effect on weight growth trajectories. We examine the association between validated 1 km2 resolution particulate matter (PM2.5) concentrations, averaged over pregnancy, and sex-specific growth trajectories from birth to age six of participants in the Boston-based Children's HealthWatch cohort (4797 participants, 84,283 measures). We compared weight trajectories, predicted using polynomial splines in mixed models, between prenatal PM2.5 above or below the median (9.5 µg/m3), and examined birth weight as an effect modifier. Females exposed to average prenatal PM2.5 ≥ 9.5 µg/m3 had higher weights compared to females exposed to < 9.5 µg/m3 throughout the study period (0.16 kg at 24 months, 0.61 kg at 60 months). In males, higher prenatal PM2.5 exposure was associated with significantly lower weights after 24 months of age, with differences increasing with time (-0.17 at 24 months, -0.72 kg at 60 months). Associations were more pronounced among low birth weight (<2500 g) females, but did not differ by birth weight status in males. Our findings demonstrate the complex association between air pollution exposures and childhood weight trajectories and emphasize the importance of sex-stratified analyses.
| S-EPMC7068568 | biostudies-literature
Project description:BackgroundAsthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Epidemiologic studies have demonstrated that exposures to environmental factors such as ambient particulate matter (PM), a major air pollutant, contribute to increased asthma prevalence and exacerbations.ObjectiveWe investigated pathophysiologic responses to Baltimore, Maryland, ambient PM (median diameter, 1.78 mum) in a murine model of asthma and attempted to identify PM-specific genomic/molecular signatures.MethodsWe exposed ovalbumin (OVA)-sensitized A/J mice intratracheally to PM (20 mg/kg), and assayed both AHR and bronchoalveolar lavage (BAL) on days 1, 4, and 7 after PM exposure. Lung gene expression profiling was analyzed in OVA- and PM-challenged mice.ResultsConsistent with this murine model of asthma, we observed significant increases in airway responsiveness in OVA-treated mice, with PM exposure inducing significant changes in AHR in both naive mice and OVA-induced asthmatic mice. PM evoked eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of type 1 T helper (T(H)1) cytokines [interferon-gamma, interleukin-6 (IL-6), tumor necrosis factor-alpha] and T(H)2 cytokines (IL-4, IL-5, eotaxin) into murine airways. Furthermore, PM consistently induced expression of genes involved in innate immune responses, chemotaxis, and complement system pathways.ConclusionThis study is consistent with emerging epidemiologic evidence and indicates that PM exposure evokes proinflammatory and allergic molecular signatures that may directly contribute to the asthma susceptibility in naive subjects and increased severity in affected asthmatics.
| S-EPMC2592270 | biostudies-literature
Project description:BackgroundFetal growth has been known to be associated with particulate matter (PM) air pollution during gestation. Given that regular working may deviate outdoor air pollution exposure, the association between air pollution and fetal growth restriction can be different across maternal working status. This study was to assess possible effect modification by maternal employment in the association between exposure to PM during pregnancy and fetal growth restriction.MethodsUsing hourly PM less than or equal to 10 and 2.5??m in diameter (PM10 and PM2.5) regulatory monitoring data for 2001-2012 and 2008-2012, respectively, and birth certificate data for 2002-2012, we computed maternal exposures with district-level averages of PM10 and PM2.5 during one year before birth, entire pregnancy, and the 1st, 2nd and 3rd trimesters. The outcomes of fetal growth restriction were assessed by small for gestational age (SGA, weighted <10th percentile in the same gestational age) as well as low birth weight (LBW, <?2.5?kg) at term. We performed logistic regression to examine the association between PM and each of fetal growth restriction outcomes adjusting for individual risk factors. For effect modification by maternal employment, we estimated adjusted odds ratio (OR) of SGA or LBW for interquartile (IQR) increases in PM10 or PM2.5 stratified by employed and non-employed mothers. We also computed relative excess risk due to interaction (RERI) to investigate additive interaction.ResultsAmong 824,011 singleton term births, 34.0% (279,856) were employed and 66.0% (544,155) were non-employed mothers. Proportions of LBW were 1.5% in employed and 1.6% in non-employed (P <?0.001). SGA occurred in 12.7% of employed and 12.8% of non- employed (P =?0.124) mothers. For non-employed mothers, we observed increased odds of SGA per IQR increase in PM10 for one year before birth (OR?=?1.02, 95% confidence intervals (CI): 1.00-1.04, P =?0.028). ORs of SGA for full pregnancy period and the 3rd trimester were also positive but did not reach statistical significance. We did not observe positive association for PM2.5. RERI was not significant both for PM10 and PM2.5.ConclusionsWe did not observe evidence of effect modification by maternal employment in the association between ambient PM and fetal growth restriction. Future studies using more refined exposure measures should confirm this finding.
| S-EPMC6632189 | biostudies-literature
Project description:Background/Objective:Wintertime thermal inversions in narrow mountain valleys create a ceiling effect, increasing concentration of small particulate matter (PM2.5). Despite potential health risks, many people continue to exercise outdoors in thermal inversions. This study measured the effects of ambient PM2.5 exposure associated with a typical thermal inversion on exercise performance, pulmonary function, and biological markers of inflammation. Methods:Healthy, active adults (5 males, 11 females) performed two cycle ergometer time trials outdoors in a counterbalanced design: 1) low ambient PM2.5 concentrations (<12??g/m3), and 2) an air quality index (AQI) ranking of "yellow." Variables of interest were exercise performance, exhaled nitric oxide (eNO), c-reactive protein (CRP), forced vital capacity (FVC), and forced expiratory volume in 1?s (FEV1). Results:Despite a significant difference in mean PM2.5 concentration of 9.3?±?3.0??g/m3 between trials (p?<?.001), there was no significant difference (p?=?.424) in the distance covered during low PM2.5 conditions (9.9?±?1.7?km) compared to high PM2.5 conditions (10.1?±?1.5?km). There were no clinically significant differences across time or between trials for eNO, CRP, FVC, or FEV1. Additionally, there were no dose-response relationships (p?>?.05) for PM2.5 concentration and the measured variables. Conclusion:An acute bout of vigorous exercise during an AQI of "yellow" did not diminish exercise performance in healthy adults, nor did it have a negative effect on pulmonary function or biological health markers. These variables might not be sensitive to small changes from acute, mild PM2.5 exposure.
| S-EPMC6323157 | biostudies-literature