Dataset Information

Associations between Ambient Particulate Matter and Nitrogen Dioxide and Chronic Obstructive Pulmonary Diseases in Adults and Effect Modification by Demographic and Lifestyle Factors.

ABSTRACT: This study was undertaken to investigate the associations between chronic exposure to particulate matter of medium aerodynamic diameter ?10 or ?2.5 µm (PM10 or PM2.5) and nitrogen dioxide (NO?) levels and lung function and to examine a possible change in these relationships by demographic and lifestyle factors. Chronic obstructive pulmonary disease (COPD) was defined using the Global Initiative for COPD criteria (forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) of <70%). Associations of lung function and COPD with PM10 or PM2.5 or NO? were examined using linear and logistic regression analyses among 1264 Korean adults. The highest tertiles of PM2.5 (?37.1 ?g/m³) and NO? (?53.8 ?g/m³) exposure were significantly associated with COPD (highest versus lowest tertile of PM2.5: adjusted odds ratio (OR) = 1.79, 95% CI: 1.02-3.13; highest versus lowest tertile of NO?: adjusted OR = 1.83, 95% CI: 1.04-3.21). A 10 ?g/m³ increase in PM10 concentration was associated with a 1.85 L (95% CI -3.65 to -0.05) decrease in FEV1 and a 1.73 L (95% CI -3.35 to -0.12) decrease in FVC, with the strongest negative association among older people and those with less education. Reduced lung function was associated with PM2.5 exposure in subjects with no physical activity. This study provides evidence that exposure to ambient air pollution has adverse effects on lung function in adults.

SUBMITTER: Lamichhane DK

PROVIDER: S-EPMC5858432 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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Associations between Ambient Particulate Matter and Nitrogen Dioxide and Chronic Obstructive Pulmonary Diseases in Adults and Effect Modification by Demographic and Lifestyle Factors.

Lamichhane Dirga Kumar DK Leem Jong Han JH Kim Hwan Cheol HC

International journal of environmental research and public health 20180219 2

This study was undertaken to investigate the associations between chronic exposure to particulate matter of medium aerodynamic diameter ≤10 or ≤2.5 µm (PM<sub>10</sub> or PM<sub>2.5</sub>) and nitrogen dioxide (NO₂) levels and lung function and to examine a possible change in these relationships by demographic and lifestyle factors. Chronic obstructive pulmonary disease (COPD) was defined using the Global Initiative for COPD criteria (forced expiratory volume in 1 second (FEV1)/forced vital capa ...[more]

PMID: 29463050

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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

Project description:ImportanceThe association between short-term exposure to air pollution and mortality has been widely documented worldwide; however, few studies have applied causal modeling approaches to account for unmeasured confounders that vary across time and space.ObjectiveTo estimate the association between short-term changes in fine particulate matter (PM2.5) and nitrogen dioxide (NO2) concentrations and changes in daily all-cause mortality rates using a causal modeling approach.Design, setting, and participantsThis cross-sectional study used air pollution and mortality data from Jiangsu, China; California; central-southern Italy; and Germany with interactive fixed-effects models to control for both measured and unmeasured spatiotemporal confounders. A total of 8 963 352 deaths in these 4 regions from January 1, 2015, to December 31, 2019, were included in the study. Data were analyzed from June 1, 2021, to October 30, 2023.ExposureDay-to-day changes in county- or municipality-level mean PM2.5 and NO2 concentrations.Main outcomes and measuresDay-to-day changes in county- or municipality-level all-cause mortality rates.ResultsAmong the 8 963 352 deaths in the 4 study regions, a 10-μg/m3 increase in daily PM2.5 concentration was associated with an increase in daily all-cause deaths per 100 000 people of 0.01 (95% CI, 0.001-0.01) in Jiangsu, 0.03 (95% CI, 0.004-0.05) in California, 0.10 (95% CI, 0.07-0.14) in central-southern Italy, and 0.04 (95% CI, 0.02- 0.05) in Germany. The corresponding increases in mortality rates for a 10-μg/m3 increase in NO2 concentration were 0.04 (95% CI, 0.03-0.05) in Jiangsu, 0.03 (95% CI, 0.01-0.04) in California, 0.10 (95% CI, 0.05-0.15) in central-southern Italy, and 0.05 (95% CI, 0.04-0.06) in Germany. Significant effect modifications by age were observed in all regions, by sex in Germany (eg, 0.05 [95% CI, 0.03-0.06] for females in the single-pollutant model of PM2.5), and by urbanicity in Jiangsu (0.07 [95% CI, 0.04-0.10] for rural counties in the 2-pollutant model of NO2).Conclusions and relevanceThe findings of this cross-sectional study contribute to the growing body of evidence that increases in short-term exposures to PM2.5 and NO2 may be associated with increases in all-cause mortality rates. The interactive fixed-effects model, which controls for unmeasured spatial and temporal confounders, including unmeasured time-varying confounders in different spatial units, can be used to estimate associations between changes in short-term exposure to air pollution and changes in health outcomes.

Project description:BackgroundTime-location information (time spent on commuting, indoors and outdoors around residential and work places and physical activity) and infiltrated outdoor pollution was less considered estimating individual exposure to ambient air pollution. Studies investigating the association between individual exposure to particulate matter (PM) with aerodynamic diameter < 10 μm (PM10) and < 2.5 μm (PM2.5) and carotid atherosclerosis presented inconsistent results. Moreover, combined effect of pollutants on carotid atherosclerosis was not fully explored. We aimed to investigate the association between long-term individual time-weighted average exposure to PM2.5 and PM10 and the risk of carotid atherosclerosis, and further explore the overall effect of co-exposure to pollutants on carotid atherosclerosis.MethodsThe study population included 3069 participants derived from the Beijing Health Management Cohort (BHMC) study. Daily concentration of ambient air pollutants was estimated by land-use regression model at both residential and work addresses, and one- and two-year time-weighted average individual exposure was calculated by further considering personal activity pattern and infiltration of ambient air pollution indoors. We explored the association of PM2.5 and PM10 with carotid atherosclerosis and pooled the overall effect of co-exposure to ambient air pollutants by quantile g-computation.ResultsA significant association between time-weighted average exposure to PM2.5 and PM10 and carotid atherosclerosis was observed. Per interquartile range increase in two-year exposure to PM2.5 (Hazard ratio (HR): 1.322, 95% confidence interval (CI): 1.219-1.434) and PM10 (HR:1.213, 95% CI: 1.116-1.319) showed the strongest association with carotid atherosclerosis, respectively. Individuals in higher quartiles of pollutants were at higher risk for carotid atherosclerosis compared with those in the lowest quartile group. Concentration response functions documented the nearly linear and nonlinear relationship and interpreted the upward trends of the risk for carotid atherosclerosis with increasing level of pollutant concentrations. Moreover, effect estimates for the mixture of pollutants and carotid atherosclerosis were larger than any of the individual pollutants (HR (95% CI) was 1.510 (1.338-1.704) and 1.613 (1.428-1.822) per quartile increase for one-year and two-year time-weighted average exposure, respectively).ConclusionsIndividual time-weighted average exposure to PM2.5 and PM10 was associated with carotid atherosclerosis. Co-exposure to ambient air pollution was also positively associated with carotid atherosclerosis.

Dataset Information

Associations between Ambient Particulate Matter and Nitrogen Dioxide and Chronic Obstructive Pulmonary Diseases in Adults and Effect Modification by Demographic and Lifestyle Factors.

Publications

Associations between Ambient Particulate Matter and Nitrogen Dioxide and Chronic Obstructive Pulmonary Diseases in Adults and Effect Modification by Demographic and Lifestyle Factors.

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