Dataset Information

The effects of fine and coarse particulate matter on lung function among the elderly.

ABSTRACT: Impaired lung function is associated with morbidity and mortality in the elderly. However, there is a paucity of data regarding the long-term effects of particulate matter (PM) on lung function among the elderly. This study evaluated the exposure-response relationship between ambient PM and different lung function indices among the elderly in Taiwan. A cross-sectional survey of individuals aged ?65 years was conducted in Taiwan from October 2015 to September 2016. Those who attended the annual health examination for the elderly in five hospitals of varying background PM concentrations were enrolled. The long-term (2015 annual mean concentration) exposure to air pollution was estimated by the Kriging method at the residence of each subject. The association between ambient PM exposure and lung function was evaluated by linear regression modeling, with adjustments for age, sex, height, weight, educational attainment, presence of asthma or chronic obstructive pulmonary disease, smoking status, season, and co-pollutants. There were 1241 subjects (mean age, 70.5 years). The mean residential PM_2.5 and PM_2.5-10 in 2015 was 26.02 and 18.01??g/m³, respectively. After adjustments for confounders and co-pollutants, the FVC decrease was best associated with fine particles (PM_2.5), whereas the FEV₁, FEF_25-75%, FEF_25% and FEF_50% decreases were best associated with coarse particles (PM_2.5-10). An IQR (10??g/m³) increase in PM_2.5 decreased FVC by 106.38?ml (4.47%), while an IQR (7.29??g/m³) increase in PM_2.5-10 decreased FEV₁ and FEF_25-75% by 91.23?ml (4.85%) and 104.44?ml/s (5.58%), respectively. Among the Taiwanese elderly, long-term PM_2.5 exposure mainly decreases the vital capacity of lung function. Moreover, PM_2.5-10 has a stronger negative effect on the function of conductive airways than PM_2.5.

SUBMITTER: Chen CH

PROVIDER: S-EPMC6794286 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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The effects of fine and coarse particulate matter on lung function among the elderly.

Chen Chi-Hsien CH Wu Chih-Da CD Chiang Hung-Che HC Chu Dachen D Lee Kang-Yun KY Lin Wen-Yi WY Yeh Jih-I JI Tsai Kun-Wei KW Guo Yue-Liang Leon YL

Scientific reports 20191015 1

Impaired lung function is associated with morbidity and mortality in the elderly. However, there is a paucity of data regarding the long-term effects of particulate matter (PM) on lung function among the elderly. This study evaluated the exposure-response relationship between ambient PM and different lung function indices among the elderly in Taiwan. A cross-sectional survey of individuals aged ≥65 years was conducted in Taiwan from October 2015 to September 2016. Those who attended the annual h ...[more]

PMID: 31616001

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Project description:BackgroundDuring the 2010 Deepwater Horizon (DWH) disaster, controlled burning was conducted to remove oil from the water. Workers near combustion sites were potentially exposed to increased fine particulate matter [with aerodynamic diameter ≤2.5μm (PM2.5)] levels. Exposure to PM2.5 has been linked to decreased lung function, but to our knowledge, no study has examined exposure encountered in an oil spill cleanup.ObjectiveWe investigated the association between estimated PM2.5 only from burning/flaring of oil/gas and lung function measured 1-3 y after the DWH disaster.MethodsWe included workers who participated in response and cleanup activities on the water during the DWH disaster and had lung function measured at a subsequent home visit (n=2,316). PM2.5 concentrations were estimated using a Gaussian plume dispersion model and linked to work histories via a job-exposure matrix. We evaluated forced expiratory volume in 1 s (FEV1; milliliters), forced vital capacity (FVC; milliliters), and their ratio (FEV1/FVC; %) in relation to average and cumulative daily maximum exposures using multivariable linear regressions.ResultsWe observed significant exposure-response trends associating higher cumulative daily maximum PM2.5 exposure with lower FEV1 (p-trend=0.04) and FEV1/FVC (p-trend=0.01). In comparison with the referent group (workers not involved in or near the burning), those with higher cumulative exposures had lower FEV1 [-166.8mL, 95% confidence interval (CI): -337.3, 3.7] and FEV1/FVC (-1.7, 95% CI: -3.6, 0.2). We also saw nonsignificant reductions in FVC (high vs. referent: -120.9, 95% CI: -319.4, 77.6; p-trend=0.36). Similar associations were seen for average daily maximum PM2.5 exposure. Inverse associations were also observed in analyses stratified by smoking and time from exposure to spirometry and when we restricted to workers without prespill lung disease.ConclusionsAmong oil spill workers, exposure to PM2.5 specifically from controlled burning of oil/gas was associated with significantly lower FEV1 and FEV1/FVC when compared with workers not involved in burning. https://doi.org/10.1289/EHP8930.

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.

Project description:Exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality. PM2.5 (<2.5 μm) and ozone exposures have been shown to associate with carotid intima media thickness in humans. Animal studies support a causal relationship between air pollution and atherosclerosis and identified adverse PM effects on HDL functionality. We aimed to determine whether brief exposures to PM2.5 and/or ozone could induce effects on HDL anti-oxidant and anti-inflammatory capacity in humans.Subjects were exposed to fine concentrated ambient fine particles (CAP) with PM2.5 targeted at 150 μg/m(3), ozone targeted at 240 μg/m(3) (120 ppb), PM2.5 plus ozone targeted at similar concentrations, and filtered air (FA) for 2 h, on 4 different occasions, at least two weeks apart, in a randomized, crossover study. Blood was obtained before exposures (baseline), 1 h after and 20 h after exposures. Plasma HDL anti-oxidant/anti-inflammatory capacity and paraoxonase activity were determined. HDL anti-oxidant/anti-inflammatory capacity was assessed by a cell-free fluorescent assay and expressed in units of a HDL oxidant index (HOI). Changes in HOI (ΔHOI) were calculated as the difference in HOI from baseline to 1 h after or 20 h after exposures.There was a trend towards bigger ΔHOI between PM2.5 and FA 1 h after exposures (p = 0.18) but not 20 h after. This trend became significant (p <0.05) when baseline HOI was lower (<1.5 or <2.0), indicating decreased HDL anti-oxidant/anti-inflammatory capacity shortly after the exposures. There were no significant effects of ozone alone or in combination with PM2.5 on the change in HOI at both time points. The change in HOI due to PM2.5 showed a positive trend with particle mass concentration (p = 0.078) and significantly associated with the slope of systolic blood pressure during exposures (p = 0.005).Brief exposures to concentrated PM2.5 elicited swift effects on HDL anti-oxidant/anti-inflammatory functionality, which could indicate a potential mechanism for how particulate air pollution induces harmful cardiovascular effects.

Project description:Fine particulate matter (PM2.5) has been widely regarded as an important environmental risk factor that has widely influenced health of both animals and humans. Lung injury is the main cause of PM2.5 affecting respiratory tract health. Gut microbiota participates in the development of lung injury in many pathological processes. However, there is still unknown the specific effects of PM2.5 on the gut-lung axis in broilers. Thus, we conducted a broiler model based on 3-wk-old male Arbor Acres broiler to explore the underlying mechanism. Our results showed that PM2.5 exposure triggered TLR4 signaling pathway and induced the increase of IL-6, IFN-γ, TNF-α expression as well as the decrease of IL-10 expression in the lung. Inhaled PM2.5 exposure significantly altered the gut microbiota diversity and community. Specifically, PM2.5 exposure decreased α diversity and altered β diversity of gut microbiota, and reduced the abundance of DTU089, Oscillospirales, Staphylococcus, and increased the Escherichia-Shigella abundance, leading to the increase of gut-derived lipopolysaccharides (LPS). Moreover, PM2.5 significantly disrupted the intestinal epithelial barrier by reducing the expression of muc2 and claudin-1 to increase intestinal permeability, which possibly facilitated the LPS translocation into the blood. Spearman analysis revealed that gut microbiota dysbiosis was positively related to TLR4, TNF-α, and IFN-γ expression in the lung. In summary, our results showed that PM2.5 exposure induced lung injury by causing inflammation and triggering TLR4 signaling pathway, and also induced gut microbiota dysbiosis resulting in the overproduction of gut-derived LPS. And gut microbiota dysbiosis may be associated with lung injury. The above results provide basis data to comprehend the potential role of gut microbiota dysbiosis in the lung injury as well as providing a new regulatory target for alleviating lung injury associated with environmental pollutants.

Project description:Fine particulate matter (PM2.5) released during the livestock industry endangers the respiratory health of animals. Our previous findings suggested that broilers exposed to PM2.5 exhibited lung inflammation and changes in the pulmonary microbiome. Therefore, this study was to investigate whether the pulmonary microbiota plays a causal role in the pathogenesis of PM2.5-induced lung inflammation. We first used antibiotics to establish a pulmonary microbiota intervention broiler model, which showed a significantly reduced total bacterial load in the lungs without affecting the microbiota composition or structure. Based on it, 45 AA broilers of similar body weight were randomly assigned to three groups: control (CON), PM2.5 (PM), and pulmonary microbiota intervention (ABX-PM). From 21 d of age, broilers in the ABX-PM group were intratracheally instilled with antibiotics once a day for 3 d. Meanwhile, broilers in the other two groups were simultaneously instilled with sterile saline. On 24 and 26 d of age, broilers in the PM and ABX-PM groups were intratracheally instilled with PM2.5 suspension to induce lung inflammation, and broilers in the CON group were simultaneously instilled with sterile saline. The lung histomorphology, inflammatory cytokines' expression levels, lung microbiome, and microbial growth conditions were analyzed to determine the effect of the pulmonary microbiota on PM2.5-induced lung inflammation. Broilers in the PM group showed lung histological injury, while broilers in the ABX-PM group had normal lung histomorphology. Furthermore, microbiota intervention significantly reduced mRNA expression levels of interleukin-1β, tumor necrosis factor-α, interleukin-6, interleukin-8, toll-like receptor 4 and nuclear factor kappa-B. PM2.5 induced significant changes in the β diversity and structure of the pulmonary microbiota in the PM group. However, no significant changes in microbiota structure were observed in the ABX-PM group. Moreover, the relative abundance of Enterococcus cecorum in the PM group was significantly higher than that in the CON and ABX-PM groups. And sterile bronchoalveolar lavage fluid from the PM group significantly promoted the growth of E. cecorum, indicating that PM2.5 altered the microbiota's growth condition. In conclusion, pulmonary microbiota can affect PM2.5-induced lung inflammation in broilers. PM2.5 can alter the bacterial growth environment and promote dysbiosis, potentially exacerbating inflammation.

Dataset Information

The effects of fine and coarse particulate matter on lung function among the elderly.

Publications

The effects of fine and coarse particulate matter on lung function among the elderly.

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