LUNG FUNCTION IN SUBJECTS WITH OCCUPATIONAL CHRONIC OBSTRUCTIVE PULMONARY DISEASE EXPOSED TO INDUSTRIAL AEROSOLS CONTAINING NANOPARTICLES

2021 ◽  
Author(s):  
L.A. Shpagina ◽  
◽  
E.B. Logashenko ◽  
E.V. Anikina ◽  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Silica Nanoparticles ◽  
Pulmonary Disease ◽  
Mass Concentration ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Lung Volumes ◽  
Obstructive Pulmonary Disease ◽  
Occupational Copd

Abstract: Despite decrease in industrial aerosol impact on workers’ health there are disproportionately high prevalence of occupational lung diseases. So, it is of interest to investigate the role of nanoparticles. Objective was to establish lung function features in subjects with occupational chronic obstructive pulmonary disease (COPD) exposed to aerosols containing nanoparticles. Methods. It was a cross-sectional observational study. Subjects with occupational COPD (GOLD 2011-2021 criteria) exposed to aerosols containing metal (n=26) or silica nanoparticles (n=24) enrolled. Comparison group – tobacco smokers with COPD (n=50). Nanoparticles at workplaces air were measured by inductively coupled plasma atomic emission spectrometry and by scanning electron microscopy. Groups were matched by gender, age, COPD duration. Results. Occupational COPD in conditions of metal nanoparticles exposure was characterized by severe airflow limitation – forced expiratory volume in one second (FEV1) was 38%(35%;42%), by prominent increase in lung volumes – functional residual capacity (FRC) was 192% (184%;203%) and by highest decrease in diffusing lung capacity for carbon monoxide (DLco/Va), 34% (31%;38%). In occupational COPD subjects exposed to silica nanoparticles mild airflow limitation, mild increase in lung volumes and substantial decrease in DLco/Va, were seen. In logistic regression model metal nanoparticles mass concentration was associated with DLco/Va, FRC, FEV1, Raw and silica nanoparticles mass concentration – with DLco and FEV1. Conclusion. Nanoparticles in industrial aerosols are associated with occupational COPD phenotype.

scholarly journals Association of NLRP1 Coding Polymorphism with Lung Function and Serum IL-1β Concentration in Patients Diagnosed with Chronic Obstructive Pulmonary Disease (COPD)

Genes ◽  
2019 ◽  
Vol 10 (10) ◽  
pp. 783 ◽  
Author(s):  
Ozretić ◽  
da Silva Filho ◽  
Catalano ◽  
Sokolović ◽  
Vukić-Dugac ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Minor Allele ◽  
Fine Tuning ◽  
Airflow Limitation ◽  
Smoking History ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
The Impact

Chronic obstructive pulmonary disease (COPD) is a chronic disease characterized by a progressive decline in lung function due to airflow limitation, mainly related to IL-1β-induced inflammation. We have hypothesized that single nucleotide polymorphisms (SNPs) in NLRP genes, coding for key regulators of IL-1β, are associated with pathogenesis and clinical phenotypes of COPD. We recruited 704 COPD individuals and 1238 healthy controls for this study. Twenty non-synonymous SNPs in 10 different NLRP genes were genotyped. Genetic associations were estimated using logistic regression, adjusting for age, gender, and smoking history. The impact of genotypes on patients’ overall survival was analyzed with the Kaplan–Meier method with the log-rank test. Serum IL-1β concentration was determined by high sensitivity assay and expression analysis was done by RT-PCR. Decreased lung function, measured by a forced expiratory volume in 1 s (FEV1% predicted), was significantly associated with the minor allele genotypes (AT + TT) of NLRP1 rs12150220 (p = 0.0002). The same rs12150220 genotypes exhibited a higher level of serum IL-1β compared to the AA genotype (p = 0.027) in COPD patients. NLRP8 rs306481 minor allele genotypes (AG + AA) were more common in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) definition of group A (p = 0.0083). Polymorphisms in NLRP1 (rs12150220; OR = 0.55, p = 0.03) and NLRP4 (rs12462372; OR = 0.36, p = 0.03) were only nominally associated with COPD risk. In conclusion, coding polymorphisms in NLRP1 rs12150220 show an association with COPD disease severity, indicating that the fine-tuning of the NLRP1 inflammasome could be important in maintaining lung tissue integrity and treating the chronic inflammation of airways.

scholarly journals Adipokines NUCB2/Nesfatin-1 and Visfatin as Novel Inflammatory Factors in Chronic Obstructive Pulmonary Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Sirpa Leivo-Korpela ◽  
Lauri Lehtimäki ◽  
Mari Hämälainen ◽  
Katriina Vuolteenaho ◽  
Lea Kööbi ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Plasma Levels ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Diffusing Capacity ◽  
Obstructive Pulmonary Disease ◽  
Pulmonary Diffusing Capacity

COPD (chronic obstructive pulmonary disease) is a common lung disease characterized by airflow limitation and systemic inflammation. Recently, adipose tissue mediated inflammation has gathered increasing interest in the pathogenesis of the disease. In this study, we investigated the role of novel adipocytokines nesfatin-1 and visfatin in COPD by measuring if they are associated with the inflammatory activity, lung function, or symptoms. Plasma levels of NUCB2/nesfatin-1 and visfatin were measured together with IL-6, IL-8, TNF-α, and MMP-9, lung function, exhaled nitric oxide, and symptoms in 43 male patients with emphysematous COPD. The measurements were repeated in a subgroup of the patients after four weeks’ treatment with inhaled fluticasone. Both visfatin and NUCB2/nesfatin-1 correlated positively with plasma levels of IL-6 (r=0.341,P=0.027andrho=0.401,P=0.008, resp.) and TNF-α(r=0.305,P=0.052andrho=0.329,P=0.033, resp.) and NUCB2/nesfatin-1 also with IL-8 (rho=0.321,P=0.036) in patients with COPD. Further, the plasma levels of visfatin correlated negatively with pulmonary diffusing capacity (r=-0.369,P=0.016). Neither of the adipokines was affected by fluticasone treatment and they were not related to steroid-responsiveness. The present results introduce adipocytokines NUCB2/nesfatin-1 and visfatin as novel factors associated with systemic inflammation in COPD and suggest that visfatin may mediate impaired pulmonary diffusing capacity.

scholarly journals Epigenome-wide association study on asthma and chronic obstructive pulmonary disease overlap reveals aberrant DNA methylations related to clinical phenotypes

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yung-Che Chen ◽  
◽  
Ying-Huang Tsai ◽  
Chin-Chou Wang ◽  
Shih-Feng Liu ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Lung Function Decline ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Dna Methylations

AbstractWe hypothesized that epigenetics is a link between smoking/allergen exposures and the development of Asthma and chronic obstructive pulmonary disease (ACO). A total of 75 of 228 COPD patients were identified as ACO, which was independently associated with increased exacerbations. Microarray analysis identified 404 differentially methylated loci (DML) in ACO patients, and 6575 DML in those with rapid lung function decline in a discovery cohort. In the validation cohort, ACO patients had hypermethylated PDE9A (+ 30,088)/ZNF323 (− 296), and hypomethylated SEPT8 (− 47) genes as compared with either pure COPD patients or healthy non-smokers. Hypermethylated TIGIT (− 173) gene and hypomethylated CYSLTR1 (+ 348)/CCDC88C (+ 125,722)/ADORA2B (+ 1339) were associated with severe airflow limitation, while hypomethylated IFRD1 (− 515) gene with frequent exacerbation in all the COPD patients. Hypermethylated ZNF323 (− 296) / MPV17L (+ 194) and hypomethylated PTPRN2 (+ 10,000) genes were associated with rapid lung function decline. In vitro cigarette smoke extract and ovalbumin concurrent exposure resulted in specific DNA methylation changes of the MPV17L / ZNF323 genes, while 5-aza-2′-deoxycytidine treatment reversed promoter hypermethylation-mediated MPV17L under-expression accompanied with reduced apoptosis and decreased generation of reactive oxygen species. Aberrant DNA methylations may constitute a determinant for ACO, and provide a biomarker of airflow limitation, exacerbation, and lung function decline.

Screening of High-risk Patients for Chronic Obstructive Pulmonary Disease in Primary Care: A Narrative Review (Preprint)

2020 ◽  
Author(s):  
Ponrathi Athilingam ◽  
Andrew Bugajski ◽  
Usha Menon
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Current Knowledge ◽  
Screening Tools ◽  
Chronic Obstructive ◽  
Early Screening ◽  
Obstructive Pulmonary Disease ◽  
Impaired Lung Function ◽  
Risk Patients

UNSTRUCTURED Chronic obstructive pulmonary disease (COPD) predominantly affects older adults, and claimed 3 million lives in 2016, making it the third leading cause of death worldwide. Over 35 million Americans aged 40 or older have lung function consistent with diagnosable COPD. COPD and cardiovascular disease (CVD) have a bidirectional relationship, in that one is a risk factor for developing the other. National and international consortiums recommend early screening of adults at risk of COPD, such as those with CVD. Recommended screening strategies include screening tools to assess symptoms, medical history, and handheld spirometry. Handheld spirometry has high diagnostic accuracy and if impaired lung function is indicated, these patients are referred for pulmonary function testing (PFT), the diagnostic gold standard for COPD. However, there is no clinical consensus for pulmonary screening in people with CVD. Current knowledge relating to the prevalence and incidence of CVD in people with COPD and the mechanisms that underlie their coexistence is key in combating the global burden of COPD.

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