Occupational exposures and asthma-COPD overlap in a clinical cohort of adult-onset asthma.
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ABSTRACT:
SUBMITTER: Tommola M
PROVIDER: S-EPMC6801214 | biostudies-literature | 2019 Oct
REPOSITORIES: biostudies-literature
Publications
Occupational exposures and asthma-COPD overlap in a clinical cohort of adult-onset asthma.
Tommola Minna M Ilmarinen Pinja P Tuomisto Leena E LE Lehtimäki Lauri L Kankaanranta Hannu H
ERJ open research 20191021 4
<b>Occupational exposure to vapours, gases, dusts or fumes (VGDF) increases the prevalence of asthma-COPD overlap (ACO) in adult-onset asthma. VGDF exposure is independently associated with ACO and an additive effect with smoking is proposed.</b> http://bit.ly/2LiMiXW. ...[more]
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Project description:Although Asthma-COPD Overlap (ACO) has been described among populations of subjects with COPD or asthma, ACO has never been described among a population of subjects with occupational asthma (OA).The aims of this study were to: 1. identify ACO in a population of subjects with OA; and 2. compare the clinical characteristics between ACO and OA.This retrospective study included all subjects diagnosed with OA between 2000 and 2017 in an OA referral center. Occupational Asthma-COPD Overlap (OACO) was defined as post-bronchodilator FEV1/FVC < 70% and smoking history ? 10 pack-years, along with a diagnosis of OA.Three hundred and four subjects were included, 262 (86.2%) were classified as OA and 42 (13.8%) as OACO. OA subjects presented higher sputum eosinophil counts after a specific-inhalation challenge than subjects with OACO (median [IQR]: 6.5 [17.0] vs 2.3 [3.5]). After adjusting for confounding factors, subjects with OACO were older (OR: 1.10 [1.05; 1.14]) and were taking higher doses of inhaled corticosteroids than OA subjects (OR, 5.20 [1.77; 16.48]). Subjects with OACO were less often atopic than OA subjects (OR, 0.19 [0.07; 0.62]).Subjects with OACO constitute a distinct clinical and inflammatory phenotype from subjects with OA.
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Project description:PurposeRecent studies suggest that occupational inhalant exposures trigger exacerbations of asthma and chronic obstructive pulmonary disease, but findings are conflicting.MethodsWe included 7,768 individuals with self-reported asthma (n = 3,215) and/or spirometric airflow limitation (forced expiratory volume in 1 second (FEV1)/ forced expiratory volume (FVC) <0.70) (n = 5,275) who participated in The Copenhagen City Heart Study or The Copenhagen General Population Study from 2001-2016. Occupational exposure was assigned by linking job codes with job exposure matrices, and exacerbations were defined by register data on oral corticosteroid treatment, emergency care unit assessment or hospital admission. Associations between occupational inhalant exposure each year of follow-up and exacerbation were assessed by Cox regression with time varying exposure and age as the underlying time scale.ResultsParticipants were followed for a median of 4.6 years (interquartile range, IQR 5.4), during which 870 exacerbations occurred. Exacerbations were not associated with any of the selected exposures (high molecular weight sensitizers, low molecular weight sensitizers, irritants or low and high levels of mineral dust, biological dust, gases & fumes or the composite variable vapours, gases, dusts or fumes). Hazards ratios ranged from 0.8 (95% confidence interval: 0.7;1.0) to 1.2 (95% confidence interval: 0.9;1.7).ConclusionExacerbations of obstructive airway disease were not associated with occupational inhalant exposures assigned by a job exposure matrix. Further studies with alternative exposure assessment are warranted.
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Project description:The coexistence of COPD and asthma is widely recognized but has not been well described. This study characterizes clinical features, spirometry, and chest CT scans of smoking subjects with both COPD and asthma.We performed a cross-sectional study comparing subjects with COPD and asthma to subjects with COPD alone in the COPDGene Study.119 (13%) of 915 subjects with COPD reported a history of physician-diagnosed asthma. These subjects were younger (61.3 vs 64.7 years old, p=0.0001) with lower lifetime smoking intensity (43.7 vs 55.1 pack years, p=0.0001). More African-Americans reported a history of asthma (33.6% vs 15.6%, p<0.0001). Subjects with COPD and asthma demonstrated worse disease-related quality of life, were more likely to have had a severe COPD exacerbation in the past year, and were more likely to experience frequent exacerbations (OR 3.55 [2.19, 5.75], p<0.0001). Subjects with COPD and asthma demonstrated greater gas-trapping on chest CT. There were no differences in spirometry or CT measurements of emphysema or airway wall thickness.Subjects with COPD and asthma represent a relevant clinical population, with worse health-related quality of life. They experience more frequent and severe respiratory exacerbations despite younger age and reduced lifetime smoking history.ClinicalTrials.gov: NCT00608764.
| S-EPMC3204243 | biostudies-literature
Project description:Individuals with chronic obstructive pulmonary disease (COPD) and asthma are an important but poorly characterised group. The genetic determinants of COPD and asthma overlap have not been studied. The aim of this study was to identify clinical features and genetic risk factors for COPD and asthma overlap. Subjects were current or former smoking non-Hispanic whites or African-Americans with COPD. Overlap subjects reported a history of physician-diagnosed asthma before the age of 40 years. We compared clinical and radiographic features between COPD and overlap subjects. We performed genome-wide association studies (GWAS) in the non-Hispanic whites and African-American populations, and combined these results in a meta-analysis. More females and African-Americans reported a history of asthma. Overlap subjects had more severe and more frequent respiratory exacerbations, less emphysema and greater airway wall thickness compared to subjects with COPD alone. The non-Hispanic white GWAS identified single nucleotide polymorphisms in the genes CSMD1 (rs11779254, p=1.57 × 10(-6)) and SOX5 (rs59569785, p=1.61 × 10(-6)) and the meta-analysis identified single nucleotide polymorphisms in the gene GPR65 (rs6574978, p=1.18 × 10(-7)) associated with COPD and asthma overlap. Overlap subjects have more exacerbations, less emphysema and more airway disease for any degree of lung function impairment compared to COPD alone. We identified novel genetic variants associated with this syndrome. COPD and asthma overlap is an important syndrome and may require distinct clinical management.
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Project description:The biological mechanisms by which cleaning products and disinfectants-an emerging risk factor-affect respiratory health remain incompletely evaluated. Studying genes by environment interactions (G × E) may help identify new genes related to adult-onset asthma.We identified interactions between genetic polymorphisms of a large set of genes involved in the response to oxidative stress and occupational exposures to low molecular weight (LMW) agents or irritants on adult-onset asthma.Our data came from three large European cohorts: Epidemiological Family-based Study of the Genetics and Environment of Asthma (EGEA), Swiss Cohort Study on Air Pollution and Lung and Heart Disease in Adults (SAPALDIA), and European Community Respiratory Health Survey in Adults (ECRHS). A candidate pathway-based strategy identified 163 genes involved in the response to oxidative stress and potentially related to exposures to LMW agents/irritants. Occupational exposures were evaluated using an asthma job-exposure matrix and job-specific questionnaires for cleaners and healthcare workers. Logistic regression models were used to detect G × E interactions, adjusted for age, sex, and population ancestry, in 2,599 adults (mean age, 47 years; 60% women, 36% exposed, 18% asthmatics). p-Values were corrected for multiple comparisons.Ever exposure to LMW agents/irritants was associated with current adult-onset asthma [OR = 1.28 (95% CI: 1.04, 1.58)]. Eight single nucleotide polymorphism (SNP) by exposure interactions at five loci were found at p < 0.005: PLA2G4A (rs932476, chromosome 1), near PLA2R1 (rs2667026, chromosome 2), near RELA (rs931127, rs7949980, chromosome 11), PRKD1 (rs1958980, rs11847351, rs1958987, chromosome 14), and PRKCA (rs6504453, chromosome 17). Results were consistent across the three studies and after accounting for smoking.Using a pathway-based selection process, we identified novel genes potentially involved in adult asthma by interaction with occupational exposure. These genes play a role in the NF-?B pathway, which is involved in inflammation. Citation: Rava M, Ahmed I, Kogevinas M, Le Moual N, Bouzigon E, Curjuric I, Dizier MH, Dumas O, Gonzalez JR, Imboden M, Mehta AJ, Tubert-Bitter P, Zock JP, Jarvis D, Probst-Hensch NM, Demenais F, Nadif R. 2017. Genes interacting with occupational exposures to low molecular weight agents and irritants on adult-onset asthma in three European studies. Environ Health Perspect 125:207-214;?http://dx.doi.org/10.1289/EHP376.
| S-EPMC5289825 | biostudies-literature
Project description:BackgroundA considerable proportion of patients have features of both asthma and chronic obstructive pulmonary disease (COPD) simultaneously, called asthma-COPD overlap (ACO).ObjectivesThe aim of this study was to identify heterogeneity of ACO from a cohort of patients with severe asthma and COPD using the same diagnostic criteria.DesignWe used the International Severe Asthma Registry (ISAR) and the Korean COPD Subgroup Study (KOCOSS) to evaluate clinical characteristics of ACO from each cohort.MethodsWe classified subjects into four groups: (1) pure severe asthma, (2) ACO from the severe asthma cohort, (3) ACO from the COPD cohort, and (4) pure COPD. ACO was defined by satisfying extreme bronchodilator response (BDR) >15% and 400 ml and/or blood eosinophil count ⩾300 /µL in patients aged 40 years or older and post-BD forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) ratio <0.7.ResultsThe ACO group had 25 (23%) of 111 in the ISAR cohort and 403 (23%) of 1781 in the KOCOSS cohort. The ACO from the COPD cohort was older with more males and more smokers, but had similar degree of airflow limitation compared with the ACO from the severe asthma cohort. ICS-containing inhaler treatment was prescribed for all severe asthma subjects, but only for 43.9% of ACO subjects from the COPD cohort. Compared with patients having pure severe asthma, the risk for exacerbation was comparable in ACO either from severe asthma or COPD cohort [adjusted odds ratio (aOR): 1.54, 95% CI: 0.22-10.95 or aOR: 2.15, 95% CI: 0.59-7.85].ConclusionThe prevalence of ACO was similar in severe asthma and COPD cohorts applying identical diagnostic criteria. ACO from the severe asthma cohort was similar to ACO from the COPD cohort in terms of lung function and exacerbation risk.
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Project description:Solvents are used in many workplaces and may be airway irritants but few studies have examined their association with asthma. We studied this question in CONSTANCES (cohort of 'CONSulTANts des Centres d'Examens de Santé'), a large French cohort. Current asthma and asthma symptom scores were defined by participant-reported respiratory symptoms, asthma medication or attacks, and the sum of 5 symptoms, in the past 12 months, respectively. Lifetime exposures to 5 organic solvents, paints and inks were assessed by questionnaire and a population-based Job-Exposure Matrix (JEM). Cross-sectional associations between exposures and outcomes were evaluated by gender using logistic and negative binomial regressions adjusted for age, smoking habits and body mass index. Analyses included 115,757 adults (54% women, mean age 47 years, 9% current asthma). Self-reported exposure to ≥1 solvent was significantly associated with current asthma in men and women, whereas using the JEM, a significant association was observed only in women. Significant associations between exposures to ≥1 solvent and asthma symptom score were observed for both self-report (mean score ratio, 95%CI, women: 1.36, 1.31-1.42; men: 1.34, 1.30-1.40) and JEM (women: 1.10, 1.07-1.15; men: 1.14, 1.09-1.18). Exposure to specific solvents was significantly associated with higher asthma symptom score. Occupational exposure to solvents should be systematically sought when caring for asthma.
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Project description:BACKGROUND:The recognition of asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) as a distinct phenotype of COPD or asthma has increased. Although ACO has worse clinical features than non-ACO COPD, limited information is available on long-term outcomes of lung function decline for ACO and non-ACO COPD. METHODS:COPD patients with at least 3 years of follow-up were selected from the Korean Obstructive Lung Disease cohort. ACO was defined based on 3 major criteria: 1) airflow limitation in individuals 40 years of age and older, 2) ?10 pack-years of smoking history, and 3) a history of asthma or bronchodilator response of >?400 mL in forced expiratory volume in 1 s (FEV1) at baseline; and at least 1 minor criterion: 1) history of atopy or allergic rhinitis, 2) two separated bronchodilator responses of ?12% and 200 mL in FEV1, or 3) peripheral blood eosinophils ?300 cells/?L. Lung function decline was compared using a linear mixed effects model for longitudinal data with random intercept and random slope. RESULTS:Among 239 patients, 47 were diagnosed with ACO (19.7%). During the follow-up period, change in smoking status, use of inhaled corticosteroids (ICS) and long-acting ?2-agonists or ICS and at least 2 exacerbations per year were similar between patients with non-ACO COPD and ACO. Over a median follow-up duration of 5.8 years, patients with non-ACO COPD experienced a faster annual decline in pre-bronchodilator FEV1 than patients with ACO (-?29.3 ml/year vs. -13.9 ml/year, P?=?0.042), which was persistent after adjustment for confounders affecting lung function decline. CONCLUSION:Patients with ACO showed favorable longitudinal changes in lung function compared to COPD patients over a median follow-up of 5.8 years.
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Project description:Adult-onset asthma and chronic obstructive pulmonary disease (COPD) are major public health burdens. This review presents a comprehensive synopsis of their epidemiology, pathophysiology, and clinical presentations; describes how they can be distinguished; and considers both established and proposed new approaches to their management. Both adult-onset asthma and COPD are complex diseases arising from gene-environment interactions. Early life exposures such as childhood infections, smoke, obesity, and allergy influence adult-onset asthma. While the established environmental risk factors for COPD are adult tobacco and biomass smoke, there is emerging evidence that some childhood exposures such as maternal smoking and infections may cause COPD. Asthma has been characterized predominantly by Type 2 helper T cell (Th2) cytokine-mediated eosinophilic airway inflammation associated with airway hyperresponsiveness. In established COPD, the inflammatory cell infiltrate in small airways comprises predominantly neutrophils and cytotoxic T cells (CD8 positive lymphocytes). Parenchymal destruction (emphysema) in COPD is associated with loss of lung tissue elasticity, and small airways collapse during exhalation. The precise definition of chronic airflow limitation is affected by age; a fixed cut-off of forced expiratory volume in 1 second/forced vital capacity leads to overdiagnosis of COPD in the elderly. Traditional approaches to distinguishing between asthma and COPD have highlighted age of onset, variability of symptoms, reversibility of airflow limitation, and atopy. Each of these is associated with error due to overlap and convergence of clinical characteristics. The management of chronic stable asthma and COPD is similarly convergent. New approaches to the management of obstructive airway diseases in adults have been proposed based on inflammometry and also multidimensional assessment, which focuses on the four domains of the airways, comorbidity, self-management, and risk factors. Short-acting beta-agonists provide effective symptom relief in airway diseases. Inhalers combining a long-acting beta-agonist and corticosteroid are now widely used for both asthma and COPD. Written action plans are a cornerstone of asthma management although evidence for self-management in COPD is less compelling. The current management of chronic asthma in adults is based on achieving and maintaining control through step-up and step-down approaches, but further trials of back-titration in COPD are required before a similar approach can be endorsed. Long-acting inhaled anticholinergic medications are particularly useful in COPD. Other distinctive features of management include pulmonary rehabilitation, home oxygen, and end of life care.
| S-EPMC4166213 | biostudies-literature
Project description:Emphysema is a distinct feature for classifying COPD, and smoking history (?10 pack-years) is one of several newly proposed criteria for asthma-COPD overlap (ACO). We studied whether or not a smoking history (?10 pack-years) and emphysema are useful markers for classifying ACO and differentiating it from asthma with chronic airflow obstruction (CAO).We retrospectively studied the mortalities and frequencies of exacerbation in 256 consecutive patients with ACO (161 with emphysema and 95 without emphysema) who had ?10 pack-years smoking history, 64 asthma patients with CAO but less of a smoking history (<10 pack-years) and 537 consecutive patients with COPD (452 with emphysema and 85 without emphysema) from 2000 to 2016. In the patients with emergent admission, the causes were classified into COPD exacerbation, asthma attack, and others.No asthma patients with CAO had emphysema according to computed tomography findings. The prognoses were significantly better in patients with asthma and CAO than in those with ACO and COPD and better in those with ACO than in those with COPD. In both ACO and COPD patients, the prognoses were better in patients without emphysema than in those with it (P=0.027 and P=0.023, respectively). The frequencies of emergent admission were higher in COPD patients than in ACO patients, and higher in patients with emphysema than in patients without emphysema. ACO/emphysema (+) patients experienced more frequent admission due to COPD exacerbation (P<0.001), while ACO/emphysema (-) patients experienced more frequent admission due to asthma attack (P=0.014).A smoking history (?10 pack-years) was found to be a useful marker for differentiating ACO and asthma with CAO, and emphysema was a useful marker for classifying ACO. These markers are useful for predicting the overall survival and frequency of exacerbation.
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