Under the U.S. Lung Allocation Score (LAS) system, older and sicker patients are prioritized for lung transplantation (LT). The impact of these changes on health‐related quality of life (HRQL) after ...transplant has not been determined. In a single‐center prospective cohort study from 2010 to 2016, we assessed HRQL before and repeatedly after LT for up to 3 years using the SF12‐Physical and Mental Health, the respiratory‐specific Airway Questionnaire 20‐Revised, and the Euroqol 5D/Visual Analog Scale utility measures by multivariate linear mixed models jointly modeled with death. We also tested changes in LT‐Valued Life Activities disability, BMI, allograft function, and 6‐min walk test exercise capacity as predictors of HRQL change. Among 211 initial participants (92% of those eligible), LT improved HRQL by all 5 measures (p < 0.05) and all but SF12‐Mental Health improved by threefold or greater than the minimally clinically important difference. Compared to younger participants, those aged ≥65 improved less in SF12‐Physical and Mental Health (p < 0.01). Improvements in disability accounted for much of the HRQL improvement. In the LAS era, LT affords meaningful and durable HRQL improvements, mediated by amelioration of disability. Identifying factors limiting HRQL improvement in selected subgroups, especially those aged ≥65, are needed to maximize the net benefits of LT.
In a prospective longitudinal adult cohort, the authors find that lung transplantation substantially improves health‐related quality of life and that this improvement is largely mediated by amelioration of physical disability, though older adults and those undergoing transplantation for diagnoses other than cystic fibrosis derive a smaller benefit in health‐related quality of life.
Full text
Available for:
BFBNIB, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The contribution of occupational exposures to chronic obstructive pulmonary disease (COPD) and, in particular, their potential interaction with cigarette smoking remains underappreciated.
Data from ...the FLOW study of 1202 subjects with COPD (of which 742 had disease classified as stage II or above by Global Obstructive Lung Disease (GOLD) criteria) and 302 referent subjects matched by age, sex and race recruited from a large managed care organisation were analysed. Occupational exposures were assessed using two methods: self-reported exposure to vapours, gas, dust or fumes on the longest held job (VGDF) and a job exposure matrix (JEM) for probability of exposure based on occupation. Multivariate analysis was used to control for age, sex, race and smoking history. The odds ratio (OR) and adjusted population attributable fraction (PAF) associated with occupational exposure were calculated.
VGDF exposure was associated with an increased risk of COPD (OR 2.11; 95% CI 1.59 to 2.82) and a PAF of 31% (95% CI 22% to 39%). The risk associated with high probability of workplace exposure by JEM was similar (OR 2.27; 95% CI 1.46 to 3.52), although the PAF was lower (13%; 95% CI 8% to 18%). These estimates were not substantively different when the analysis was limited to COPD GOLD stage II or above. Joint exposure to both smoking and occupational factors markedly increased the risk of COPD (OR 14.1; 95% CI 9.33 to 21.2).
Workplace exposures are strongly associated with an increased risk of COPD. On a population level, prevention of both smoking and occupational exposure, and especially both together, is needed to prevent the global burden of disease.
As the environments in which livestock are reared become more variable, animal robustness becomes an increasingly valuable attribute. Consequently, there is increasing focus on managing and breeding ...for it. However, robustness is a difficult phenotype to properly characterise because it is a complex trait composed of multiple components, including dynamic elements such as the rates of response to, and recovery from, environmental perturbations. In this review, the following definition of robustness is used: the ability, in the face of environmental constraints, to carry on doing the various things that the animal needs to do to favour its future ability to reproduce. The different elements of this definition are discussed to provide a clearer understanding of the components of robustness. The implications for quantifying robustness are that there is no single measure of robustness but rather that it is the combination of multiple and interacting component mechanisms whose relative value is context dependent. This context encompasses both the prevailing environment and the prevailing selection pressure. One key issue for measuring robustness is to be clear on the use to which the robustness measurements will employed. If the purpose is to identify biomarkers that may be useful for molecular phenotyping or genotyping, the measurements should focus on the physiological mechanisms underlying robustness. However, if the purpose of measuring robustness is to quantify the extent to which animals can adapt to limiting conditions then the measurements should focus on the life functions, the trade-offs between them and the animal’s capacity to increase resource acquisition. The time-related aspect of robustness also has important implications. Single time-point measurements are of limited value because they do not permit measurement of responses to (and recovery from) environmental perturbations. The exception being single measurements of the accumulated consequence of a good (or bad) adaptive capacity, such as productive longevity and lifetime efficiency. In contrast, repeated measurements over time have a high potential for quantification of the animal’s ability to cope with environmental challenges. Thus, we should be able to quantify differences in adaptive capacity from the data that are increasingly becoming available with the deployment of automated monitoring technology on farm. The challenge for future management and breeding will be how to combine various proxy measures to obtain reliable estimates of robustness components in large populations. A key aspect for achieving this is to define phenotypes from consideration of their biological properties and not just from available measures.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
ABSTRACT
There is a severe tension between the observed star formation rate (SFR)–stellar mass (M⋆) relations reported by different authors at z = 1–4. In addition, the observations have not been ...successfully reproduced by state-of-the-art cosmological simulations that tend to predict a factor of 2–4 smaller SFRs at a fixed M⋆. We examine the evolution of the SFR–M⋆ relation of z = 1–4 galaxies using the skirt simulated spectral energy distributions of galaxies sampled from the Evolution and Assembly of GaLaxies and their Environments simulations. We derive SFRs and stellar masses by mimicking different observational techniques. We find that the tension between observed and simulated SFR–M⋆ relations is largely alleviated if similar methods are used to infer the galaxy properties. We find that relations relying on infrared wavelengths (e.g. 24 ${\rm \, \mu m}$, MIPS – 24, 70, and 160 ${\rm \, \mu m}$ or SPIRE – 250, 350, and 500 ${\rm \, \mu m}$) have SFRs that exceed the intrinsic relation by 0.5 dex. Relations that rely on the spectral energy distribution fitting technique underpredict the SFRs at a fixed stellar mass by −0.5 dex at z ∼ 4 but overpredict the measurements by 0.3 dex at z ∼ 1. Relations relying on dust-corrected rest-frame ultraviolet luminosities, are flatter since they overpredict/underpredict SFRs for low/high star-forming objects and yield deviations from the intrinsic relation from 0.10 to −0.13 dex at z ∼ 4. We suggest that the severe tension between different observational studies can be broadly explained by the fact that different groups employ different techniques to infer their SFRs.
BackgroundAlthough chronic obstructive pulmonary disease (COPD) is a common cause of death and disability, little is known about the effects of socioeconomic status (SES) and race–ethnicity on health ...outcomes.MethodsThe aim of this study is to determine the independent impacts of SES and race–ethnicity on COPD severity status, functional limitations and acute exacerbations of COPD among patients with access to healthcare. Data were used from the Function, Living, Outcomes and Work cohort study of 1202 Kaiser Permanente Northern California Medical Care Plan members with COPD.ResultsLower educational attainment and household income were consistently related to greater disease severity, poorer lung function and greater physical functional limitations in cross-sectional analysis. Black race was associated with greater COPD severity, but these differences were no longer apparent after controlling for SES variables and other covariates (comorbidities, smoking, body mass index and occupational exposures). Lower education and lower income were independently related to a greater prospective risk of acute COPD exacerbation (HR 1.5; 95% CI 1.01 to 2.1; and HR 2.1; 95% CI 1.4 to 3.4, respectively).ConclusionLow SES is a risk factor for a broad array of adverse COPD health outcomes. Clinicians and disease management programs should consider SES as a key patient-level marker of risk for poor outcomes.
Full text
Available for:
BFBNIB, CMK, NMLJ, NUK, PNG, SAZU, UL, UM, UPUK
Health‐related quality of life (HRQL) has been assessed in various lung transplantation (LT) investigations but never analyzed systematically across multiple studies. We addressed this knowledge gap ...through a systematic literature review. We searched the PubMed, CINAHL and PsychInfo databases for publications from January 1, 1983 to December 31, 2011. We performed a thematic analysis of published studies of HRQL in LT. Using a comparative, consensus‐based approach, we identified themes that consistently emerged from the data, classifying each study according to primary and secondary thematic categories as well as by study design. Of 749 publications initially identified, 73 remained after exclusions. Seven core themes emerged: (1) Determinants of HRQL; (2) Psychosocial factors in HRQL; (3) Pre‐ and posttransplant HRQL comparisons; (4) Long‐term longitudinal HRQL studies; (5) HRQL effects of therapies and interventions; (6) HRQL instrument validation and methodology; (7) HRQL prediction of clinical outcomes. Overall, LT significantly and substantially improves HRQL, predominantly in domains related to physical health and functioning. The existing literature demonstrates substantial heterogeneity in methodology and approach; relatively few studies assessed HRQL longitudinally within the same persons. Opportunity for future study lies in validating existing and potential novel HRQL instruments and further elucidating the determinants of HRQL through longitudinal multidimensional investigation.
In this systematic review of health‐related quality of life in lung transplantation, the authors use thematic analysis to synthesize and categorize the existing biomedical literature into seven emergent themes, and they highlight limitations in the literature and offer a roadmap for future study.
Full text
Available for:
BFBNIB, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
There is accumulating evidence that the workplace environment contributes significantly to the general burden of asthma. The purpose of this review is to explore the respiratory health and ...socioeconomic consequences of work-related asthma by addressing a series of controversial issues: 1) what is the natural history of occupational asthma and in what ways does ongoing exposure to the causal agent impact clinical outcomes?; 2) how does the natural history of irritant-induced asthma differ in its health outcomes from immunologically-mediated occupational asthma?; 3) do working conditions have a significant impact on asthma regardless of the aetiology of the disease?; 4) what is the scope of work disability from work-related-asthma in social and economic terms?; 5) what is the clinician's role in reducing the respiratory health consequences of work-related asthma? 6) to what extent do existing compensation and other social insurance schemes successfully address occupational asthma and work-aggravated asthma?
Although chronic obstructive pulmonary disease (COPD) is attributed predominantly to tobacco smoke, occupational exposures are also suspected risk factors for COPD. Estimating the proportion of COPD ...attributable to occupation is thus an important public health need. A randomly selected sample of 2,061 US residents aged 55-75 yrs completed telephone interviews covering respiratory health, general health status and occupational history. Occupational exposure during the longest-held job was determined by self-reported exposure to vapours, gas, dust or fumes and through a job exposure matrix. COPD was defined by self-reported physician's diagnosis. After adjusting for smoking status and demography, the odds ratio for COPD related to self-reported occupational exposure was 2.0 (95% confidence interval (CI) 1.6-2.5), resulting in an adjusted population attributable risk (PAR) of 20% (95% CI 13-27%). The adjusted odds ratio based on the job exposure matrix was 1.6 (95% CI 1.1-2.5) for high and 1.4 (95% CI 1.1-1.9) for intermediate probability of occupational dust exposure; the associated PAR was 9% (95% CI 3-15%). A narrower definition of COPD, excluding chronic bronchitis, was associated with a PAR based on reported occupational exposure of 31% (95% CI 19-41%). Past occupational exposures significantly increased the likelihood of chronic obstructive pulmonary disease, independent of the effects of smoking. Given that one in five cases of chronic obstructive pulmonary disease may be attributable to occupational exposures, clinicians and health policy-makers should address this potential avenue of chronic obstructive pulmonary disease causation and its prevention.
This review critically evaluates the recent scientific literature relevant to occupational risk factors for chronic obstructive pulmonary disease (COPD) and chronic bronchitis. The 2003 American ...Thoracic Society statement on the occupational contribution to the burden of airway disease
synthesized relevant data on this topic through 1999. Since 2000, 14 separate studies have published values or provide data that allow estimation of the population attributable risk per cent (PAR%) for the proportion of chronic bronchitis or COPD due to work-related factors. Based on data
since 2000, the median PAR% value for both chronic bronchitis and COPD is 15%. A number of additional studies have been published that underscore the association between specific occupational exposures and airflow obstruction. In addition, data are emerging that indicate the extent to which
COPD is a cause of work disability; limited data raise the possibility that among those with occupational COPD, disability may be even more prominent. This review supports previous analyses concluding that there is a causal association between work-related exposures and COPD.
Workplace inhalational hazards remain common worldwide, even though they are ameliorable. Previous American Thoracic Society documents have assessed the contribution of workplace exposures to asthma ...and chronic obstructive pulmonary disease on a population level, but not to other chronic respiratory diseases. The goal of this document is to report an in-depth literature review and data synthesis of the occupational contribution to the burden of the major nonmalignant respiratory diseases, including airway diseases; interstitial fibrosis; hypersensitivity pneumonitis; other noninfectious granulomatous lung diseases, including sarcoidosis; and selected respiratory infections.
Relevant literature was identified for each respiratory condition. The occupational population attributable fraction (PAF) was estimated for those conditions for which there were sufficient population-based studies to allow pooled estimates. For the other conditions, the occupational burden of disease was estimated on the basis of attribution in case series, incidence rate ratios, or attributable fraction within an exposed group.
Workplace exposures contribute substantially to the burden of multiple chronic respiratory diseases, including asthma (PAF, 16%); chronic obstructive pulmonary disease (PAF, 14%); chronic bronchitis (PAF, 13%); idiopathic pulmonary fibrosis (PAF, 26%); hypersensitivity pneumonitis (occupational burden, 19%); other granulomatous diseases, including sarcoidosis (occupational burden, 30%); pulmonary alveolar proteinosis (occupational burden, 29%); tuberculosis (occupational burden, 2.3% in silica-exposed workers and 1% in healthcare workers); and community-acquired pneumonia in working-age adults (PAF, 10%).
Workplace exposures contribute to the burden of disease across a range of nonmalignant lung conditions in adults (in addition to the 100% burden for the classic occupational pneumoconioses). This burden has important clinical, research, and policy implications. There is a pressing need to improve clinical recognition and public health awareness of the contribution of occupational factors across a range of nonmalignant respiratory diseases.
PDF
