https://www.commed.vcu.edu/Chronic_Disease/2012/cochranrvwrschbias.pdf

The Cochrane Collaboration's tool for assessing risk of bias in randomised trials

Impact of air pollution on the burden of chronic respiratory diseases in China: time for urgent action

Beyond PM2.5: The role of ultrafine particles on adverse health effects of air pollution.

Rationale: 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. Methods: 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. Results: 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%). Conclusions: 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/the-occupational-burden-of-nonmalignant-respiratory-diseases-2nfso7zaui.pdf

The Occupational Burden of Nonmalignant Respiratory Diseases. An Official American Thoracic Society and European Respiratory Society Statement.

Spirometry is the main pulmonary function test and is essential for the evaluation and monitoring of respiratory diseases Its utility transcends the field of Respiratory Medicine, is becoming increasingly important in primary care and applications have even been described outside the field of respiratory diseases This document is therefore intended to serve as support for all health professionals who use spirometry, providing recommendations based on the best scientific evidence available An update of the indications and contraindications of the test is proposed The document sets out recommendations on the requirements necessary for conventional spirometers and portable office equipment, as well as on spirometer hygiene and quality control measures Spirometric parameters that must be considered, performance of manoeuvres, criteria for acceptability and repeatability of measurements and their quality control are defined A proposal is also established for presentation of the results and an evaluation and interpretation is proposed according to information generated in recent years Finally, lines of adaptation and integration of spirometry in the field of new technologies are considered

Spirometry. Spanish Society of Pulmonology and Thoracic Surgery (SEPAR).

Environmental ultrafine particulate matter (PM) is capable of inducing airway injury, while the detailed molecular mechanisms remain largely unclear. Here, we demonstrate pivotal roles of autophagy in regulation of inflammation and mucus hyperproduction induced by PM containing environmentally persistent free radicals in human bronchial epithelial (HBE) cells and in mouse airways. PM was endocytosed by HBE cells and simultaneously triggered autophagosomes, which then engulfed the invading particles to form amphisomes and subsequent autolysosomes. Genetic blockage of autophagy markedly reduced PM-induced expression of inflammatory cytokines, e.g. IL8 and IL6, and MUC5AC in HBE cells. Mice with impaired autophagy due to knockdown of autophagy-related gene Becn1 or Lc3b displayed significantly reduced airway inflammation and mucus hyperproduction in response to PM exposure in vivo. Interference of the autophagic flux by lysosomal inhibition resulted in accumulated autophagosomes/amphisomes, and intriguingly, this process significantly aggravated the IL8 production through NFKB1, and markedly attenuated MUC5AC expression via activator protein 1. These data indicate that autophagy is required for PM-induced airway epithelial injury, and that inhibition of autophagy exerts therapeutic benefits for PM-induced airway inflammation and mucus hyperproduction, although they are differentially orchestrated by the autophagic flux.

https://www.tandfonline.com/doi/pdf/10.1080/15548627.2015.1124224

Autophagy is essential for ultrafine particle-induced inflammation and mucus hyperproduction in airway epithelium

Should FEV1/FEV6 replace FEV1/FVC ratio to detect airway obstruction? A metaanalysis.

Background
Nontypeable Haemophilus influenzae (NTHi) is an important respiratory pathogen implicated as an infectious trigger in chronic obstructive pulmonary disease, but its molecular interaction with human lung epithelial cells remains unclear. Herein, we tested that the hypothesis that NTHi induces the expression of cyclooxygenase (COX)-2 and prostaglandin E2 (PGE2) via activation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappa B in pulmonary alveolar epithelial cells.

/pdf/nontypeable-haemophilus-influenzae-induces-cox-2-and-pge2-20nk9m19zd.pdf

Nontypeable Haemophilus influenzae induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B

Background and objective:  Pulmonary alveolar proteinosis (PAP) is a rare pulmonary disease. It was first described in China in 1965, and more cases have been reported subsequently. A systematic review was performed on 241 cases of PAP in China and progress in the diagnosis and treatment of this disease is discussed.



Methods:  The Chinese biological and medical databases from 1965 to 2006 were searched and 241 cases with complete clinical and pathological data were identified. The clinical characteristics of the disease were summarized and longitudinal comparisons were made of diagnostic and treatment methods over time.



Results:  The morbidity associated with PAP has increased in recent years. The clinical manifestations were non-specific. Progressive dyspnoea, cough and sputum were the most common symptoms. The percentage of patients undergoing CT examination has increased over the years. The combination of bronchoscopic biopsy and bronchoalveolar lavage (BAL) was usually sufficient to establish the diagnosis. Treatment was reported for a total of 142 cases. BAL and whole lung lavage were both effective and were only required once by most patients.



Conclusions:  The demographic characteristics and clinical manifestations of PAP patients in China are largely consistent with previous reports. Morbidity has increased dramatically in recent years, mainly due to the broad application of bronchoscopy since 1995. CT is very important for diagnosis of the disease. The long-term effects of treatment by whole lung lavage and BAL are similar.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1440-1843.2009.01539.x

Pulmonary alveolar proteinosis in China: a systematic review of 241 cases.

Hypomagnesemia is commonly seen but frequently overlooked in critically ill patients in intensive care unit (ICU). However, the strength and consistency of the effect of hypomagnesemia on outcomes in critically ill patients remain controversial. In this report, we performed a systematic review and meta-analysis to evaluate the association of serum magnesium level with prognosis of critically ill patients upon admission to the ICU. A comprehensive search for clinical trials was performed, and 10 studies comprising 1,122 cases and 630 controls were finally selected for analysis. The patients with hypomagnesemia had higher mortality rate (risk ratio [RR] 1.76; 95% confidence interval [CI] 1.54-2.00; P <0.00001), more frequently had sepsis (RR 2.04; 95% CI 1.21-3.42; P = 0.0007) and more frequent need for ventilatory support (RR 1.36; 95% CI 1.21 to 1.53; P <0.00001). Length of ICU stay was also higher in the hypomagnesemia group (RR 1.85; 95% CI 0.43- 3.26; P = 0.01). Collectively, our data indicated that hypomagnesemia appears associated with greater risk of mortality, sepsis, mechanical ventilation, and the length of ICU stay in patients admitted to ICU. The role of magnesium therapy for improving outcomes in critically ill patients is needed to further study.

Feng Xu

Papers

Autophagy is essential for ultrafine particle-induced inflammation and mucus hyperproduction in airway epithelium

Should FEV1/FEV6 replace FEV1/FVC ratio to detect airway obstruction? A metaanalysis.

Nontypeable Haemophilus influenzae induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B

Pulmonary alveolar proteinosis in China: a systematic review of 241 cases.

Does Hypomagnesemia Impact on the Outcome of Patients Admitted to the Intensive Care Unit? A Systematic Review and Meta-Analysis.