scholarly journals Work Lung Disease Due to Rice Dust

2020 ◽  
Vol 6 (3) ◽  
pp. 79
Author(s):  
Ariani Permatasari ◽  
Reagen Irwan Kolibu

Indonesia is one of the third largest rice producers globally; therefore, rice dust-related lung diseases will be more significant. Rice dust is easily exposed to humans, triggers lung damage, and decline the lung function. Rice dust exposure is associated with occupational lung diseases, for instance, acute reversible airflow obstruction, chronic obstructive pulmonary disease, grain fever, organic dust syndrome, and hypersensitivity pneumonitis. Smoking and the environment might aggravate rice dust-related respiratory problems. The average tolerated dose of rice dust is about less than 3 mg/m3. Avoiding exposure to rice dust is primer prevention.

2021 ◽  
pp. 55-68
Author(s):  
Vyacheslav S. Lotkov ◽  
Anton Vladimirovich Glazistov ◽  
Antonina G. Baykova ◽  
Marina Yuryevna Vostroknutova ◽  
Natalia E. Lavrentieva

The formation and progression of chronic dust bronchitis and chronic bronchitis of toxic-chemical etiology, chronic obstructive pulmonary disease is accompanied by an increase in the degree of ventilation disorders, echocardiographic signs of hypertrophy and dilatation of the right ventricle are formed, typical for chronic pulmonary heart disease. The progression of disturbances in the function of external respiration in dusty lung diseases leads to a decrease in myocardial contractility. The detection of hemodynamic disturbances at the early stages of the development of occupational lung diseases indicates the need for individual monitoring of the functional state of the cardiovascular system in the process of contact with industrial aerosols, especially in groups of workers with long-term exposure.


2015 ◽  
Vol 24 (137) ◽  
pp. 428-435 ◽  
Author(s):  
George A. Margaritopoulos ◽  
Eirini Vasarmidi ◽  
Joseph Jacob ◽  
Athol U. Wells ◽  
Katerina M. Antoniou

For many years has been well known that smoking could cause lung damage. Chronic obstructive pulmonary disease and lung cancer have been the two most common smoking-related lung diseases. In the recent years, attention has also focused on the role of smoking in the development of interstitial lung diseases (ILDs). Indeed, there are three diseases, namely respiratory bronchiolitis-associated ILD, desquamative interstitial pneumonia and pulmonary Langerhans cell histiocytosis, that are currently considered aetiologically linked to smoking and a few others which are more likely to develop in smokers. Here, we aim to focus on the most recent findings regarding the role of smoking in the pathogenesis and clinical behaviour of ILDs.


2022 ◽  
Vol 8 ◽  
Author(s):  
Lan Chai ◽  
Qi Wang ◽  
Caijuan Si ◽  
Wenyan Gao ◽  
Lun Zhang

Objective:Lung microbiota is increasingly implicated in multiple types of respiratory diseases. However, no study has drawn a consistent conclusion regarding the relationship between changes in the microbial community and lung diseases. This study verifies the association between microbiota level and lung diseases by performing a meta-analysis.Methods:Literature databases, including PubMed, ISI Web of Science, Embase, Google Scholar, PMC, and CNKI, were used to collect related articles published before March 20, 2021. The standard mean deviation (SMD) and related 95% confidence intervals (CIs) were calculated using a random-effects model. Subgroup, sensitivity, and publication bias analyses were also conducted.Results:Six studies, comprising 695 patients with lung diseases and 176 healthy individuals, were included in this meta-analysis. The results indicated that the microbiota level was higher in patients with lung diseases than in healthy individuals (SMD = 0.39, 95% CI = 0.22–0.55, I2 = 91.5%, P < 0.01). Subgroup analysis based on country demonstrated that the microbiota level was significantly higher in Chinese (SMD = 1.90, 95% CI = 0.87–2.93, I2 = 62.3%, P < 0.01) and Korean (SMD = 0.24, 95% CI = 0.13–0.35, I2 = 78.7%, P < 0.01) patients with lung diseases. The microbiota level of patients with idiopathic pulmonary fibrosis (IPF) (SMD = 1.40, 95% CI = 0.42–2.38, I2 = 97.3%, P = 0.005), chronic obstructive pulmonary disease (COPD) (SMD = 0.30, 95% CI = 0.09–0.50, I2 = 83.9%, P = 0.004), and asthma (SMD = 0.19, 95% CI = 0.06–0.32, I2 = 69.4%, P = 0.004) were significantly higher than those of the healthy group, whereas a lower microbiota level was found in patients with chronic hypersensitivity pneumonitis (CHP). The microbiota level significantly increased when the disease sample size was >50. Subgroup analysis based on different microbiota genera, indicated that Acinetobacter baumannii and Pseudomonas aeruginosa were significantly increased in COPD and asthma diseases.Conclusion:We observed that patients with IPF, COPD, and asthma had a higher microbiota level, whereas patients with CHP had a lower microbiota level compared to the healthy individuals. The level of A. baumannii and P. aeruginosa were significantly higher in patients with COPD and asthma, and thus represented as potential microbiota markers in the diagnosis and treatment of lung diseases.


2019 ◽  
Vol 116 (31) ◽  
pp. 15625-15634 ◽  
Author(s):  
Sara Bruzzaniti ◽  
Marialuisa Bocchino ◽  
Marianna Santopaolo ◽  
Gaetano Calì ◽  
Anna Agnese Stanziola ◽  
...  

Chronic obstructive pulmonary disease (COPD) is an inflammatory condition associated with abnormal immune responses, leading to airflow obstruction. Lungs of COPD subjects show accumulation of proinflammatory T helper (Th) 1 and Th17 cells resembling that of autoreactive immune responses. As regulatory T (Treg) cells play a central role in the control of autoimmune responses and their generation and function are controlled by the adipocytokine leptin, we herein investigated the association among systemic leptin overproduction, reduced engagement of glycolysis in T cells, and reduced peripheral frequency of Treg cells in different COPD stages. These phenomena were also associated with an impaired capacity to generate inducible Treg (iTreg) cells from conventional T (Tconv) cells. At the molecular level, we found that leptin inhibited the expression of forkhead-boxP3 (FoxP3) and its splicing variants containing the exon 2 (FoxP3-E2) that correlated inversely with inflammation and weakened lung function during COPD progression. Our data reveal that the immunometabolic pathomechanism leading to COPD progression is characterized by leptin overproduction, a decline in the expression of FoxP3 splicing forms, and an impairment in Treg cell generation and function. These results have potential implications for better understanding the autoimmune-like nature of COPD and the pathogenic events leading to lung damage.


2021 ◽  
Vol 22 (9) ◽  
pp. 5018
Author(s):  
Michael C. McKelvey ◽  
Ryan Brown ◽  
Sinéad Ryan ◽  
Marcus A. Mall ◽  
Sinéad Weldon ◽  
...  

Dysregulated protease activity has long been implicated in the pathogenesis of chronic lung diseases and especially in conditions that display mucus obstruction, such as chronic obstructive pulmonary disease, cystic fibrosis, and non-cystic fibrosis bronchiectasis. However, our appreciation of the roles of proteases in various aspects of such diseases continues to grow. Patients with muco-obstructive lung disease experience progressive spirals of inflammation, mucostasis, airway infection and lung function decline. Some therapies exist for the treatment of these symptoms, but they are unable to halt disease progression and patients may benefit from novel adjunct therapies. In this review, we highlight how proteases act as multifunctional enzymes that are vital for normal airway homeostasis but, when their activity becomes immoderate, also directly contribute to airway dysfunction, and impair the processes that could resolve disease. We focus on how proteases regulate the state of mucus at the airway surface, impair mucociliary clearance and ultimately, promote mucostasis. We discuss how, in parallel, proteases are able to promote an inflammatory environment in the airways by mediating proinflammatory signalling, compromising host defence mechanisms and perpetuating their own proteolytic activity causing structural lung damage. Finally, we discuss some possible reasons for the clinical inefficacy of protease inhibitors to date and propose that, especially in a combination therapy approach, proteases represent attractive therapeutic targets for muco-obstructive lung diseases.


Chapter 18 covers the basic science and clinical topics relating to respiratory medicine which trainees are required to learn as part of their basic training and demonstrate in the MRCP. The chapter starts with an introduction to the respiratory system, before covering respiratory defence and physiology, respiratory investigations, respiratory failure, pneumonia, tuberculosis, cystic fibrosis, bronchiectasis, pleural effusion, chronic obstructive pulmonary Disease, adult respiratory distress syndrome, asthma , fungal lung diseases, pulmonary embolism , lung cancer, pulmonary fibrosis, extrinsic allergic alveolitis, occupational lung diseases, sarcoidosis, Cor pulmonale and pulmonary hypertension, pneumothorax, cough and haemoptysis, pulmonary eosinophilia, and obstructive sleep apnoea.


2017 ◽  
Author(s):  
Cora S Sack ◽  
Sverre Vedal ◽  
Joel D Kaufman

Environmental and occupational lung diseases encompass a diverse group of lung diseases caused by the inhalation of potentially harmful substances. Although workplace regulations and the changing economy in the United States have significantly decreased incidence, these diseases remain both common and associated with significant morbidity. In addition, novel exposures continue to be recognized as new causes of disease. This review provides the medical student and clinician with a framework for approaching and categorizing environmental and occupational lung disease. It also presents an in-depth discussion of the epidemiology, biological mechanisms, diagnosis, and clinical care of some of the more commonly encountered diseases. Occupational lung diseases that affect the airways, such as work-related asthma and chronic obstructive pulmonary disease, and malignant neoplasms are covered. This review concludes with general strategies to help prevent disease incidence and progression.     This review contains 1 figure, 5 tables, and 56 references. Key words: bronchiolitis obliterans, chronic obstructive pulmonary disease, irritant-induced occupational asthma, mesothelioma, occupational asthma, occupational lung disease, occupational lung neoplasm, work-related asthma


2017 ◽  
Author(s):  
Cora S Sack ◽  
Sverre Vedal ◽  
Joel D Kaufman

Environmental and occupational lung diseases encompass a diverse group of lung diseases caused by the inhalation of potentially harmful substances. Although workplace regulations and the changing economy in the United States have significantly decreased incidence, these diseases remain both common and associated with significant morbidity. In addition, novel exposures continue to be recognized as new causes of disease. This review provides the medical student and clinician with a framework for approaching and categorizing environmental and occupational lung disease. It also presents an in-depth discussion of the epidemiology, biological mechanisms, diagnosis, and clinical care of some of the more commonly encountered diseases. Occupational lung diseases that affect the airways, such as work-related asthma and chronic obstructive pulmonary disease, and malignant neoplasms are covered. This review concludes with general strategies to help prevent disease incidence and progression.     This review contains 1 figure, 5 tables, and 56 references. Key words: bronchiolitis obliterans, chronic obstructive pulmonary disease, irritant-induced occupational asthma, mesothelioma, occupational asthma, occupational lung disease, occupational lung neoplasm, work-related asthma


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Junghyun Kim ◽  
Bom Kim ◽  
So Hyeon Bak ◽  
Yeon-Mok Oh ◽  
Woo Jin Kim

Abstract Background The clinical and radiological presentation of chronic obstructive pulmonary disease (COPD) is heterogenous depending on the characterized sources of inflammation. This study aimed to evaluate COPD phenotypes associated with specific dust exposure. Methods This study was designed to compare the characteristics, clinical outcomes and radiological findings between two prospective COPD cohorts representing two distinguishing regions in the Republic of Korea; COPD in Dusty Area (CODA) and the Korean Obstructive Lung Disease (KOLD) cohort. A total of 733 participants (n = 186 for CODA, and n = 547 for KOLD) were included finally. A multivariate analysis to compare lung function and computed tomography (CT) measurements of both cohort studies after adjusting for age, sex, education, body mass index, smoking status, and pack-year, Charlson comorbidity index, and frequency of exacerbation were performed by entering the level of FEV1(%), biomass exposure and COPD medication into the model in stepwise. Results The mean wall area (MWA, %) became significantly lower in COPD patients in KOLD from urban and metropolitan area than those in CODA cohort from cement dust area (mean ± standard deviation [SD]; 70.2 ± 1.21% in CODA vs. 66.8 ± 0.88% in KOLD, p = 0.028) after including FEV1 in the model. COPD subjects in KOLD cohort had higher CT-emphysema index (EI, 6.07 ± 3.06 in CODA vs. 20.0 ± 2.21 in KOLD, p < 0.001, respectively). The difference in the EI (%) was consistently significant even after further adjustment of FEV1 (6.12 ± 2.88% in CODA vs. 17.3 ± 2.10% in KOLD, p = 0.002, respectively). However, there was no difference in the ratio of mean lung density (MLD) between the two cohorts (p = 0.077). Additional adjustment for biomass parameters and medication for COPD did not alter the statistical significance after entering into the analysis with COPD medication. Conclusions Higher MWA and lower EI were observed in COPD patients from the region with dust exposure. These results suggest that the imaging phenotype of COPD is influenced by specific environmental exposure.


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