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Introduction Interactions have been demonstrated between cigarette smoking (CS) and occupational exposures to several particles. This study tested the postulate that CS interacts with coal mine dust exposure to impact and change radiological and histological endpoints of coal mine dust lung disease. Methods A retrospective evaluation of coalminers with a high-resolution computed tomography (HRCT) of the chest was conducted at West Virginia University Hospital (2015- 2022). There was a consensus review of both radiology and histology findings and their comparative analysis with a non-miner surgical resection cohort collected from thoracic oncology clinic. Results The study cohort (n=556) was divided into groups: coal-/smoking- (8.3%), coal-/smoking+ (26.6%), coal+/smoking- (22.3%), and coal+/smoking+ (42.8%). Miners were older males with a median duration of coal mine work (CMW) of 30-years. Ever-smokers (66% of miner cohort and 76% of non-miner cohort) smoked 35 and 28 composite pack years (CPY) respectively, where miners had greater intensity of smoking (22 vs 18 cigarettes/day) compared to non-miners. On HRCT, 1/3 rd and 1/5 th of miners had simple and complicated coal workers’ pneumoconiosis (sCWP and cCWP), respectively. 35% of ever-smoking miners had radiologic patterns for probable usual interstitial pneumonitis, nonspecific interstitial pneumonitis, desquamative interstitial pneumonitis, and combined pulmonary fibrosis and emphysema. Radiologically, both coal-/smoking+ and coal+/smoking+ showed excessive emphysema (70-80%). Histologically, miners had more fibrosis (47% and 50% in coal+/smoking- and coal+/smoking+ vs. 11% and 28% in coal-/smoking- and coal-/smoking+). Never-smoking miners demonstrated more histological evidence of CWP than ever-smokers (60% and 27%); in addition, they had radiologic and histologic emphysema (30%), radiologic interstitial lung disease (ILD) (14.5%) and histologic evidence of fibrosis (47%). Ever-smokers demonstrated histologic emphysema more frequently (33% and 67% in coal+/smoking- and coal+/smoking+ vs. 24% and 72% in coal-/smoking- and coal-/smoking+). Logistic regression modeling showed the following associations: radiologic and histologic emphysema with CPY; histologic fibrosis, any ILD (not including RB-ILD), CPFE and anthracosis with both CPY and CMW; radiologic RB-ILD inclusive of small-opacities, cCWP with both CMW and silica; and sCWP and pulmonary artery dilation with CMW. Interestingly, CPY≥30 negatively correlated with radiologic cCWP and histologic CWP. Mortality was increased in smokers (14% and 29% in coal+/smoking- and coal+/smoking+ vs. 4% and 20% in coal-/smoking- and coal-/smoking+) with predictors being radiologic ILD, histologic CWP, and related co-morbid diseases including COPD, chronic kidney disease, and gastroesophageal reflux. Conclusion CS demonstrated a major impact on miners’ health including changing radiologic and histologic endpoints of interstitial lung diseases and emphysema.

Cigarette smoking (CS)-related monocytosis contributes to the development of chronic lung injuries via complex mechanisms. We aim to determine correlations between measures of CS and monocytes, their capacities to predict chronic lung diseases, and their associations with mortality. A single-center retrospective study of patients undergoing surgical resection for suspected lung nodules/masses was performed. CS was quantified as cigarettes smoked per day (CPD), duration of smoking, composite pack years (CPY), current smoking status, and smoking cessation years. A multivariate logistic regression analysis was performed. Of 382 eligible patients, 88% were ever smokers. In this group, 45% were current smokers with mean CPD of 27.2±40.0. CPY and duration of smoking showed positive linear correlations with percentage monocyte count. Physiologically, CPY was associated with progressive obstruction, hyperinflation, and reduced diffusion capacity (DL ). Across the quartiles of smoking, there was an accumulation of radiologic and histologic abnormalities. Anthracosis and emphysema were associated with CPD, while lung cancer, respiratory bronchiolitis (RB), emphysema, and honeycombing were statistically related to duration of smoking. Analysis using consecutive CPY showed associations with lung cancer (≥10 and <30), fibrosis (≥20 and <40), RB (≥50), anthracosis and emphysema (≥10 and onwards). Percentage monocytes correlated with organizing pneumonia (OP), fibrosis, and emphysema. The greater CPY increased mortality across the groups. Significant predictors of mortality included percentage monocyte, anemia, GERD, and reduced DL . Indices of CS and greater monocyte numbers were associated with endpoints of chronic lung disease suggesting a participation in pathogenesis. Application of these easily available metrics may support a chronology of CS-induced chronic lung injuries. While a relative lesser amount of smoking can be associated with lung cancer and fibrosis, greater CPY increases the risk for emphysema. Monocytosis predicted lung fibrosis and mortality. Duration of smoking may serve as a better marker of monocytosis and associated chronic lung diseases.

Background Cigarette smoking is a risk factor for interstitial lung abnormalities (ILAs) and interstitial lung diseases (ILDs). Investigation defining the relationships between ILAs/ILDs and clinical, radiographic, and pathologic findings in smokers have been incomplete. Employing a cohort undergoing surgical resection for lung nodules/masses, we (1) define the prevalence of ILAs/ILDs, (2) delineate their clinical, radiographic and pathologic predictors, and (3) determine their associations with mortality. Methods Patients undergoing resection of lung nodules/masses between 2017 and 2020 at a rural Appalachian, tertiary medical center were retrospectively investigated. Predictors for ILAs/ILDs and mortality were assessed using multivariate logistic regression analysis. Results In the total study cohort of 352 patients, radiographic ILAs and ILDs were observed in 35.2% and 17.6%, respectively. Among ILA patterns, subpleural reticular changes (14.8%), non-emphysematous cysts, centrilobular (CL) ground glass opacities (GGOs) (8% each), and mixed CL-GGO and subpleural reticular changes (7.4%) were common. ILD patterns included combined pulmonary fibrosis emphysema (CPFE) (3.1%), respiratory bronchiolitis (RB)-ILD (3.1%), organizing pneumonitis (2.8%) and unclassifiable (4.8%). The group with radiographic ILAs/ILDs had a significantly higher proportion of ever smokers (49% vs. 39.9%), pack years of smoking (44.57 ± 36.21 vs. 34.96 ± 26.22), clinical comorbidities of COPD (35% vs. 26.5%) and mildly reduced diffusion capacity (% predicated 66.29 ± 20.55 vs. 71.84 ± 23). Radiographic centrilobular and paraseptal emphysema (40% vs. 22.2% and 17.6% vs. 9.6%, respectively) and isolated traction bronchiectasis (10.2% vs. 4.2%) were associated with ILAs/ILDs. Pathological variables of emphysema (34.9% vs. 18.5%), any fibrosis (15.9% vs. 4.6%), peribronchiolar metaplasia (PBM, 8% vs. 1.1%), RB (10.3% vs. 2.5%), and anthracosis (21.6% vs. 14.5%) were associated with ILAs/ILDs. Histologic emphysema showed positive correlations with any fibrosis, RB, anthracosis and ≥ 30 pack year of smoking. The group with ILAs/ILDs had significantly higher mortality (9.1% vs. 2.2%, OR 4.13, [95% CI of 1.84–9.25]). Conclusions In a rural cohort undergoing surgical resection, radiographic subclinical ILAs/ILDs patterns were highly prevalent and associated with ever smoking and intensity of smoking. The presence of radiographic ILA/ILD patterns and isolated honeycomb changes were associated with increased mortality. Subclinical ILAs/ILDs and histologic fibrosis correlated with clinical COPD as well as radiographic and pathologic emphysema emphasizing the co-existence of these pulmonary injuries in a heavily smoking population.

It is proposed that the mechanistic basis for non-neoplastic lung injury with cigarette smoking is a disruption of iron homeostasis in cells after exposure to cigarette smoke particle (CSP). Following the complexation and sequestration of intracellular iron by CSP, the host response (eg, inflammation, mucus production, and fibrosis) attempts to reverse a functional metal deficiency. Clinical manifestations of this response can present as respiratory bronchiolitis, desquamative interstitial pneumonitis, pulmonary Langerhans' cell histiocytosis, asthma, pulmonary hypertension, chronic bronchitis, and pulmonary fibrosis. If the response is unsuccessful, the functional deficiency of iron progresses to irreversible cell death evident in emphysema and bronchiectasis. The subsequent clinical and pathological presentation is a continuum of lung injuries, which overlap and coexist with one another. Designating these non-neoplastic lung injuries after smoking as distinct disease processes fails to recognize shared relationships to each other and ultimately to CSP, as well as the common mechanistic pathway (ie, disruption of iron homeostasis).

Background Accurate staging systems are essential for assessing the severity of idiopathic pulmonary fibrosis (IPF) and guiding clinical management. This study aimed to evaluate the prognostic value of pulmonary comorbidities and body mass index (BMI) in IPF, develop a nomogram predicting overall survival (OS), and create a nomogram‐based survival prediction model. Methods Patients with IPF were identified from electronic medical records of the West Virginia hospital system. Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression analysis was used for variable selection, and a nomogram was constructed. Risk groups were defined based on the nomogram's probability tertiles. The performance of the nomogram‐based model was evaluated using Harrell's concordance index (C‐index) and the Hosmer–Lemeshow test. Results The study included 152 patients with IPF. The majority of the patients were elderly, male, and had a BMI above 24 kg/m2. The median survival duration was 7.6 years. The survival rates were 91% at 1 year, 78% at 3 years, and 68% at 5 years. LASSO regression selected carbon monoxide lung diffusion capacity percentage predicted (DLco%), BMI, pulmonary hypertension, pulmonary embolism, and sleep apnea as independent predictive variables. The nomogram demonstrated good discrimination (C‐index = 0.71) and calibration. Conclusions Pulmonary comorbidities and BMI have significant prognostic value in IPF, emphasizing the necessity for consistent screening, assessment, and management of these factors in IPF care. Furthermore, the nomogram‐based staging system showed promising performance in predicting OS and represents an actionable staging system that could potentially improve clinical management in IPF. Further validation of the nomogram is warranted to confirm its utility in clinical practice. In our study, we developed a nomogram‐based risk‐staging system for idiopathic pulmonary fibrosis based on inpatient data from West Virginia University Medicine hospitals. We identified DLco%, body mass index (used as an indicator of malnutrition), pulmonary hypertension, pulmonary embolism, and sleep apnea as independent predictors of overall survival. Nomograms offer a reliable visualization of multivariable prognostic models.

Background The St. George’s Respiratory Questionnaire (SGRQ) and its idiopathic pulmonary fibrosis (IPF) version (SGRQ-I) are widely used to assess health-related quality of life in IPF. However, the psychometric properties of these questionnaires in the IPF population have not been thoroughly evaluated. This systematic review assessed and summarized the available evidence on the psychometric properties of the SGRQ and SGRQ-I in IPF patients. Methods Seven electronic databases were searched to identify relevant studies. The eligibility criteria included full-text studies focusing on the psychometric properties of the SGRQ and SGRQ-I in patients with IPF. The risk of bias, criteria for good measurement properties, and strength of evidence were assessed based on the COnsensus-based Standards for the selection of health Measurement INstruments (COSMIN). The inverse-variance heterogeneity (IVhet) model was used to pool results for construct validity. Results A total of 24 studies were included; 19 assessed the psychometric properties of the SGRQ, and seven evaluated the SGRQ-I. Structural validity was assessed in one study for the SGRQ-I. Most domains of the SGRQ and SGRQ-I, except for the symptom domain of the SGRQ, had acceptable internal consistency. Both questionnaires demonstrated adequate test–retest reliability, known-groups validity, and responsiveness. Regarding construct validity, there were moderate to strong correlations with respiratory-specific measures, yet weaker correlations were observed with pulmonary function tests. Interpretability analysis revealed minor floor and ceiling effects. Conclusion The SGRQ and SGRQ-I have the potential to capture essential dimensions of health-related quality of life (HRQoL) in IPF. However, further research should focus on ensuring that the items and domains of these questionnaires truly reflect the unique challenges and experiences faced by patients with IPF through content validity studies.

Idiopathic pulmonary fibrosis (IPF) is currently defined as a progressive fibrosing interstitial lung disease (ILD) associated with a histopathologic and radiologic pattern of usual interstitial pneumonia (UIP). The relationship between IPF and particles is described, and a pathogenesis for the disease is proposed based on an association with these exposures. In clinical studies and epidemiological investigations, the majority of IPF diagnoses are associated with particle exposures. Cigarette smoking presents the greatest particle challenge in any society, and a relationship with IPF has repeatedly been demonstrated. Environmental exposures to particles other than cigarette smoking, including biomass fuel smoke and ambient air pollution, as well as numerous occupational particle exposures, have also been associated with IPF. The pathogenesis of the disease includes a complexation and sequestration of cell iron at the particle surface, which results in a functional cell deficiency of the requisite metal. In response to the insufficiency of metal in cells, there is the synthesis of biopolymers, including exopolysaccharides (e.g., hyaluronic acid), which accumulate in the extracellular matrix. These biopolymers complex iron and, following depolymerization, facilitate the delivery of the metal intracellularly via receptor-mediated uptake. This process reverses the functional iron deficiency introduced by the particle. Pulmonary fibrosis after particle exposure reflects a response to the modification of a functional intracellular iron deficiency in the lower respiratory tract. The temporal and spatial heterogeneity of IPF results from a dose–response with retained particles and reversibility of the fibrosis.

Osimertinib is an oral epithelial growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) used primarily in the treatment of metastatic non-small cell lung cancer. It is usually well tolerated with less than 5% of patients developing significant pulmonary toxicity from the medication, typically within the first few months after initiation. Previously reported pulmonary adverse reactions include pneumonitis (nonspecific interstitial pneumonia or other forms of acute interstitial process), fleeting asymptomatic infiltrates on imaging, and eosinophilic pneumonia. We present an interesting case of a 65-year-old female with recurrent metastatic adenocarcinoma of the lung, treated with Osimertinib for 4 months, who developed a previously unreported toxicity of diffuse alveolar hemorrhage (DAH) requiring mechanical ventilatory support.

Theories of disease pathogenesis following asbestos exposure have focused on the participation of iron. After exposure, an open network of negatively charged functional groups on the fiber surface complexes host metals with a preference for iron. Competition for iron between the host and the asbestos results in a functional metal deficiency. The homeostasis of iron in the host is modified by the cell response, including increased import to correct the loss of the metal to the fiber surface. The biological effects of asbestos develop in response to and are associated with the disruption of iron homeostasis. Cell iron deficiency in the host following fiber exposure activates kinases and transcription factors, which are associated with the release of mediators coordinating both inflammatory and fibrotic responses. Relative to serpentine chrysotile, the clearance of amphiboles is incomplete, resulting in translocation to the mesothelial surface of the pleura. Since the biological effect of asbestos is dependent on retention of the fiber, the sequestration of iron by the surface, and functional iron deficiency in the cell, the greater clearance (i.e., decreased persistence) of chrysotile results in its diminished impact. An inability to clear asbestos from the lower respiratory tract initiates a host process of iron biomineralization (i.e., asbestos body formation). Host cells attempt to mobilize the metal sequestered by the fiber surface by producing superoxide at the phagosome membrane. The subsequent ferrous cation is oxidized and undergoes hydrolysis, creating poorly crystalline iron oxyhydroxide (i.e., ferrihydrite) included in the coat of the asbestos body.

Paraneoplastic diarrhea is a commonly described complication of gastrointestinal tract or endocrine malignancies. It is an extremely rare complication of lung adenocarcinoma, with only one previously reported case in the literature. A 46-year-old female with newly diagnosed stage IVb lung adenocarcinoma presented to our intensive care unit in hypovolemic shock with symptoms suggestive of diabetes insipidus (DI) as well as profuse large volume watery diarrhea. Exhaustive serological and microbiological workup revealed the diarrhea to be paraneoplasitc in nature. This case represents the second known case of paraneoplastic diarrhea secondary to lung adenocarcinoma. Clinicians should be aware of this rare phenomenon.