Objective: Occupational dust exposure has been associated with accelerated lung function decline, which in turn is associated with overall morbidity and mortality. In the current study, we assess potential benefits on lung function of hypothetical interventions that would reduce occupational exposure to fine particulate matter (PM) while adjusting for the healthy worker survivor effect.
Methods: Analyses were performed in a cohort of 6485 hourly male workers in an aluminium manufacturing company in the USA, followed between 1996 and 2013. We used the parametric g-formula to assess lung function decline over time under hypothetical interventions while also addressing time-varying confounding by underlying health status, using a composite risk score based on health insurance claims.
Results: A counterfactual scenario envisioning a limit on exposure equivalent to the 10th percentile of the observed exposure distribution of 0.05 mg/m was associated with an improvement in forced expiratory volume in one second (FEV) equivalent to 37.6 mL (95% CI 13.6 to 61.6) after 10 years of follow-up when compared with the observed. Assuming a linear decrease and (from NHANES reference values), a 20 mL decrease per year for a 1.8 m-tall man as they age, this 37.6 mL FEV loss over 10 years associated with observed exposure would translate to approximately a 19% increase to the already expected loss per year from age alone.
Conclusions: Our results indicate that occupational PM exposure in the aluminium industry accelerates lung function decline over age. Reduction in exposure may mitigate accelerated loss of lung function over time in the industry.
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http://dx.doi.org/10.1136/oemed-2019-105908 | DOI Listing |
Discov Nano
January 2025
Institute of Physiology II, University of Münster, Robert-Koch-Str. 27b, 48149, Münster, Germany.
Metastatic cancer cells undergo metabolic reprogramming, which involves changes in the metabolic fluxes, including endocytosis, nucleocytoplasmic transport, and mitochondrial metabolism, to satisfy their massive demands for energy, cell division, and proliferation compared to normal cells. We have previously demonstrated the ability of two different types of compounds to interfere with linchpins of metabolic reprogramming, Pitstop-2 and 1,6-hexanediol (1,6-HD). 1,6-HD disrupts glycolysis enzymes and mitochondrial function, enhancing reactive oxygen species production and reducing cellular ATP levels, while Pitstop-2 impedes clathrin-mediated endocytosis and small GTPases activity.
View Article and Find Full Text PDFAm J Respir Crit Care Med
January 2025
The University of Alabama at Birmingham, Division of Pulmonary, Allergy, and Critical Care Medicine, Birmingham, Alabama, United States.
Am J Physiol Lung Cell Mol Physiol
January 2025
Division of Pulmonology, Asthma, Cystic Fibrosis, and Sleep, Emory University School of Medicine, Atlanta, GA, USA.
Secondhand smoke exposure (SHSe) is a public health threat for people with cystic fibrosis (CF) and other lung diseases. Primary smoking reduces CFTR channel function, the causative defect in CF. We reported that SHSe worsens respiratory and nutritional outcomes in CF by disrupting immune responses and metabolic signaling.
View Article and Find Full Text PDFAnn Am Thorac Soc
January 2025
Royal Women's Hospital, Newborn Research, Parkville, Victoria, Australia.
The effect of moderate-late preterm (MLP; 32 to 36 completed weeks' gestation) birth on childhood respiratory health is unclear. To assess the effect of being born MLP, compared with being born at term (≥37 completed weeks' gestation), on lung function and respiratory morbidity at 9-10 years of age. Prospective cohort of children born MLP or at term at the Royal Women's Hospital, Victoria, Australia.
View Article and Find Full Text PDFPediatr Pulmonol
January 2025
University Hospitals Cleveland Medical Center, Division of Pulmonary, Critical Care and Sleep Medicine, Cleveland, Ohio, USA.
Objective: Although studies have examined changes in C-reactive protein (CRP) during pulmonary exacerbations (PEX) in people with cystic fibrosis (PwCF), few have evaluated CRP profiles across age groups. Here, we characterize age-related CRP responses to PEX treatment.
Methods: We measured CRP concentrations at the beginning and end of intravenous (IV) antibiotic therapy for PEX in 100 pediatric and 147 adult PwCF at 10 US CF Centers.
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