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This study investigated the protective role of Heme Oxygenase-1 (HO-1) against pulmonary function deterioration in workers exposed to artificial stone dust. The researchers analyzed one hundred stone workers, comparing current smokers, ex-smokers, and never smokers through low-resolution computed tomography, pulmonary function tests, and induced sputum analysis. Results indicated that current smokers exhibited higher HO-1 gene expression and a significantly lower decline in pulmonary function over time compared to non-smokers, alongside a reduced fraction of small particles in their sputum. The authors concluded that smoking may confer a protective effect via HO-1 mechanisms, although this finding requires careful interpretation given the known health risks of tobacco use. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.
Abstract
Background: The Heme Oxygenase system, along with its catabolism products, is involved in a variety of crucial physiological functions, including cytoprotection, inflammation, anti-oxidative effects, apoptosis, angiogenesis, and vascular regulation. Objectives: To analyze the Heme Oxygenase -1 (HO-1) mediated effect of mild deterioration of pulmonary function testing (PFT) in exposed artificial stone smoking workers. Methods: One hundred stone workers divided into current smokers, ex-smokers and never smokers underwent Low Resolution Computed Tomography, PFT, induced sputum (IS) Particle Size Distribution (PSD) and Real Time PCR in IS samples. Results: Smoking status had no significant effect on PFT results but it altered the IS differential cell counts. There was significantly less decline in PFT over time for the smokers group. There was a significantly lower fraction of small particles (<2 μm) in the IS of the current smokers group compared to the never- and ex-smokers groups. HO-1 gene expression was higher among smokers compared to never- and ex-smokers groups. A low percentage of small particles (<5 μm) correlated negatively to the percentage of neutrophils and positively to the percentage of macrophages in the sputum of the smokers group. Conclusions: We found significantly lower risk for decreased PFT deterioration among smokers workers exposed to artificial stone dust with higher HO-1 gene expression suggesting a possible protective effect of smoking by the involvement of HO-1 mechanism. (Sarcoidosis Vasc Diffuse Lung Dis 2018; 35: 276-284).
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HO-1 protects smokers exposed to artificial stone dust for pulmonary function tests deterioration
Abstract
Background: The Heme Oxygenase system, along with its catabolism products, is involved in a variety of crucial physiological functions, including cytoprotection, inflammation, anti-oxidative effects, apoptosis, angiogenesis, and vascular regulation. Objectives: To analyze the Heme Oxygenase -1 (HO-1) mediated effect of mild deterioration of pulmonary function testing (PFT) in exposed artificial stone smoking workers. Methods: One hundred stone workers divided into current smokers, ex-smokers and never smokers underwent Low Resolution Computed Tomography, PFT, induced sputum (IS) Particle Size Distribution (PSD) and Real Time PCR in IS samples. Results: Smoking status had no significant effect on PFT results but it altered the IS differential cell counts. There was significantly less decline in PFT over time for the smokers group. There was a significantly lower fraction of small particles (<2 µm) in the IS of the current smokers group compared to the never- and ex-smokers groups. HO-1 gene expression was higher among smokers compared to never- and ex-smokers groups. A low percentage of small particles (<5 µm) correlated negatively to the percentage of neutrophils and positively to the percentage of macrophages in the sputum of the smokers group. Conclusions: We found significantly lower risk for decreased PFT deterioration among smokers workers exposed to artificial stone dust with higher HO-1 gene expression suggesting a possible protective effect of smoking by the involvement of HO-1 mechanism.
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