Literature DB >> 32476913

HO-1 protects smokers exposed to artificial stone dust for pulmonary function tests deterioration.

Noa Ophir1, Amir Bar-Shai1,2, Mordechai R Kramer3, Ahuva Grubstein3, Lilach Shani Israeli2, Elizabeth Fireman1.   

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). Copyright:
© 2018.

Entities:  

Keywords:  artificial stone; inflammation; lung function; occupational disease; silicosis

Year:  2018        PMID: 32476913      PMCID: PMC7170158          DOI: 10.36141/svdld.v35i3.6968

Source DB:  PubMed          Journal:  Sarcoidosis Vasc Diffuse Lung Dis        ISSN: 1124-0490            Impact factor:   0.670


  40 in total

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Authors:  Moshe Stark; Yehuda Lerman; Arik Kapel; Asher Pardo; Yehuda Schwarz; Lee Newman; Lisa Maier; Elizabeth Fireman
Journal:  Arch Environ Occup Health       Date:  2014       Impact factor: 1.663

4.  Effect of cigarette smoking on the development of murine chronic pigeon breeder's lung. The difference between a short-term and a long-term exposure.

Authors:  Masashi Furuiye; Shuji Miyake; Yasunari Miyazaki; Yoshio Ohtani; Naohiko Inase; Takeshi Umino; Yasuyuki Yoshizawa
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Authors:  A Nemmar; P H M Hoet; B Vanquickenborne; D Dinsdale; M Thomeer; M F Hoylaerts; H Vanbilloen; L Mortelmans; B Nemery
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Authors:  T D Sterling; J J Weinkam
Journal:  J Occup Med       Date:  1976-11

8.  Increased intestinal expression of heme oxygenase-1 and its localization in patients with ulcerative colitis.

Authors:  Tomohisa Takagi; Yuji Naito; Katsura Mizushima; Yayoi Nukigi; Hitomi Okada; Takahiro Suzuki; Ikuhiro Hirata; Tatsushi Omatsu; Tetsuya Okayama; Osamu Handa; Satoshi Kokura; Hiroshi Ichikawa; Toshikazu Yoshikawa
Journal:  J Gastroenterol Hepatol       Date:  2008-12       Impact factor: 4.029

9.  Human alveolar epithelial cell injury induced by cigarette smoke.

Authors:  Beata Kosmider; Elise M Messier; Hong Wei Chu; Robert J Mason
Journal:  PLoS One       Date:  2011-12-07       Impact factor: 3.240

10.  Tobacco smoke: involvement of reactive oxygen species and stable free radicals in mechanisms of oxidative damage, carcinogenesis and synergistic effects with other respirable particles.

Authors:  Athanasios Valavanidis; Thomais Vlachogianni; Konstantinos Fiotakis
Journal:  Int J Environ Res Public Health       Date:  2009-02-02       Impact factor: 3.390

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