Increased alveolar nitric oxide and systemic inflammation markers in silica-exposed workers
R Sauni, P Oksa, L Lehtimäki, P Toivio… - Occupational and …, 2012 - oem.bmj.com
R Sauni, P Oksa, L Lehtimäki, P Toivio, P Palmroos, R Nieminen, E Moilanen, J Uitti
Occupational and environmental medicine, 2012•oem.bmj.comBackground Exposure to silica dust may cause inflammatory responses, primarily in the
lungs, although systemic effects have also been reported. Alveolar inflammation can be
demonstrated by increased alveolar concentration of nitric oxide (NO), but information on the
effects of silica dust on exhaled NO is sparse. Inflammatory mediators including cytokines
are known to take part in silica-induced processes, but the role of adipokines has not been
studied previously. Objectives The aim of the study was to investigate the pulmonary and …
lungs, although systemic effects have also been reported. Alveolar inflammation can be
demonstrated by increased alveolar concentration of nitric oxide (NO), but information on the
effects of silica dust on exhaled NO is sparse. Inflammatory mediators including cytokines
are known to take part in silica-induced processes, but the role of adipokines has not been
studied previously. Objectives The aim of the study was to investigate the pulmonary and …
Background
Exposure to silica dust may cause inflammatory responses, primarily in the lungs, although systemic effects have also been reported. Alveolar inflammation can be demonstrated by increased alveolar concentration of nitric oxide (NO), but information on the effects of silica dust on exhaled NO is sparse. Inflammatory mediators including cytokines are known to take part in silica-induced processes, but the role of adipokines has not been studied previously.
Objectives
The aim of the study was to investigate the pulmonary and systemic inflammatory responses to occupational exposure to silica dust.
Methods
The authors examined 94 silica-exposed workers and 35 healthy volunteers. The authors also measured alveolar NO concentration, bronchial NO flux and the plasma levels of proinflammatory cytokines, interleukin (IL)-6 and IL-8, and the adipokines, adipsin, leptin, adiponectin and resistin.
Results
After adjusting for age, body mass index and pack-years of tobacco smoking, silica exposure was associated with significantly higher levels of alveolar NO (p=0.001), indicating inflammatory effects of silica in the peripheral lung. In addition, increased plasma concentrations of IL-6, adiponectin, adipsin and resistin were significantly associated with silica exposure (p=0.002, p=0.034, p<0.001 and p=0.048, respectively).
Conclusions
In conclusion, measurement of alveolar NO concentration and plasma cytokine and adipokine levels seems to offer a modern means to demonstrate the inflammatory effects of exposure to silica. These measures might be useful in finding subjects with a significant immune response to silica particles and thus at higher risk of developing silicosis or other immunological diseases associated with exposure to silica, but further research is needed.
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