Journal of occupational and environmental medicine · 2022
An Increase in Plasma Adipsin Levels Is Associated With Higher Cumulative Dust Exposure and Airway Obstruction in Foundry Workers.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Koskela Kirsi, Sauni Riitta, Uitti Jukka, Oksa Panu, Moilanen Eeva, Hämäläinen Mari, Lehtimäki Lauri
Аннотация
OBJECTIVE: The aim of the study was to assess whether plasma adipokine levels (adipsin, adiponectin, leptin, and resistin) are associated with pulmonary function in foundry workers.
METHODS: We examined 65 dust-exposed foundry workers and 40 nonexposed controls and analyzed their lung function and plasma adipokine levels at baseline and after approximately 7 years of follow-up.
RESULTS: A higher increase in plasma adipsin was associated with the development of airway obstruction in exposed subjects during follow-up after adjusting for body mass index changes during the follow-up period. Furthermore, the increase in adipsin levels was positively associated with cumulative dust exposure even after adjusting for smoking and body mass index changes during follow-up ( P = 0.015).
CONCLUSION: The results suggest that plasma adipsin is involved in the pathogenesis of subclinical airway inflammation and the development of chronic obstruction and is induced by occupational dust exposure.
METHODS: We examined 65 dust-exposed foundry workers and 40 nonexposed controls and analyzed their lung function and plasma adipokine levels at baseline and after approximately 7 years of follow-up.
RESULTS: A higher increase in plasma adipsin was associated with the development of airway obstruction in exposed subjects during follow-up after adjusting for body mass index changes during the follow-up period. Furthermore, the increase in adipsin levels was positively associated with cumulative dust exposure even after adjusting for smoking and body mass index changes during follow-up ( P = 0.015).
CONCLUSION: The results suggest that plasma adipsin is involved in the pathogenesis of subclinical airway inflammation and the development of chronic obstruction and is induced by occupational dust exposure.