Lung function and IFN-gamma levels in the sera of silica-exposed workers.
Excessive exposure to respirable particles of crystalline silica is an occupational health problem in developing countries and can cause a variety of pulmonary diseases, such as silicosis, chronic obstructive pulmonary disease (COPD), and malignancy, in susceptible hosts. In addition to the well-documented role of pulmonary macrophages, lymphocytes occasionally have been suggested to influence the pneumoconiotic process, but their potential role is not clearly understood. Interferon-gamma (IFN-gamma), a lymphocyte cytokine, is recognized as the most important cytokine in converting macrophages from a resting to an activated state. The aim of the present study was to investigate serum IFN-gamma levels and pulmonary function changes in silica-exposed workers and in silicosis. Twenty-seven silica workers (aged 35.6 +/- 8.2 years with 5.11 +/- 2.98 years exposure duration) and 18 unexposed office workers (aged 33.8 +/- 12 years) were included in the study. Mean spirometry parameters and smoking history were comparable to the values of the office workers, but COPD prevalence was higher in the silica-exposed group, and the age-adjusted ratio was more sensitive than fixed quotient criteria for airway obstruction. We found silicosis in 4 silica workers. The mean serum IFN-gamma level was increased in silica-exposed workers (10.22 +/- 22.68 pg/mL) although it was undetectable in all office workers and even in the workers with silicosis. Evaluating pulmonary function tests (PFT) using an age-adjusted quotient may prevent underestimation of airflow limitation, especially in the young population with risk factors. Although serum IFN-gamma may increase initially in response to silica, low levels of IFN-gamma in later stages may be considered a risk factor for silicosis because this cytokine downregulates the fibroblast responses to transforming growth factor-beta (TGF-beta) and decreases collagen production. Additional research to determine the exact role of this potent cytokine may offer insight into the pathogenesis of silicosis.
Polatli
Mehmet
M
Chest Disease Department, Adnan Menderes University School of Medicine, Aydin, Turkey. mpolatli@ttmail.com; mpolatli@adu.edu.tr
Tuna
Handan T
HT
Yenisey
Cigdem
C
Serter
Mukadder
M
Cildag
Orhan
O
D000328:Adult; D006801:Humans; D007371:Interferon-gamma / Q000097:blood*; D016273:Occupational Exposure; D012129:Respiratory Function Tests; D012822:Silicon Dioxide / Q000008:administration & dosage*; D012829:Silicosis / Q000097:blood* / Q000503:physiopathology*
D012822:Silicon Dioxide; D007371:Interferon-gamma