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.
Chest Disease Department, Adnan Menderes University School of Medicine, Aydin, Turkey. mpolatli@ttmail.com; mpolatli@adu.edu.tr
Mehmet
M
Polatli
Handan T
HT
Tuna
Cigdem
C
Yenisey
Mukadder
M
Serter
Orhan
O
Cildag
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