Abstract
Inhalation of metal-rich PM2.5 produces reactive oxygen species (ROS) in the body, which may cause Maillard reactions, produce advanced glycation end products (AGEs). The interaction between the receptor of AGEs (RAGE) and its ligand AGEs triggers the inflammatory signal transduction, elevating risk of chronic diseases including diabetes mellitus. This study was assess the association between exposure to metal fume fine particle matter and production of AGE and RAGE.This study conducted in cross-sectional design and consisted of 52 welding workers and 29 office workers. The exposure assessment was performed for all individuals with a personal sampler to measure eight working hours exposure to metal-rich PM2.5 on Monday. On Tuesday morning, participants were instructed to fast for at least 10 hours prior to urine and blood sampling. Urinary metals were measured by ICP-MS. AGE and RAGE product was analyzed by ELISA and Flow Cytometry respectively. Multivariable linear regression model was used to assess association between urinary metals concentration and AGE and RAGE expression.PM2.5 exposure concentrations were 379.93±4.71 μg/m3 and 154.47±3.56 μg/m3 in welders and administrative personnel, respectively. RAGE expressions were 1500.78±1743.56 a. u. and 741.05± 537.03 a. u. in welders and administrative personnel, respectively. However, AGE did not significantly differ between these two groups. There was no significant correlation between PM2.5 and AGE or RAGE. After adjusted for confounders, urinary chromium concentration (β=0.242, 95%CI 0.024-0.339, P=0.025) and urinary cadmium concentration (β=0.333, 95%CI 0.017-0.165, P=0.017) were significantly associated with RAGE expression. However, no significant effect of urinary metals concentration on AGE was found.Exposure to metal fume particulate matter in welders were significantly associated with increasing RAGE expression. Inflammatory response of increased RAGE expression of welders should be further investigated.
Published Version
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