Occupational exposure to gasoline in gasoline station male attendants promotes M1 polarization in macrophages

Several studies have reported the toxicological implications of exposure to petroleum hydrocarbon fumes in animal models. There is little documentation on the effect of such exposure on oxidative stress levels and immune response. To our knowledge, no documentation of M1 polarization in macrophages in gasoline station male attendants. Therefore, this study aimed to evaluate the harmful effects of gasoline vapors in 62 male attendants (16-70 years) compared to 29 age- and sex-matched-unexposed controls. The attendants were recruited from Damietta governorate gasoline stations. Gasoline exposure induced a significant increase in tumor necrosis factor-alpha (TNF-alpha) level (p < 0.05) as well as a slight but non-significant increase in the activity of acidic mammalian chitinase (AMCase) (p > 0.05). Further TNF-alpha/AMCase ratio was significantly increased (p < 0.01) in sera of the attendants when compared to those of the healthy controls. Also, the total leucocytic and lymphocytic counts were significantly increased (p < 0.01 and p < 0.001, respectively). On contrary, neutrophils to lymphocytes ratio (NLR) and platelets to lymphocytes ratio (PLR) were significantly decreased (p < 0.05 and p < 0.001, respectively). In addition, significant reduction in hemoglobin (Hb) concentration, plasma glutathione reduced form (GSH), and catalase, as well as superoxide dismutase (SOD) activities in red blood cells were observed in the exposed attendants. As a result, malondialdehyde (MDA), nitric oxide (NO) levels, and NO/AMCase ratio were significantly increased (p < 0.05). In conclusion, this study inferred that prolonged gasoline exposure can mediate immune activation, especially M1 macrophages polarization, possibly via oxidative stress-mediated mechanism.

Automated summary

Exposure to gasoline vapors among male attendants at gas stations leads to immune activation, especially polarization of M1 macrophages, possibly through an oxidative stress-mediated pathway. This exposure also triggers cellular-level inflammatory responses and alterations in blood parameters.