Adverse pulmonary impacts of environmental concentrations of oil mist particulate matter in normal human bronchial epithelial cell

Abstract

Airborne oil mist particulate matter (OMPM) is generated during industrial processes such as metalworking and may be associated with pulmonary dysfunction. In this study, we employed the normal human bronchial epithelial BEAS-2B cell line to elucidate the association between pulmonary toxicity and OMPM of 2.5-10 μm, 1.0-2.5 μm and <1.0 μm particle sizes (OMPM_10-2.5, OMPM_2.5-1.0 and OMPM_1.0). We measured OMPM concentrations at a precision machinery factory to estimate lung deposition rates and select realistic environmental concentrations for testing. All OMPMs (1-50 μg/cm²) significantly decreased BEAS-2B cell viability (>38% of control), except for low-dose OMPM_1.0 (1 μg/cm²). OMPM_10-2.5 and OMPM_2.5-1.0, but not OMPM_1.0, induced oxidative stress (1.5-4-fold increase compared with the control) and increased the production of proinflammatory cytokines (1.5-3-fold). However, only OMPM_1.0 induced pulmonary epithelial barrier dysfunction via depletion of zonula occludens (0.65-0.8-fold) and α1-antitrypsin proteins (0.65-0.8-fold). In conclusion, a higher risk of lung disease was associated with smaller particle size OMPM. Exposure to OMPM_1.0 may be a potential risk factor for chronic obstructive pulmonary disease. The evidence also demonstrates that occupational exposure to OMPM may cause pulmonary disease at very low concentrations.

Keywords: Epithelial barrier integrity; Inflammation; Oil mist particulate matter; Oxidative stress; α1-Antitrypsin proteins.