Diesel engine exhaust
AOPs Including This Stressor
|Oxidative stress [MIE] Leading to Decreased Lung Function [AO]||Low|
Events Including This Stressor
|Decrease, Lung function|
|User term||DTXID||Preferred name||Casrn||jchem_inchi_key||indigo_inchi_key|
|Diesel engine exhaust||DTXSID1024043||Diesel engine exhaust||NOCAS_24043|
Incubation of human primary bronchial epithelial cells differentiated at the air-liquid interface with Diesel exhaust particles (DEP; 100 µg/mL = 16.26 ng/mL phenanthrene, 3.65 ng/mL fluoranthene, 2.53 ng/mL pyrene) attenuated CBF in a time- and dose-dependent manner. Exposure to 10 µg/mL DEP decreased CBF by 40% (Q1 = 19, Q3 = 46) from baseline after 24-h incubation. Similarly, exposure to 50 µg/mL DEP, filtered DEP solution, or 100 µg/mL DEP decreased CBF by 51% (Q1 = 49, Q3 = 56), 33% (Q1 = 26, Q3 = 36), and 73% (Q1 = 65, Q3 = 83), respectively, from baseline after 24-h incubation. Changes in CBF started to become significant at 4 h with 50 µg/mL DEP and at 2 h with 100 µg/mL DEP compared to untreated cultures (Bayram et al., 1998).
In a study of 733 adult females who had lived in the Tokyo metropolitan area for more than 3 years, the higher the level of air pollution, the more significantly the FEV1 was reduced (Sekine et al., 2004).
In a study in 29 healthy subjects, exposure to DE inside diesel-powered trains for 3 days was associated with reduced lung function (Andersen et al., 2019).
In workers who tested diesel engines in an assembly unit of a manufacturing plant, FEV1, FEV1/FVC, FEV25-75 and MEF were significantly reduced compared to non-exposed workers (Zhang et al., 2017).