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Background: Numerous epidemiological studies have recently observed that exposure to traffic-related air pollution (TRAP) is associated with increased risk of various respiratory diseases. Major gaps in knowledge remain regarding the toxicological effects., Objectives: We examined the toxicological effects of the gasoline exhaust particles (GEP), a paradigm of TRAP, in rats, with an objective to provide the evidence, obtain the biomarkers, and suggest effective intervention measure., Methods: We measured the airway hyperresponsiveness (AHR), inflammatory cells in the bronchoalveolar lavage (BAL) fluid, histological changes in the lung tissues, and the biomarkers so as to systematically examine the toxicological effects of GEPs at different dose levels (0.5, 2.5, 5 mg/kg BW). The intervention of vitamin E (VE), a natural antioxidant, on the toxicological effects was investigated., Results: The lung injury caused by GEP exposure was first indicated by the airway hyperresponsiveness (AHR). Compared with the control group, GEP exposure significantly increased the airway resistances and decreased the lung compliance; the higher the dose of GEP, the more serious the lung injury. Lung injury was also revealed by the increase of inflammatory cells, including the lymphocytes and neutrophils, in the BAL fluid. With the increase of GEP dose, histological changes in the lung tissues were further observed: inflammatory cell infiltration increased and alveolar wall thickened. The toxicology of GEP was demonstrated by the increase of the biomarkers of the oxidative stress, the pro-inflammatory cytokines and the apoptosis cytokine. However, administration of VE was found to be effective in restoring airway injury., Conclusion: The toxicological effects of traffic-related air pollution (TRAP) on rat lungs are supported by evidence and biomarkers, and vitamin E intervention is feasible., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Although health benefits of physical activity are well known, the risk of physical activity in polluted air is unclear. Our objective is to investigate health effects resulting from physical activity in polluted air by looking at particle deposition in human tracheobronchial (TB) airways. Airflow and particle deposition in TB airways were investigated using a computational fluid dynamics (CFD) method. We chose three regional airways: upper (G3-G5), central (G9-G11) and lower (G14-G16). Physical activity was described by breathing rate at the mouth, for three levels of activity: sedentary (15 l/min), moderate (30 l/min) and intense (60 l/min). We found that particle deposition was strongly affected by physical activity. Particles are deposited in greater number in the lower airways (G14-G16) during sedentary activity, more in the upper airways (G3-G5) during intense activity, and uniformly in the airways during moderate activity. The difference in the deposition pattern was due to the reason that physical activity increased the airflow which increased inertial impaction. Our modeling of particle deposition in the human respiratory airways shows that there are different health effects for different activity levels: sedentary activity leads to chronic health effects, intense activity results in acute effects, and moderate activity minimizes the adverse health effects of physical activity in polluted air., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Although ambient particulate matter or particles have been found to be associated with morbidity and mortality all over the world, specific health effects of particles from different sources need further elucidation. The objective of this work is to predict the deposition of particles from different sources in the human lung. The whole lung, consisting of 24 generations of branches from trachea to alveoli, was approximated using a one-dimensional lumped "trumpet" model with a variable cross-sectional area. The aerosol dynamics equation was numerically solved using a finite difference method to investigate the transport and deposition of particles in the lung model. Particles from various sources were assumed to be different in both size and density. We found that in general, coarse particles (> 2.5 µm) were mainly deposited in the tracheobronchial (TB) region by impaction, and fine particles (< 2.5 µm) were mainly deposited in the pulmonary (P) region by sedimentation and diffusion. However, the coarse particles with low density can be deposited in P region by sedimentation. As a comparison, our results found that soil particles, which are coarse with low density, were deposited in the deep lung more than traffic particles, which are fine with high density. Modeling of particle deposition in the human lung indicated that coarse particles generated by crustal sources may have adverse health effects as strong as those resulting from fine particles generated from combustion sources., (Copyright © 2018 Elsevier Inc. All rights reserved.)

The plasticizer di(2-ethylhexyl) phthalate (DEHP) is ubiquitous in the environment and considered as carcinogen; however, the carcinogenic risk of human exposure to DEHP in the air via inhalation is lacking. A probabilistic incremental lifetime cancer risk (ILCR) model was implemented to quantitatively estimate the potential cancer risk of DEHP via human inhalation by using Monte Carlo simulation. We assessed the cancer risk in different age groups (children, adolescents, and adults) exposed to different DEHP concentrations (background low, indoor moderate, and occupational high) for different durations (2, 8, and 20 years). Results showed that the cancer risk of exposure to DEHP was below the acceptable limit (10 -6 ) in the ambient air but was serious in indoor and occupational environments even at short exposure duration (2 years). The cancer risk of DEHP via inhalation in children was lower than that in adolescents and adults, but the risk in children via dermal and oral exposure to indoor dust and soft PVC toys should be considered. Sensitivity analysis indicated that the exposure concentration of DEHP was the strongest factor that influenced ILCR. Our work provides the evidence of cancer risk of DEHP via inhalation and highlights the risk in indoor and occupational environments.