Responses of reconstituted human bronchial epithelia from normal and health-compromised donors to non-volatile particulate matter emissions from an aircraft turbofan engine

Abstract

Health effects of particulate matter (PM) from aircraft engines have not been adequately studied since controlled laboratory studies reflecting realistic conditions regarding aerosols, target tissue, particle exposure and deposited particle dose are logistically challenging. Due to the important contributions of aircraft engine emissions to air pollution, we employed a unique experimental setup to deposit exhaust particles directly from an aircraft engine onto reconstituted human bronchial epithelia (HBE) at air-liquid interface under conditions similar to in vivo airways to mimic realistic human exposure. The toxicity of non-volatile PM (nvPM) from a CFM56-7B26 aircraft engine was evaluated under realistic engine conditions by sampling and exposing HBE derived from donors of normal and compromised health status to exhaust for 1 h followed by biomarker analysis 24 h post exposure. Particle deposition varied depending on the engine thrust levels with 85% thrust producing the highest nvPM mass and number emissions with estimated surface deposition of 3.17 × 10⁹ particles cm^-2 or 337.1 ng cm^-2. Transient increase in cytotoxicity was observed after exposure to nvPM in epithelia derived from a normal donor as well as a decrease in the secretion of interleukin 6 and monocyte chemotactic protein 1. Non-replicated multiple exposures of epithelia derived from a normal donor to nvPM primarily led to a pro-inflammatory response, while both cytotoxicity and oxidative stress induction remained unaffected. This raises concerns for the long-term implications of aircraft nvPM for human pulmonary health, especially in occupational settings.

Keywords: Aerosol; Aircraft engine exhaust; Bronchial epithelial cell culture; Cellular response; Non-volatile particulate matter.

Fig. 1.

Deposition of non-volatile particulate matter (nvPM) from a CFM56-7B26 turbofan onto reconstituted human bronchial epithelia (HBE). a) Recorded diffusion charging current for each thrust level (0.32mv/fA). b) Size distributions of deposited particles. c) Mass of nvPM deposited per surface area of cell culture after 1 h of exposure. d) Number of nvPM deposited per surface area of cell culture after 1 h of exposure. Highest deposition is observed for 85% thrust and lowest for the second lowest thrust level (7%), which is less deposition than after exposure to ground idle (GI, 3%). Data for diffusion current, particle mass and number are reported as mean and SD of four (85%) or three (7%, GI) independent aerosol generations for cell exposures.

Fig. 2.

Morphology of non-volatile particulate matter (nvPM) soot emissions. Transmission electron microscopy (TEM) images showing the larger size and higher abundance of soot particles, a) at 85% thrust compared to b) ground idle (GI) condition. Scale bar: 200 nm.

Fig. 3.

Biological responses in bronchial epithelia of a normal donor after 1 h of exposure to non-volatile particulate matter (nvPM) from different thrust levels. a) Adenylate kinase (AK) released from damaged cells into the apical compartment, presented as fold change over particle-filtered (P-free) controls, at 1 h and 24 h post exposure (hpe). b) HMOX-1 gene expression 24 hpe as determined by qPCR, presented as fold change over P-free controls. c) IL-6, d) MCP-1, and e) IL-8 secretions into the basal compartment 24 hpe as determined by ELISA, presented as pg mL⁻¹. Data is presented as mean ± SD and n = 9–18 cultures from three independent exposures. Statistical significance was assessed using a non-matching two-way analysis of variance (ANOVA) with Sidak’s multiple comparison test (AK release) or a non-matching one-way analysis of variance (ANOVA) with Tukey’s multiple comparison test (HMOX-1, IL-6, MCP-1, IL-8): *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

Fig. 4.

Comparison of biological responses after 1 h of exposure to ground idle thrust conditions in three individual donors. a) Adenylate kinase (AK) released from damaged cells into the apical compartment, presented as fold change over particle-free (P-free) controls, at 1 and 24 h post exposure (hpe). b) HMOX-1 gene expression 24 hpe as determined by qPCR, presented as fold change over P-free controls. c) IL-6, MCP-1, and IL-8 secretions into the basal compartment 24 hpe as determined by ELISA, presented as pg mL⁻¹. Data is presented as mean ± SD and n = 9–18 cultures from three independent exposures. Statistical significance was assessed using a non-matching one-way analysis of variance (ANOVA) with Tukey’s multiple comparison test (HMOX-1, IL-6, MCP-1, IL-8): ***p < 0.001, and ****p < 0.0001.