Engine-operating load influences diesel exhaust composition and cardiopulmonary and immune responses

Abstract

Background: The composition of diesel engine exhaust (DEE) varies by engine type and condition, fuel, engine operation, and exhaust after treatment such as particle traps. DEE has been shown to increase inflammation, susceptibility to infection, and cardiovascular responses in experimentally exposed rodents and humans. Engines used in these studies have been operated at idle, at different steady-state loads, or on variable-load cycles, but exposures are often reported only as the mass concentration of particulate matter (PM), and the effects of different engine loads and the resulting differences in DEE composition are unknown.

Objectives: We assessed the impacts of load-related differences in DEE composition on models of inflammation, susceptibility to infection, and cardiovascular toxicity.

Methods: We assessed inflammation and susceptibility to viral infection in C57BL/6 mice and cardiovascular toxicity in APOE-/- mice after being exposed to DEE generated from a single-cylinder diesel generator operated at partial or full load.

Results: At the same PM mass concentration, partial load resulted in higher proportions of particle organic carbon content and a smaller particle size than did high load. Vapor-phase hydrocarbon content was greater at partial load. Compared with high-load DEE, partial-load DEE caused greater responses in heart rate and T-wave morphology, in terms of both magnitude and rapidity of onset of effects, consistent with previous findings that systemic effects may be driven largely by the gas phase of the exposure atmospheres. However, high-load DEE caused more lung inflammation and greater susceptibility to viral infection than did partial load.

Conclusions: Differences in engine load, as well as other operating variables, are important determinants of the type and magnitude of responses to inhaled DEE. PM mass concentration alone is not a sufficient basis for comparing or combining results from studies using DEE generated under different conditions.

Figure 1

Mass composition of PM in the three exposure conditions. Abbreviations: Alkanes C15–C30, compounds with 15–30 carbon chain lengths; dae, aerodymanic particle size equivelant; dlogDP, differential log of particle size range; dm, differential mass; m, mass; Oxy-PAH, oxygenated polycyclic aromatic hydrocarbons. (A) The full mass composition of PM primarily dominated by carbon. Elemental (black) carbon accounted for most of the high-load exhaust, but its concentration was low in the partial-load operating condition. (B) Contributions from ammonium, sulfate, and nitrate to PM mass. Partial-load PM had much greater contributions from organic carbon, ammonium, sulfate, and nitrate material than did high-load PM. (C) Nonmethane volatile organic compounds (NMVOC) and CO for the three exposure conditions. The partial-load atmosphere consisted of much greater mass of both components than did the high-load or control atmospheres. (D) Relative proportions of major volatile organic compound classes, including semivolatile organic compounds (SVOCs) in the three experimental atmospheres. (E and F) PM mass size distributions did not differ between high- and partial-load modes, but the particle number size distributions did; the y-axis label [(dm/m)/dlogDp] refers to the differential mass, normalized to total mass within a specified particle size range. The black circles show the particle number size distribution.

Figure 2

Changes in markers of pulmonary inflammation, HO-1 (A), IFN-γ (B), and TNF-α (C), for control [filtered air (FA)], partial-load DEE, and high-load DEE exposures (mean + SE). Inflammatory proteins were measured in homogenates of the right caudal and middle lung lobes (C57BL/6 mice, 6 per group). *p < 0.05 versus control, and **p < 0.05 versus control and partial load, by two-way ANOVA (n = 5 per group).

Figure 3

Pathology and viral clearance in C57BL/6 mice exposed to filtered air (FA; control), partial-load DEE, or high-load DEE, and RSV administration (mean + SE). *p < 0.05 versus control.

Figure 4

Lung pathology images of C57BL/6 mice exposed to filtered air (A), partial-load DEE (B), or high-load DEE (C) and RSV. H&E-stained lungs (left) show substantial increases in inflammation in mice exposed to both RSV and high-load DEE. Additionally, airway epithelial cells stained for Clara cell secretory protein (right) show more advanced pathology and differentiation after exposure to high-load DEE. *p < 0.05 versus control.

Figure 5

HR (A) and T-wave area (B) changes (mean ± SE) in ApoE^–/– mice exposed to filtered air, partial-load DEE, or high-load DEE. We obtained ECG signals continuously via radiotelemetry, and we derived data from the ECG and reported hourly data for analysis. Average HRs were 692 ± 13, 685 ± 40, and 648 ± 26 BPM for control, partial load, and high load, respectively. *p < 0.05 versus control, and **p < 0.05 versus control and high load, by two-way ANOVA (n = 5 per group).