Cytotoxicity and Epithelial Barrier Toxicity of Fine Particles from Residential Biomass Pellet Burning

Abstract

Rising environmental concerns associated with the domestic use of solid biofuels have driven the search for clean energy alternatives. This study investigated the in vitro toxicological characteristics of PM_2.5 emissions from residential biomass pellet burning using the A549 epithelial cell line. The potential of modern pellet applications to reduce PM_2.5 emissions was evaluated by considering both mass reduction and toxicity modification. PM_2.5 emissions from raw and pelletized biomass combustion reduced cell viability, indicative of acute toxicity, and also protein expression associated with epithelial barrier integrity, implying further systemic toxicity, potentially via an oxidative stress mechanism. Toxicity varied between PM_2.5 emissions from raw biomass and pellets, with pelletized straw and wood inducing cytotoxicity by factors of 0.54 and 1.30, and causing epithelial barrier damage by factors of 1.76 and 2.08, respectively, compared to their raw counterparts. Factoring in both mass reduction and toxicity modifications, PM_2.5 emissions from pelletized straw and wood dropped to 1.83 and 5.07 g/kg, respectively, from 30.1 to 9.32 g/kg for raw biomass combustion. This study underscores the effectiveness of pelletized biomass, particularly straw pellets, as a sustainable alternative to traditional biofuels and highlights the necessity of considering changes in toxicity when assessing the potential of clean fuels to mitigate emissions of the PM_2.5 complex.

Keywords: PM2.5 emissions; ROS; cytotoxicity; epithelial barrier damage; pellets; solid biofuels.

Figure 1

Cell viability after incubation with PM_2.5 emitted from pelletized straw and wood fuels compared to their feedstock. (A) Dose–response relationships between PM_2.5 exposure and cell viability quantified using the CCK-8 assay. (B) Lethal Concentration 50 (LC50) values calculated from the dose–response relationships.

Figure 2

Cellular expression of proteins maintaining cellular junctions after exposure to PM_2.5 emissions from pelletized straw and wood fuels compared to their feedstock. (A) Visualization of cellular ZO-1 protein through fluorescence microscopy images, with the ZO-1 protein depicted in green, nuclei in blue, and cytoplasmic membranes in red. (B) Gene expression of the ZO-1 protein. (C) Gene expression of the Claudin-5 protein.

Figure 3

ROS generation induced by exposure to PM_2.5 from burning pelletized biomass (A) compared with their feedstock (B). Asterisks indicate the significance of the difference relative to the control test (p < 0.05).

Figure 4

Physicochemical properties of PM_2.5 emissions from burning raw and pelletized biomass fuels, including appearance and size distribution (A), pristine size (B), hydrodynamic size (C), ζ potential (D), surface O-functional group percentage (E), and the content of element carbon (EC) (F), organic carbon (OC) (G), heavy metals (H), and polycyclic aromatic hydrocarbon (PAHs) (I). Asterisks on the columns of pellets indicate the significance of the difference relative to their corresponding raw feedstock (*: p < 0.05; **: p < 0.01).

Figure 5

Relative importance of physicochemical properties of PM_2.5 emissions in explaining the variability of the cytotoxicity (A) and epithelial barrier damage (B), denoted by cell viability and gene expression of ZO-1, respectively. Tested properties include the hydrodynamic size (HySize), ζ potential (ZePo), surface oxygen/carbon ratio (O/C), the content of element carbon (EC), organic carbon (OC), heavy metal (HMs), and polycyclic aromatic hydrocarbon (PAHs).

Figure 6

Potential reductions in PM_2.5 emissions, achieved by switching from the combustion of raw straw (A) and wood (B) to their pelletized counterparts as fuels. Data are presented as mean values with 95% confidence intervals.