Differentiating the in vitro toxicity of solid-surface composite dust: A comparison of material components and...

Workers fabricating solid-surface composite (SSC) materials like Corian® are exposed to airborne particulate matter (PM) containing aluminum trihydrate (ATH) and potentially abrasive particles from sanding tools, leading to concerns about respiratory health effects like pulmonary fibrosis. However, the relative toxicological contributions of the SSC material versus the sandpaper abrasives remain unclear.

This study aimed to compare the in vitro cellular responses induced by respirable dust generated from sanding SSC with different commercial sandpapers (aluminum oxide [Al2O3], ceramic, silicon carbide [SiC]) to the responses elicited by ATH and corresponding abrasive analogue particles.

Respirable dust (PM with an aerodynamic diameter less than 5 µm) was generated from sanding Corian® using the three sandpaper types via a fluidized bed generator coupled with a cyclone separator. Human monocytic THP-1 cells, differentiated into macrophage-like cells, were exposed for 48 h to suspensions of these SSC dusts, ATH, or Al2O3, ceramic, and SiC abrasive analogue particles (10 µg/well). Cytotoxicity (LDH release), apoptosis (Caspase 3/7 activity), necrosis (propidium iodide uptake), cell cycle distribution, and nuclear morphology (including mono-, bi-, multi-, and micronucleation) and the Nuclear Division Index were assessed.

Exposure to SSC dusts generated with any sandpaper type, as well as ATH, resulted in significant increases in apoptosis compared to controls. However, these exposures did not cause significant LDH release or alterations in cell cycle progression or mitotic indices. Conversely, the Al2O3, ceramic, and SiC abrasive analogue particles induced significant disruptions in cell cycle (S phase population reduction) and mitosis (increased multinucleation, micronucleation, and NDI), alongside apoptosis (Al2O3, SiC) or necrosis (ceramic, SiC), but also caused minimal LDH release.

Under these in vitro conditions, the apoptotic response to respirable SSC sanding dust appears primarily driven by components inherent to the SSC material itself, consistent with the effects of ATH. This response profile was distinct from the cell cycle arrest and mitotic disruption prominently caused by the abrasive analogue particles. These findings suggest the intrinsic properties of SSC material components are key drivers of initial macrophage responses in vitro, differing significantly from the effects of the abrasive materials alone.