Abstract
Combustion-derived nanomaterials are noxious ultrafine (<100 nm) aerosol by-products of human activity. They pose threats to pulmonary health due to their small size, allowing them to penetrate alveoli causing detrimental responses downstream. Information regarding the cellular activity that connects nanocarbon particle exposure to poor pulmonary health remains lacking. We hypothesized that low-dose and long-term administrations of carbonaceous nanoparticles contribute to lung irritation by adversely affecting respiratory cells that function as the first line of defense. Responses to ultrafine black carbon (UBC), a key component of airborne pollutants, by human lung A549, murine lung LA4 epithelial cells, human peripheral-blood monocytes THP1, and murine macrophages RAW264.7 were investigated. The cells were first plated on day zero and were fed fresh UBC suspended in culture media on days one, four, and seven. The exposure regimen included three different concentrations of UBC. On day ten, all cells were harvested, washed, and assayed. The impact on cellular viability revealed that UBC was only moderately cytotoxic, while metabolic activity was significantly diminished in a dose-dependent manner. Additionally, beta-galactosidase proportionally increased with UBC concentration compared to untreated cells, indicating that cellular senescence was promoted across all cell types. The implemented regimen caused minimal toxicity yet demonstrated different cellular modifications across the cell lines of both species, inducing changes to enzyme vitality and cellular fitness. The data suggested that compounding nanosized black carbon exposure could negatively impair overall pulmonary health by distinctively modifying intracellular behavior.