Particle-induced artifacts in the MTT and LDH viability assays.

In vitro testing is a common first step in assessing combustion-generated and engineered nanoparticle-related health hazards. Commercially available viability assays are frequently used to compare the toxicity of different particle types and to generate dose-response data. Nanoparticles, well-known for having large surface areas and chemically active surfaces, may interfere with viability assays, producing a false assessment of toxicity and making it difficult to compare toxicity data.

Oxidative stress induced by zero-valent iron nanoparticles and Fe(II) in human bronchial epithelial cells.

To identify the mechanism through which nanoparticulate zero-valent iron (nZVI; Fe0(s)) damages cells, a series of experiments were conducted in which nZVI in phosphate-buffered saline (PBS) was exposed to oxygen in the presence and absence of human bronchial epithelial cells. When nZVI is added to PBS, a burst of oxidants is produced as Fe0 and ferrous iron (Fe[II]) are converted to ferric iron (Fe[II]). Cytotoxicity and internal reactive oxygen species (ROS) production in cells exposed to nZVI is equivalent to the response observed when cells are exposed to the same concentration of dissolved Fe(II).

Cellular response to diesel exhaust particles strongly depends on the exposure method.

In vitro exposure to aerosols at the air-liquid interface (ALI) preserves the physical and chemical characteristics of aerosol particles. Although frequently described as being a more physiologic exposure method, ALI exposure has not been directly compared with conventional in vitro exposures where the particles are suspended in medium. We exposed immortalized human bronchial epithelial cells (16HBE14o) to aerosolized diesel exhaust particles at the ALI and to suspensions of collected particles.

Inflammatory response of lung cells exposed to whole, filtered, and hydrocarbon denuded diesel exhaust.

In vitro studies with the organic extracts of diesel particles have suggested that hydrocarbons such as PAH may play a role in an inflammatory response, but these have been limited by the possible artifacts introduced in the particle collection and processing. In this study, we avoid these artifacts and use an activated carbon denuder to remove hydrocarbons from the exhaust stream to investigate their role in the inflammatory response. Human bronchial epithelial cells (16HBE14o) were exposed at the air-cell interface to diluted and aged exhaust from a diesel generator operated at partial and no load conditions.

Distribution and accumulation of a mixture of arsenic, cadmium, chromium, nickel, and vanadium in mouse small intestine, kidneys, pancreas, and femur following oral administration in water or feed.

Manufactured gas plant (MGP) sites are contaminated with coal tar and may contain metals such as arsenic (As), cadmium (Cd), chromium (Cr), nickel (Ni), and vanadium (V). These metals are known to cause cancer or other adverse health conditions in humans, and the extent and cost of remediating MGP sites may be influenced by the presence of these metals. Studies assessed the distribution of these metals in female B6C3F1 mice ingesting (1) a metal mixture in water or (2) an MGP mixture in NIH-31 feed.

Evaluation of gastrointestinal solubilization of petroleum hydrocarbon residues in soil using an in vitro physiologically based model.

Petroleum hydrocarbon residues in weathered soils may pose risks to humans through the ingestion pathway. To understand the factors controlling their gastrointestinal (GI) absorption, a newly developed experimental extraction protocol was used to model the GI solubility of total petroleum hydrocarbon (TPH) residues in highly weathered soils from different sites. The GI solubility of TPH residues was significantly higher for soil contaminated with diesel than with crude oil.

Characterization of a major aromatic DNA adduct detected in human breast tissues.

A bulky DNA adduct (Spot 1) was previously detected in normal adjacent breast tissues of 41% (36/87) of women with breast cancer and in none (0/29) of the noncancer controls by (32)P-postlabeling. To characterize this adduct, it was chromatographically compared with DNA adduct profiles generated in several in vitro and in vivo experimental systems. First, MCF-7 cells were exposed to a number of chemical carcinogens, that is, benzo[a]pyrene (B[a]P), 4-OH-B[a]P, 9-OH-B[a]P, 11-OH-B[a]P, B[a]P-trans-4,5-dihydrodiol, 1-nitropyrene, 6-nitrochrysene, dibenzo[a,l]pyrene, benzo[c]phenanthrene, dibenzo[a,h]anthracene, 3-methylcholanthrene, and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine.