Effect of Treatment Media on the Agglomeration of Titanium Dioxide Nanoparticles: Impact on Genotoxicity, Cellular Interaction, and Cell Cycle

The widespread use of titanium dioxide (TiO₂) nanoparticles in consumer products increases the probability of exposure to humans and the environment. Although TiO₂ nanoparticles have been shown to induce DNA damage (comet assay) and chromosome damage (micronucleus assay, MN) <i>in vitro</i>, no study has systematically assessed the influence of medium composition on the physicochemical characteristics and genotoxicity of TiO₂ nanoparticles. We assessed TiO₂ nanoparticle agglomeration, cellular interaction, induction of genotoxicity, and influence on cell cycle in human lung epithelial cells using three different nanoparticle-treatment media: keratinocyte growth medium (KGM) plus 0.1% bovine serum albumin (KB); a synthetic broncheoalveolar lavage fluid containing PBS, 0.6% bovine serum albumin and 0.001% surfactant (DM); or KGM with 10% fetal bovine serum (KF). The comet assay showed that TiO₂ nanoparticles induced similar amounts of DNA damage in all three media, independent of the amount of agglomeration, cellular interaction, or cell-cycle changes measured by flow cytometry. In contrast, TiO₂ nanoparticles induced MN only in KF, which is the medium that facilitated the lowest amount of agglomeration, the greatest amount of nanoparticle cellular interaction, and the highest population of cells accumulating in S phase. These results with TiO₂ nanoparticles in KF demonstrate an association between medium composition, particle uptake, and nanoparticle interaction with cells, leading to chromosomal damage as measured by the MN assay

Photochemical Conversion of Surrogate Emissions for Use in Toxicological Studies: Role of Particulate- and Gas-Phase Products

The production of photochemical atmospheres under controlled conditions in an irradiation chamber permits the manipulation of parameters that influence the resulting air-pollutant chemistry and potential biological effects. To date, no studies have examined how contrasting atmospheres with a similar Air Quality Health Index (AQHI), but with differing ratios of criteria air pollutants, might differentially affect health end points. Here, we produced two atmospheres with similar AQHIs based on the final concentrations of ozone, nitrogen dioxide, and particulate matter (PM_2.5). One simulated atmosphere (SA-PM) generated from irradiation of ∼23 ppmC gasoline, 5 ppmC α-pinene, 529 ppb NO, and 3 μg m^–3 (NH₄)₂SO₄ as a seed resulted in an average of 976 μg m^–3 PM_2.5, 326 ppb NO₂, and 141 ppb O₃ (AQHI 97.7). The other atmosphere (SA-O₃) generated from 8 ppmC gasoline, 5 ppmC isoprene, 874 ppb NO, and 2 μg m^–3 (NH₄)₂SO₄ resulted in an average of 55 μg m^–3 PM_2.5, 643 ppb NO₂, and 430 ppb O₃ (AQHI of 99.8). Chemical speciation by gas chromatography showed that photo-oxidation degraded the organic precursors and promoted the de novo formation of secondary reaction products such as formaldehyde and acrolein. Further work in accompanying papers describe toxicological outcomes from the two distinct photochemical atmospheres

Progressive Increase in Disinfection Byproducts and Mutagenicity from Source to Tap to Swimming Pool and Spa Water: Impact of Human Inputs

Pools and spas are enjoyed throughout the world for exercise and relaxation. However, there are no previous studies on mutagenicity of disinfected spa (hot tub) waters or comprehensive identification of disinfection byproducts (DBPs) formed in spas. Using 28 water samples from seven sites, we report the first integrated mutagenicity and comprehensive analytical chemistry of spas treated with chlorine, bromine, or ozone, along with pools treated with these same disinfectants. Gas chromatography (GC) with high-resolution mass spectrometry, membrane-introduction mass spectrometry, and GC-electron capture detection were used to comprehensively identify and quantify DBPs and other contaminants. Mutagenicity was assessed by the <i>Salmonella</i> mutagenicity assay. More than 100 DBPs were identified, including a new class of DBPs, bromoimidazoles. Organic extracts of brominated pool/spa waters were 1.8× more mutagenic than chlorinated ones; spa waters were 1.7× more mutagenic than pools. Pool and spa samples were 2.4 and 4.1× more mutagenic, respectively, than corresponding tap waters. The concentration of the sum of 21 DBPs measured quantitatively increased from finished to tap to pool to spa; and mutagenic potency increased from finished/tap to pools to spas. Mutagenic potencies of samples from a chlorinated site correlated best with brominated haloacetic acid concentrations (Br-HAAs) (<i>r</i> = 0.98) and nitrogen-containing DBPs (N-DBPs) (<i>r</i> = 0.97) and the least with Br-trihalomethanes (<i>r</i> = 0.29) and Br–N-DBPs (<i>r</i> = 0.04). The mutagenic potencies of samples from a brominated site correlated best (<i>r</i> = 0.82) with the concentrations of the nine HAAs, Br-HAAs, and Br-DBPs. Human use increased significantly the DBP concentrations and mutagenic potencies for most pools and spas. These data provide evidence that human precursors can increase mutagenic potencies of pools and spas and that this increase is associated with increased DBP concentrations