Human-Cell Mutagens in Respirable Airborne Particles in the Northeastern United States. 1. Mutagenicity of Fractionated Samples

Abstract

Few studies have characterized the regional scale (300-500 km) variability of the mutagenicity of respirable airborne particles (PM2.5). We previously collected 24-h PM2.5 samples for 1 year from background, suburban, and urban sites in Massachusetts (MA) and rural and urban sites in upstate New York (NY) (n = 53-60 samples per site). Bimonthly composites of these samples were mutagenic to human cells. The present report describes our effort to identify chemical classes responsible for the mutagenicity of the samples, to quantify spatial differences in mutagenicity, and to compare the mutagenicity of samples composited in different ways. Organic extracts and HPLC fractions (two nonpolar, one semipolar, and one polar) of annual composites were tested for mutagenicity in the h1A1v2 cells, a line of human B-lymphoblastoid cells that express cytochrome P450 CYP1A1 cDNA. The mutagenic potency (induced mutant fraction per microg organic carbon) of the semipolarfractions was the highest at all five sites, accounting for 35-82% of total mutagenic potency of the samples, vs the nonpolar (4-38%) and polar (14-32%) fractions. These results are consistent with previous studies. While unfractionated extracts exhibited no spatial variations, the mutagenicity of semipolar fractions at the NY sites was approximately 2-fold higher than at the MA sites. This suggests there may be significant regional differences in the sources and/ or transport and transformation of mutagenic compounds in PM2.5. In addition, mutagenic potency was sensitive to whether samples were fractionated and how they were composited: unfractionated annual composite samples at the NY sites were significantly less mutagenic than their semipolar fractions and the annual average of bimonthly composites; spatial differences in the mutagenic potency of bimonthly composites and the semipolar fractions were not apparent in the annual composites.

Occurrence and Potential Sources of Quinones Associated with PM2.5 in Guadalajara, Mexico

“…In addition to direct mutagenicity and carcinogenicity [4,5], in vivo assays have shown that quinones are highly redox active, cascading the formation of reactive oxygen species (ROS) within the cell [6]. The presence of ROS can cause severe oxidative stress within cells [7] and lead to the development of diseases and pathological conditions such as asthma, cardiovascular diseases, Alzheimer, diabetes, or cancer [8].…”

Particle size distribution of nitrated and oxygenated polycyclic aromatic hydrocarbons (NPAHs and OPAHs) on traffic and suburban sites of a European megacity: Paris (France)

“…Due to their recognized or potential mutagenic activity (Arey et al, 1988;Durant et al, 1996;Ishii et al, 2000;Pedersen et al, 2004Pedersen et al, , 2005, the study of PAH derivatives according to the particle size distribution is of prime interest. However, to date, only 8 authors reported results on the size distribution of NPAHs (Ladji et al, 2009;Hayakawa et al, 1995b;Albinet et al, 2008a;Cecinato et al, 1999;Di Filippo et al, 2010;Hayakawa et al, 1995a;Jinhui and Lee, 2000;Kawanaka et al, 2004Kawanaka et al, , 2008Teixeira et al, 2011), and only 4 papers focused on the particle size distribution of OPAHs (Albinet et al, 2008a;Allen, 1997;Allen et al, 1997;Ladji et al, 2009).…”

Seasonal Influence on Vapor-and Particle-Phase Polycyclic Aromatic Hydrocarbon Concentrations in School Communities Located in Southern California

“…There is ample literature showing that PM is toxic to humans (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans 1989; Peng et al 2005). More recently, a direct link between the PAH content of atmospheric PM and adverse health effects has been established (Pedersen et al 2004;Xia et al 2004). …”