Correlations of asthma mortality with traffic-related factors: use of catalytic converters and radial tires.

OBJECTIVE: : The objective of this study was to test the hypotheses that the post-1970 rise in asthma mortality in industrialized nations was related to introduction of catalytic converters and/or radial tires. METHODS: : Annual asthma mortality data were plotted on linear coordinates for fraction of automobile fleet with converters or radial tires in Canada, Germany, Japan, and the United States. RESULTS: : Catalytic converter association could not account for asthma mortality that rose in Germany before general adoption of the technology there. Radial tire use was, however, linearly correlated with asthma mortality in all four countries. CONCLUSION: : Rising exposure to materials related to radial tire use may account for a substantial fraction of increased asthma mortality risk since approximately 1970.

Effects of temperature and soil components on emissions from pyrolysis of pyrene-contaminated soil.

Effects of temperature and soil on yields and identities of light gases (H2, CH4, C2H2, C2H4, C2H6, CO, and CO2) and polycyclic aromatic hydrocarbons (PAH) from thermal treatment of a pyrene-contaminated (5 wt%) soil in the absence of oxygen were determined for a U.S. EPA synthetic soil matrix prepared to proxy U.S. Superfund soils. Shallow piles (140-170 mg) of contaminated soil particles and as controls, neat (non-contaminated) soil (140-160 mg), neat pyrene (10-15 mg), neat sand (230 mg), and pyrene-contaminated sand (160 mg), were heated in a ceramic boat inside a 1.65 cm i.d. pyrex tube at temperatures from 500 to 1100 degrees C under an axial flow of helium. Volatile products spent 0.2-0.4s at temperature before cooling. Light gases, PAH and a dichloromethane extract of the residue in the ceramic boat, were analyzed by gas chromatography or high pressure liquid chromatography (HPLC). Over 99% pyrene removal was observed when heating for a few tens of seconds in all investigated cases, i.e., at 500, 650, 750, 1000, and 1100 degrees C for soil, and 750 and 1000 degrees C for sand. However, each of these experiments gave significant yields (0.2-16 wt% of the initial pyrene) of other PAH, e.g., cyclopenta[cd]pyrene (CPP), which mutates bacterial cells and human cells in vitro. Heating pyrene-polluted soil gave pyrene conversions and yields of acetylene, CPP, and other PAH exceeding those predicted from similar, but separate heating of neat soil and neat pyrene. Up to 750 degrees C, recovered pyrene, other PAH, and light gases accounted for all or most of the initial pyrene whereas at 1000 and 1100 degrees C conversion to soot was significant. A kinetic analysis disentangled effects of soil-pyrene interactions and vapor phase pyrolysis of pyrene. Increase of residence time was found to be the main reason for the enhanced conversion of pyrene in the case of the presence of a solid soil or sand matrix. Light gas species released due to the thermal treatment, such as acetylene and methane, lead the formation of other, pyrene-derived PAH, e.g., methylpyrenes, cyclopenta[cd]pyrene, and benzo[a]pyrene. Implications of these findings for the chemistry of soil thermal decontamination and for diagnosing potential defects in soil thermal cleaning, e.g., incomplete elimination of targeted pollutants and formation of adverse by-products, are discussed.

Human cell mutagens in respirable airborne particles from the northeastern United States. 2. Quantification of mutagens and other organic compounds.

Few reports have characterized mutagenic compounds in respirable airborne particles (<2.5 micrometers in diameter; PM2.5) collected at different sites on a regional scale (hundreds of km). Previously, we reported differences in the human (h1A1v2) cell mutagenicity of whole and fractionated organic extracts of PM2.5 samples collected in Boston, MA, Rochester, NY, and Quabbin Reservoir, a rural site in western MA. Herein we describe the analysis of mutagens and other organic compounds in these samples. Gas chromatography-mass spectrometry (GC-MS) was used to quantify approximately 150 organic compounds, including 31 known human cell mutagens. Molecular weight (MW) 226-302 amu PAHs were the most important mutagens identified: cyclopenta[cd]pyrene accounted for 1-2% of the measured mutagenicity of the samples, MW 252 PAHs accounted for 4-6%, MW 276-278 PAHs accounted for 2-5%, and MW 302 PAHs accounted for 2-3%. 6H-benzo-[cd]pyren-6-one, a PAH ketone, accounted for 3-5% of the mutagenicity. The same compounds accounted for similar portions of the total attributed mutagenicity in each sample. Mutagen levels were similar in the Boston and Rochester samples, and both were significantly higher than the Quabbin sample. This may explain whythe mutagenicities of the Boston and Rochester samples were higher than the Quabbin sample. The levels of mutagens found in semipolar fractions, however, could not explain why the mutagenicity of semipolar fractions was 2-fold higher in the Rochester sample than in the Boston sample. Known mutagens accounted for only 16-26% of the total mutagenicity of the unfractionated extracts, and only approximately 20% of the mutagenicity of the nonpolar and semipolar fractions. The remaining mutagenicity is likely attributable to other, as-yet unknown, semipolar and polar mutagens, or to interactions among chemical constituents of the samples. These findings are consistent with similar studies performed on airborne particles from Los Angeles and Washington, DC, thus indicating that PAHs, PAH-ketones, and as-yet unidentified polar organic compounds are widely distributed airborne human cell mutagens.

Human-cell mutagens in respirable airborne particles in the northeastern United States. 1. Mutagenicity of fractionated samples.

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.