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High concentrations of pollution particles, including "soot" or black carbon, exist over the Indian Ocean, but their sources and geographical origins are not well understood. We measured emissions from the combustion of biofuels, used widely in south Asia for cooking, and found that large amounts of carbonaceous aerosols are emitted per kilogram of fuel burnt. We calculate that biofuel combustion is the largest source of black carbon emissions in India, and we suggest that its control is central to climate change mitigation in the south Asian region.

The proinflammatory effects of particulate pollutants, including diesel exhaust particles (DEP), are related to their content of redox cycling chemicals and their ability to generate oxidative stress in the respiratory tract. An antioxidant defense pathway, which involves phase II enzyme expression, protects against the pro-oxidative and proinflammatory effects of DEP. The expression of enzymes, including heme oxygenase-1 (HO-1) and GST, is dependent on the activity of a genetic antioxidant response element in their promoters. In this study we investigated the mechanism by which redox cycling organic chemicals, prepared from DEP, induce phase II enzyme expression as a protective response. We demonstrate that aromatic and polar DEP fractions, which are enriched in polycyclic aromatic hydrocarbons and quinones, respectively, induce the expression of HO-1, GST, and other phase II enzymes in macrophages and epithelial cells. We show that HO-1 expression is mediated through accumulation of the bZIP transcription factor, Nrf2, in the nucleus, and that Nrf2 gene targeting significantly weakens this response. Nrf2 accumulation and subsequent activation of the antioxidant response element is regulated by the proteasomal degradation of Nrf2. This pathway is sensitive to pro-oxidative and electrophilic DEP chemicals and is also activated by ambient ultrafine particles. We propose that Nrf2-mediated phase II enzyme expression protects against the proinflammatory effects of particulate pollutants in the setting of allergic inflammation and asthma.

Motor vehicles are a significant source of polycyclic aromatic hydrocarbon (PAH) emissions. Improved understanding of the relationship between fuel composition and PAH emissions is needed to determine whether fuel reformulation is a viable approach for reducing PAH emissions. PAH concentrations were quantified in gasoline and diesel fuel samples collected in summer 1997 in northern California. Naphthalene was the predominant PAH in both fuels, with concentrations of up to 2600 mg L-1 in gasoline and 1600 mg L-1 in diesel fuel. Particle-phase PAH size distributions and exhaust emission factors were measured in two bores of a roadway tunnel. Emission factors were determined separately for light-duty vehicles and for heavy-duty diesel trucks, based on measurements of PAHs, CO, and CO2. Particle-phase emission factors, expressed per unit mass of fuel burned, ranged up to 21 μg kg-1 for benzo[ghi]perylene for light-duty vehicles and up to ∼1000 μg kg-1 for pyrene for heavy-duty diesel vehicles. Light-duty vehicles were found to be a significant source of heavier (four- and five-ring) PAHs, whereas heavy-duty diesel engines were the dominant source of three-ring PAHs, such as fluoranthene and pyrene. While no correlation between heavy-duty diesel truck PAH emission factors and PAH concentrations in diesel fuel was found, light-duty vehicle PAH emission factors were found to be correlated with PAH concentrations in gasoline, suggesting that gasoline reformulation may be effective in reducing PAH emissions from motor vehicles.

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