Particulate matter (PM) emissions from stationary combustion sources burning coal, fuel oil, biomass, and waste, and PM from internal combustion (IC) engines burning gasoline and diesel, are a significant source of primary particles smaller than 2.5 µm (PM 2.5 ) in urban areas. Combustion-generated particles are generally smaller than geologically produced dust and have unique chemical composition and morphology. The fundamental processes affecting formation of combustion PM and the emission characteristics of important applications are reviewed. Particles containing transition metals, ultrafine particles, and soot are emphasized because these types of particles have been studied extensively, and their emissions are controlled by the fuel composition and the oxidant-temperature-mixing history from the flame to the stack. There is a need for better integration of the combustion, air pollution control, atmospheric chemistry, and inhalation health research communities. Epidemiology has demonstrated that susceptible individuals are being harmed by ambient PM. Particle surface area, number of ultrafine particles, bioavailable transition metals, polycyclic aromatic hydrocarbons (PAH), and other particle-bound organic compounds are suspected to be more important than particle mass in determining the effects of air pollution. Time-and size-resolved PM measurements are needed for testing mechanistic toxicological hypotheses, for characterizing the relationship between combustion operating conditions and transient emissions, and for source apportionment studies to develop air quality plans. Citations are provided to more specialized reviews, and the concluding comments make suggestions for further research.

Inhalation of environmental particulate matter (PM) is correlated with adverse health effects in humans, but gene products that couple detection with cellular responses, and the specific properties of PM that target different pathways, have not been fully elucidated. TRPA1 and V1 are two cation channels expressed by sensory neurons and non-neuronal cells of the respiratory tract that have been implicated as possible mediators of PM toxicity. The goals of this research were to determine if environmental PM preferentially activated TRPA1 and to elucidate the criteria responsible for selectivity. Quantification of TRPA1 activation by 4 model PM revealed that diesel exhaust PM (DEP) and coal fly ash PM (CFA1) were TRPA1 agonists at concentrations >0.077 mg/ml. DEP was more potent and approximately 97% of the activity of DEP was recovered by serial extraction of the solid DEP with ethanol and hexane:n-butyl chloride. Modification of the electrophile/agonist binding sites on TRPA1 (C621, C641, C665 and K710) to non-nucleophilic residues reduced TRPA1 activation by DEP and abolished activation by DEP extracts as well as multiple individual electrophilic chemical components of DEP. However, responses to CFA1 and DEP solids were not affected by these mutations. Activity-guided fractionation of DEP and high resolution mass spectroscopy identified several new DEP-derived TRPA1 agonists and activation of mouse dorsal root ganglion neurons demonstrated TRPA1 is a primary target for DEP in a heterogeneous population of primary sensory nerves. It is concluded that TRPA1 is a specific target for electrophilic chemical components of DEP and proposed that activation of TRPA1 in the respiratory tract is likely to be an important mechanism for DEP pneumotoxicity.

Background: The induction of cytokines by airway cells in vitro has been widely used to assess the effects of ambient and occupational particles. This study measured cytotoxicity and the release of the proinflammatory cytokines IL-6 and IL-8 by human bronchial epithelial cells treated with manufactured nano-and micron-sized particles of Al 2 O 3 , CeO 2 , Fe 2 O 3 , NiO, SiO 2 , and TiO 2 , with soil-derived particles from fugitive dust sources, and with the positive controls LPS, TNF-α, and VOSO 4 .

There is ongoing concern regarding the toxicity of nanoparticles with sizes less than 100 nm as compared to larger particles of the same nominal substance. Two commercial ZnO types, one sold as a 8-10 nm powder and the other described as -325 mesh (<44 mum) powder, were evaluated in human colon-derived RKO cells. The powders had a volume-to-surface area ratio equivalent to 40 and 330 nm spheres, respectively. Both materials formed micrometer-sized agglomerates in cell culture media. The nanosized ZnO was more cytotoxic than the micrometer-sized ZnO with LC(50) values of 15 +/- 1 and 29 +/- 4 mug/cm(2), respectively. Transfer of Zn from the solid phase to the cell culture media in the presence of RKO cells was time- and concentration-dependent. However, direct particle-cell contact was required for RKO cell cytotoxicity, and the toxicity of particles was independent of the amount of soluble Zn in the cell culture media. The mechanism of cell death includes the disruption of mitochondrial function. Robust markers of apoptosis, Annexin V staining, loss of mitochondrial potential, and increased generation of superoxide were observed when cells were treated with ZnO particulate matter but not when treated with comparable concentration of a soluble Zn salt. Both ZnO samples induced similar mechanisms of toxicity, but there was a statistically significant increase in potency per unit mass with the smaller particles.