[1] Field studies have been performed in Lindon, Utah (February 2003) and Rubidoux, California (July 2003) to determine if the Rupprecht and Patashnick (R&P) Filter Dynamic Measurement System (FDMS) determines total fine particulate mass, including the semivolatile ammonium nitrate and organic material. Collocated measurements were made with the FDMS, a conventional tapered element oscillating microbalance (TEOM) monitor with a heated filter, an R&P differential TEOM monitor, the Brigham Young University (BYU) Real-Time Total Ambient Mass Sampler (RAMS), the BYU particle concentrator-organic sampling system (PC-BOSS), a PM 2.5 Federal Reference Method (FRM), a PM 2.5 speciation sampler, an R&P continuous nitrate monitor, and two Sunset continuous carbon monitors (one to measure quartz filter-retained particulate carbon and one to measure particulate semivolatile carbonaceous material lost from the particles on a filter during sampling). The RAMS and PC-BOSS samplers have been shown to determine fine particulate material, including both the semivolatile and the nonvolatile components. Linear regression analysis at the Lindon site between the FDMS (X) and the PC-BOSS (Y), and the FDMS (X) and the RAMS (Y), resulted in zero-intercept slopes of 1.01 ± 0.06 (r 2 = 0.63) and 1.00 ± 0.01 (r 2 = 0.69), respectively. At the Rubidoux sampling site, linear regression analysis between the PC-BOSS (X) and the FDMS (Y) gave a zero-intercept slope of 0.96 ± 0.02 (r 2 = 0.90). Linear regression analysis between the FDMS (X) and the RAMS (Y) resulted in a zero-intercept slope of 0.99 ± 0.01 (r 2 = 0.80). Measurements made at the two sites indicate that the FDMS and the R&P differential TEOM monitors do measure total fine particulate mass, including the semivolatile ammonium nitrate and organic material. Both the heated TEOM monitor and PM 2.5 FRM did not measure the semivolatile material. The difference between the FDMS and a heated TEOM monitor was explained by the semivolatile ammonium nitrate and organic material measured by the various chemical composition monitors.

Quantitative models of Förster resonance energy transfer (FRET)-pioneered by Förster-define our understanding of FRET and underpin its widespread use. However, multicolour FRET (mFRET), which arises between multiple, stochastically distributed fluorophores, lacks a mechanistic model and remains intractable. mFRET notably arises in fluorescently barcoded microparticles, resulting in a complex, non-orthogonal fluorescence response that impedes their encoding and decoding. Here, we introduce an ensemble mFRET (emFRET) model, and apply it to guide barcoding into regimes with extreme FRET. We further introduce a facile, proportional multicolour labelling method using oligonucleotides as homogeneous linkers. A total of 580 barcodes were rapidly designed and validated using four dyes-with FRET efficiencies reaching 76%-and used for multiplexed immunoassays with cytometric readout and fully automated decoding. The emFRET model helps to expand the barcoding capacity of barcoded microparticles using common organic dyes and will benefit other applications subject to stochastic mFRET.

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Exposure to particulate matter (PM) has been implicated in oxidative stress (OxS) and inflammation as underlying mechanisms of lung damage and cardiovascular alterations. PM is a chemical mixture that can be subdivided according to their aerodynamic size into coarse (CP), fine (FP), and ultrafine (UFP) particulates. We investigated, in a rat model, the induction of OxS (protein oxidation and antioxidant response), carcinogen-DNA adduct formation, and inflammatory mediators in lung in response to different airborne particulate fractions, CP, FP, and UFP, after an acute and subchronic exposure. In addition, OxS was evaluated in the aorta to assess the effects beyond the lungs. Exposure to CP, FP, and UFP induced time-and size-dependent lung protein oxidation and DNA adduct formation. After acute and subchronic exposure, nuclear factor erythroid-2 (Nrf2) activation was observed in the lung, by electrophoretic mobility shift assay, and the induction of mRNA antioxidant enzymes in the FP and UFP groups, but not in the CP. Cytokine concentration of interleukin 1, interleukin 6, and macrophage inflammatory protein-2 was significantly increased in bronchoalveolar lavage fluid after acute exposure to FP and UFP. Activation of Nrf2 and expression of mRNA antioxidant enzymes were observed only after the subchronic exposure to FP and UFP in the aorta. Our results indicate that FP and UFP were mainly accountable for the oxidant toxic effects in the lung; OxS is spread from the lung to the cardiovascular system. We conclude that the biological mechanisms associated with transient OxS and inflammation are particle size and timedependent exposure resulting in acute lung injury, which later reaches the vascular system.

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