Abstract. We synthesised observations of total particle number (CN) concentration from 36 sites around the world. We found that annual mean CN concentrations are typically 300-2000 cm −3 in the marine boundary layer and free troposphere (FT) and 1000-10 000 cm −3 in the continental boundary layer (BL). Many sites exhibit pronounced seasonality with summer time concentrations a factor of 2-10 greater than wintertime concentrations. We used these CN obserCorrespondence to: D. V. Spracklen (dominick@env.leeds.ac.uk) vations to evaluate primary and secondary sources of particle number in a global aerosol microphysics model. We found that emissions of primary particles can reasonably reproduce the spatial pattern of observed CN concentration (R 2 =0.46) but fail to explain the observed seasonal cycle (R 2 =0.1). The modeled CN concentration in the FT was biased low (normalised mean bias, NMB=−88%) unless a secondary source of particles was included, for example from binary homogeneous nucleation of sulfuric acid and water (NMB=−25%). Simulated CN concentrations in the continental BL were also biased low (NMB=−74%) unless the number emission of anthropogenic primary particles was increased or a Published by Copernicus Publications on behalf of the European Geosciences Union. 4776 D. V. Spracklen et al.: Explaining global aerosol number concentrations mechanism that results in particle formation in the BL was included. We ran a number of simulations where we included an empirical BL nucleation mechanism either using the activation-type mechanism (nucleation rate, J , proportional to gas-phase sulfuric acid concentration to the power one) or kinetic-type mechanism (J proportional to sulfuric acid to the power two) with a range of nucleation coefficients. We found that the seasonal CN cycle observed at continental BL sites was better simulated by BL particle formation (R 2 =0.3) than by increasing the number emission from primary anthropogenic sources (R 2 =0.18). The nucleation constants that resulted in best overall match between model and observed CN concentrations were consistent with values derived in previous studies from detailed case studies at individual sites. In our model, kinetic and activation-type nucleation parameterizations gave similar agreement with observed monthly mean CN concentrations.

Cigarette smoke exposure is a major determinant of adverse lung health, but the molecular processes underlying its effects on inflammation and immunity remain poorly understood. Therefore, we sought to understand whether inflammatory and host defense determinants are affected during subchronic cigarette smoke exposure. Dose-response and time course studies of lungs from Balb/c mice exposed to smoke generated from 3, 6, and 9 cigarettes/day for 4 days showed macrophage- and S100A8-positive neutrophil-rich inflammation in lung tissue and bronchoalveolar lavage (BAL) fluid, matrix metalloproteinase (MMP) and serine protease induction, sustained NF-kappaB translocation and binding, and mucus cell induction but very small numbers of CD3+CD4+ and CD3+CD8+ lymphocytes. Cigarette smoke had no effect on phospho-Akt but caused a small upregulation of phospho-Erk1/2. Activator protein-1 and phospho-p38 MAPK could not be detected. Quantitative real-time PCR showed upregulation of chemokines (macrophage inflammatory protein-2, monocyte chemoattractant protein-1), inflammatory mediators (TNF-alpha, IL-1beta), leukocyte growth and survival factors [granulocyte-macrophage colony-stimulating factor, colony-stimulating factor (CSF)-1, CSF-1 receptor], transforming growth factor-beta, matrix-degrading MMP-9 and MMP-12, and Toll-like receptor (TLR)2, broadly mirroring NF-kappaB activation. No upregulation was observed for MMP-2, urokinase-type plasminogen activator, tissue-type plasminogen activator, and TLRs 3, 4, and 9. In mouse strain comparisons the rank order of susceptibility was Balb/c > C3H/HeJ > 129SvJ > C57BL6. Partition of responses into BAL macrophages vs. lavaged lung strongly implicated macrophages in the inflammatory responses. Strikingly, except for IL-10 and MMP-12, macrophage and lung gene profiles in Balb/c and C57BL/6 mice were very similar. The response pattern we observed suggests that subchronic cigarette smoke exposure may be useful to understand pathogenic mechanisms triggered by cigarette smoke in the lungs including inflammation and alteration of host defense.

Abstract. The southern hemisphere marine Aerosol Characterization Experiment (ACE 1) was the first of a series of experiments that will quantify the chemical and physical processes controlling the evolution and properties of the atmospheric aerosol relevant to radiative forcing and climate. The goals of this series of process studies are to reduce the overall uncertainty in the calculation of climate forcing by aerosols and to understand the multiphase atmospheric chemical system sufficiently to be able to provide a prognostic analysis of future radiative forcing and climate response. ACE 1, which was conducted from November 15 to December 14, 1995, over the southwest Pacific Ocean, south of Australia, quantified the chemical, physical, radiative, and cloud nucleating properties and furthered our understanding of the processes controlling the aerosol properties in this minimally polluted marine atmosphere. The experiment involved the efforts of scientists from 45 research institutes in 11 countries.

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The vapor pressure of H2SO4 over 98.01 mass‐% sulfuric acid solution has been determined experimentally over the temperature interval 338 to 445 K. Values of the enthalpy and entropy changes upon vaporization deduced from the data accord well with other estimates available in the literature. Extrapolation to 99.0 mass‐% and 296.15 K allows us to confirm another recent vapor pressure determination, thereby supporting the conclusion that the vapor pressures most often used in nucleation calculations in the past are as much as an order of magnitude high.