Role of Secondary Organic Matter on Soot Particle Toxicity in Reconstituted Human Bronchial Epithelia Exposed at the Air-Liquid Interface.

Secondary organic matter (SOM) formed from gaseous precursors constitutes a major mass fraction of fine particulate matter. However, there is only limited evidence on its toxicological impact. In this study, air-liquid interface cultures of human bronchial epithelia were exposed to different series of fresh and aged soot particles generated by a miniCAST burner combined with a micro smog chamber (MSC). Soot cores with geometric mean mobility diameters of 30 and 90 nm were coated with increasing amounts of SOM, generated from the photo-oxidation of mesitylene and ozonolysis of α-pinene. At 24 h after exposure, the release of lactate dehydrogenase (LDH), indicating cell membrane damage, was measured and proteome analysis, i.e. the release of 102 cytokines and chemokines to assess the inflammatory response, was performed. The data indicate that the presence of the SOM coating and its bioavailability play an important role in cytotoxicity. In particular, LDH release increased with increasing SOM mass/total particle mass ratio, but only when SOM had condensed on the outer surface of the soot cores. Proteome analysis provided further evidence for substantial interference of coated particles with essential properties of the respiratory epithelium as a barrier as well as affecting cell remodeling and inflammatory activity.

Responses of reconstituted human bronchial epithelia from normal and health-compromised donors to non-volatile particulate matter emissions from an aircraft turbofan engine.

Health effects of particulate matter (PM) from aircraft engines have not been adequately studied since controlled laboratory studies reflecting realistic conditions regarding aerosols, target tissue, particle exposure and deposited particle dose are logistically challenging. Due to the important contributions of aircraft engine emissions to air pollution, we employed a unique experimental setup to deposit exhaust particles directly from an aircraft engine onto reconstituted human bronchial epithelia (HBE) at air-liquid interface under conditions similar to in vivo airways to mimic realistic human exposure. The toxicity of non-volatile PM (nvPM) from a CFM56-7B26 aircraft engine was evaluated under realistic engine conditions by sampling and exposing HBE derived from donors of normal and compromised health status to exhaust for 1 h followed by biomarker analysis 24 h post exposure. Particle deposition varied depending on the engine thrust levels with 85% thrust producing the highest nvPM mass and number emissions with estimated surface deposition of 3.17 × 109 particles cm-2 or 337.1 ng cm-2. Transient increase in cytotoxicity was observed after exposure to nvPM in epithelia derived from a normal donor as well as a decrease in the secretion of interleukin 6 and monocyte chemotactic protein 1. Non-replicated multiple exposures of epithelia derived from a normal donor to nvPM primarily led to a pro-inflammatory response, while both cytotoxicity and oxidative stress induction remained unaffected. This raises concerns for the long-term implications of aircraft nvPM for human pulmonary health, especially in occupational settings.

Non-volatile particle emissions from aircraft turbine engines at ground-idle induce oxidative stress in bronchial cells.

Aircraft emissions contribute to local and global air pollution. Health effects of particulate matter (PM) from aircraft engines are largely unknown, since controlled cell exposures at relevant conditions are challenging. We examined the toxicity of non-volatile PM (nvPM) emissions from a CFM56-7B26 turbofan, the world's most used aircraft turbine using an unprecedented exposure setup. We combined direct turbine-exhaust sampling under realistic engine operating conditions and the Nano-Aerosol Chamber for In vitro Toxicity to deposit particles onto air-liquid-interface cultures of human bronchial epithelial cells (BEAS-2B) at physiological conditions. We evaluated acute cellular responses after 1-h exposures to diluted exhaust from conventional or alternative fuel combustion. We show that single, short-term exposures to nvPM impair bronchial epithelial cells, and PM from conventional fuel at ground-idle conditions is the most hazardous. Electron microscopy of soot reveals varying reactivity matching the observed cellular responses. Stronger responses at lower mass concentrations suggest that additional metrics are necessary to evaluate health risks of this increasingly important emission source.

Charge-based personal aerosol samplers.

There are several good reasons to use personal monitors for exposure control and health effect studies. But current personal monitoring methods are either not sensitive enough to measure typical ambient concentrations, work offline (masking short exposures to high concentrations), and/or require trained personnel to analyze the data, which makes them difficult to use. For this reason, we propose the use of a diffusion charging sensor as an online personal monitoring method, and present a miniaturized device (45 x 80 x 200 mm, 770 g) that works on this principle. Our device has a high time resolution and covers typically encountered ambient concentration ranges. It can measure very low particle concentrations of a few hundred particles per cubic centimeter even for ultrafine particles (i.e., two to three orders of magnitude more sensitive than rival technologies), while the upper detection limit is 1 million particles/cm(3), which hardly ever occurs in ambient settings. While other methods measure a fixed quantity, the response of our device can be tuned to be proportional to the particle diameter to the power of x, with at least 0.3

Methane balance of a bioreactor landfill in Latin America.

This paper presents results from a methane (CH4) gas emission characterization survey conducted at the Loma Los Colorados landfill located 60 km from Santiago, Chile. The landfill receives approximately 1 million metric tons (t) of waste annually, and is equipped with leachate control systems and landfill gas collection systems. The collected leachate is recirculated to enable operation of the landfill as a bioreactor. For this study, conducted between April and July 2000, a total of 232 surface emission measurements were made over the 23-ha surface area of the landfill. The average surface flux rate of CH4 emissions over the landfill surface was 167 g x m(-2) x day(-1), and the total quantity of surface emissions was 13,320 t/yr. These values do not include the contribution made by "hot spots," originating from leachate pools caused by "daylighting" of leachate, that were identified on the landfill surface and had very high CH4 emission rates. Other point sources of CH4 emissions at this landfill include 20 disconnected gas wells that vent directly to the atmosphere. Additionally, there are 13 gas wells connected to an incinerator responsible for destroying 84 t/yr of CH4. The balance also includes CH4 that is being oxidized on the surface of the landfill by meth-anotrophic bacteria. Including all sources, except leachate pool emissions, the emissions were estimated to be 14,584 t/yr CH4. It was estimated that less than 1% of the gas produced by the decomposition of waste was captured by the gas collection system and 38% of CH4 generated was emitted to the atmosphere through the soil cover.