Short-term exposure to stone minerals used in asphalt affect lung function and promote pulmonary inflammation among healthy adults.

Objective: Stone minerals are a partially ignored environmental challenge but a significant contributor to urban air pollution. We examined if short-term exposure to two stone minerals - quartz diorite and rhomb porphyry - commonly used in asphalt pavement would affect lung function, promote pulmonary inflammation, and affect bronchial reactivity differently.

Methods: Our randomized crossover study included 24 healthy, non-smoking young adults exposed to the stone minerals quartz diorite, rhomb porphyry, and control dust (lactose).

Particulate Matter 2.5 Exposure and Self-Reported Use of Wood Stoves and Other Indoor Combustion Sources in Urban Nonsmoking Homes in Norway.

Few studies have examined particulate matter (PM) exposure from self-reported use of wood stoves and other indoor combustion sources in urban settings in developed countries. We measured concentrations of indoor PM < 2.5 microns (PM2.

Wood smoke particles from different combustion phases induce similar pro-inflammatory effects in a co-culture of monocyte and pneumocyte cell lines.

Background: Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season.

DNA damage and DNA damage responses in THP-1 monocytes after exposure to spores of either Stachybotrys chartarum or Aspergillus versicolor or to T-2 toxin.

We have characterized cell death in THP-1 cells after exposure to heat-treated spores from satratoxin G-producing Stachybotrys chartarum isolate IBT 9631, atranone-producing S. chartarum isolate IBT 9634, and sterigmatocystin-producing Aspergillus versicolor isolate IBT 3781, as well as the trichothecenes T-2 and satratoxin G. Spores induced cell death within 3-6 h, with Stachybotrys appearing most potent.

Involvement of NADPH oxidase and iNOS in rodent pulmonary cytokine responses to urban air and mineral particles.

We have investigated the potential of two complex mineral particles (feldspar and mylonite), quartz (Min-U-Sil), and suspended particulate matter (SRM-1648) (SPM) from urban air to induce inflammatory cytokine responses in primary rat alveolar type 2 cells and alveolar macrophages, and the involvement of cellular formation of free radicals in these responses. All particle types induced an increased release of interleukin (IL)-6 and macrophage inflammatory protein (MIP)-2 from type 2 cells. Diphenyleneiodonium chloride (DPI), a selective inhibitor of NADPH-oxidase, reduced the IL-6 and MIP-2 responses to quartz, SPM and mylonite.

Pattern of cell death after in vitro exposure to GDMA, TEGDMA, HEMA and two compomer extracts.

Objectives: In vitro exposure to chemical compounds in dental materials may cause cell death by apoptosis, necrosis or a combination of both. The aim of this paper was to evaluate aqueous extracts of freshly cured compomers Freedom (SDI) and F2000 (3M ESPE), and constituents identified in the extracts, GDMA (glycerol dimethacrylate), TEGDMA (triethylene glycol dimethacrylate) and HEMA (2-hydroxyethyl methacrylate) for their ability to induce necrosis and apoptosis in primary rat alveolar macrophages and the J744A1 macrophage cell line.

Methods: The cells were exposed to either extracts of freshly cured samples of the products or to one of the constituents identified in the extracts.