Particle Toxicity in vitro

BrooklynDodger fears complexity in particle response will found a new line of Houdini risk assessments to avoid a single particle limit, either in the community or at work.  Appropriate recognition of varying responses of several cell types and several particle types would explain some contrasting whole animal people responses.  The Dodger fears slicing and dicing of response data to attempt multiple limits.

So here the investigators find 3 types of inflammatory cells in the airways: neutrophils (PMN), eosinophils and monocytes (Mo), and alveolar macrophages (AM).  They chose 6 types of particles:  transition metal-rich residual oil fly ashes (ROFAs), coal fly ashes, diesel, SiO2, TiO2 and fugitive dusts [which contained aluminum silicates].  The particles were of various sizes.  Different cells reacted differently to different particles of different size and source.  There’s at least an 18 cell matrix showing relative sensitivity of cell type vs. particle type.

The main message is that the so called inert material, titanium dioxide, reacted with all these cell types.  Diesel, theoretically a carbon particle coated with PAC’s [PAC’s not being acutely reactive?] also had effect.

The claims of those who believe no physiological basis for fine particle epidemiology are clearly weakened.

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 Toxicol In Vitro. 2002 Jun;16(3):209-18
Differential particulate air pollution induced oxidant stress in human granulocytes, monocytes and alveolar macrophages.Becker S, Soukup JM, Gallagher JE.US EPA, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Research Triangle Park, NC 27711, USA. becker.susanne@epamail.epa.gov Individuals with pre-existing airways inflammation, such as chronic obstructive pulmonary disease (COPD), lung infection or asthma are likely most sensitive to particulate pollution. These diseases are characterized by a presence of inflammatory cells in the airways including neutrophils (PMN), eosinophils and monocytes (Mo), and increased numbers of alveolar macrophages (AM).  Particles including transition metal-rich residual oil fly ashes (ROFAs), coal fly ashes, diesel, SiO2, TiO2 and fugitive dusts were co-cultured with AM, Mo and PMN. A strong oxidant response of AM was restricted to oil fly ashes, while the PMN were most reactive to the dusts containing aluminium silicate. In general, the Mo response was less vigorous, but overlapped both AM- and PMN-stimulating dusts. The response of AM to SiO2 of various sizes and TiO2 in the fine size range obtained from different commercial sources, was highly variable, implying that composition rather than size was responsible for the oxidant response. These results suggest that oxidant activation by various sources of particulate matter is cell specific. Therefore, the inflamed lung is likely to be more susceptible to harm of ambient air particulates because of the oxidant stress posed by a broader range of particles.