The acute toxic effects of particulate matter in mouse lung are related to size and season of collection

Farina, Francesca; Sancini, Giulio; Mantecca, Paride; Gallinotti, Daniele; Camatini, Marina; Palestini, Paola

doi:10.1016/j.toxlet.2011.01.031

Cited by 99 publications

(92 citation statements)

References 51 publications

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“…As known to all, the particles aggregate easily in sterile saline. For this reason, the PM 2.5 suspension was sonicated to make particles dispersed just before intratracheal instillation into mice (Farina et al, 2011;Jin et al, 2017). We also determined that the chemical composition of PM 2.5 samples was rich in some metals such as Zn, Al, Pb, Fe and part of PAHs.…”

Section: Discussionmentioning

confidence: 99%

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Wu¹,

Zhang²

2018

J. Toxicol. Sci.

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-Epidemiological studies have confirmed that ambient fine particulate matter (PM 2.5 ) exposure is associated with cardiovascular disease (CVD). However, the underlying mechanisms in PM 2.5 exposure-induced heart injury are largely unknown. It has been acknowledged that NADPH oxidase (Nox) 4 plays a critical role in CVD development. To investigate the acute effects of PM 2.5 on the mouse heart and the role of Nox4 in PM 2.5 exposure-induced cardiac injury, C57BL/6J mice were instilled with saline or 1.5, 3.0, 6.0 mg/kg BW PM 2.5 suspension for two weeks (five days per week). The levels of malondialdehyde (MDA), super oxide dismutase (SOD), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β in heart supernatants were determined using related kits. The expression of Nox4, p67 phox , p47 phox and p22 phox in heart tissue was evaluated by immunofluorescence staining or Western blotting, respectively. Protein levels of p53, Bax, Bcl-2 and Caspase-3 in the heart were examined using immunohistochemical staining and Western blotting. TUNEL assay was used to measure myocardial apoptosis. PM 2.5 exposure leads to obvious cardiac injury. PM 2.5 exposure increases MDA level and iNOS activity, and decreases activity of SOD in heart supernatants of mice. High levels of TNF-α and IL-1β in heart supernatants of mice with PM 2.5 instillation were determined. Nox4 and Noxassociated subunits such as p67 phox , p47 phox and p22 phox expression levels were increased in heart tissue of mice after PM 2.5 exposure. Additionally, PM 2.5 exposure causes myocardial apoptosis in the mouse heart. This study suggested that Nox4 is involved in PM 2.5 exposure-induced cardiac injury in mice.

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Section: Discussionmentioning

confidence: 99%

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Wu¹,

Zhang²

2018

J. Toxicol. Sci.

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“…Particles larger than 10 µm are likely to land in proximal airways, but fine particles reach the lungs and are deposited in the alveoli [7]. Therefore PM 2.5 may be more harmful than larger ones [8]. Ambient fine particulate pollution was associated with increased risk of cardiovascular diseases [9].…”

Section: Human Exposure To Air Pollution: the Route Of Air Pollutantsmentioning

confidence: 99%

Impact of Air Pollution on Public Health

Marchwińska-Wyrwał¹,

Dziubanek²,

Hajok³

et al. 2011

The Impact of Air Pollution on Health, Economy, Environment and Agricultural Sources

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“…Traditionally, the toxicity of PM is estimated by collecting particles and then resuspending them in a liquid medium that can be instilled onto in vitro cells or into the lungs of test animals (Steenhof et al, 2011;Tsukue et al, 2010;Weldy et al, 2011;Farina et al, 2011). Additionally, in toxicology studies, filter samples are routinely left exposed to laboratory air for extended periods of time and/or autoclaved.…”

Section: Potential Differences To Traditional Pm Toxicity Assessmentsmentioning

confidence: 99%

“…Many toxicological studies focus on single species, or single primary pollutants, in the search for an entity that can be assigned causality for health outcomes observed in epidemiology studies (e.g., Steenhof et al, 2011;Farina et al, 2011;Schlesinger et al, 2006;Dreher, 2000). While it is useful to examine the effects of single pollutants, these studies ignore atmospheric ageing and the photochemical evolution of species that occurs during the day in the ambient environment.…”

Section: Introductionmentioning

confidence: 99%

Gaseous VOCs rapidly modify particulate matter and its biological effects – Part 2: Complex urban VOCs and model PM

et al. 2012

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Abstract. This is the second study in a three-part study designed to demonstrate dynamic entanglements among gaseous organic compounds (VOCs), particulate matter (PM), and their subsequent potential biological effects. We study these entanglements in increasingly complex VOC and PM mixtures in urban-like conditions in a large outdoor chamber, both in the dark and in sunlight. To the traditional chemical and physical characterizations of gas and PM, we added new measurements of gas-only-and PM-onlybiological effects, using cultured human lung cells as model living receptors. These biological effects are assessed here as increases in cellular damage or expressed irritation (i.e., cellular toxic effects) from cells exposed to chamber air relative to cells exposed to clean air. Our exposure systems permit side-by-side, gas-only-and PM-only-exposures from the same air stream containing both gases and PM in equilibria, i.e., there are no extractive operations prior to cell exposure for either gases or PM.In Part 1 (Ebersviller et al., 2012a), we demonstrated the existence of PM "effect modification" (NAS, 2004) for the case of a single gas-phase toxicant and an inherently nontoxic PM (mineral oil aerosol, MOA). That is, in the presence of the single gas-phase toxicant in the dark, the initially non-toxic PM became toxic to lung cells in the PM-onlybiological exposure system. In this Part 2 study, we used sunlit-reactive systems to create a large variety of gas-phase toxicants from a complex mixture of oxides of nitrogen and 54 VOCs representative of those measured in US city air. In these mostly day-long experiments, we have designated the period in the dark just after injection (but before sunrise) as the "Fresh" condition and the period in the dark after sunset as the "Aged" condition. These two conditions were used to expose cells and to collect chemical characterization samples. We used the same inherently non-toxic PM from the Part 1 study as the target PM for "effect modification". Fortunately, in the absence of "seed particles", the complex highly-reactive VOC system used does not create any secondary aerosol in situ. All PM present in these tests were, therefore, introduced by injection of MOA to serve as PM-to-be-modified by the gaseous environment. PM addition was only done during dark periods, either before or after the daylight period. The purpose of this design is to test if a non-toxic PM becomes toxic in initially unreacted ("Fresh"), or in reacted ("Aged") complex VOC conditions. To have a complete design, we also tested the effects of clean air and the same VOC conditions, but without introducing any PM. Thus, there were six exposure treatment conditions that were evaluated with the side-by-side, gas-only-and PMonly-effects exposure systems; five separate chamber experiments were performed: two with clean air and three with the complex VOC/NO x mixture.For all of these experiments and exposures, chemical composition data and matching biological effects results for two end-points were compared. Chemic...

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The acute toxic effects of particulate matter in mouse lung are related to size and season of collection

Cited by 99 publications

References 51 publications

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Impact of Air Pollution on Public Health

Gaseous VOCs rapidly modify particulate matter and its biological effects – Part 2: Complex urban VOCs and model PM

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