Short term inhalation toxicity of a liquid aerosol of glutaraldehyde-coated CdS/Cd(OH)2 core shell quantum dots in rats

Ma‐Hock, Lan; Farias, Patrícia M. A.; Hofmann, Thomas; Andrade, Arnaldo C. D. S.; Silva, J.N.; Arnaud, Thatiana Montenegro Stamford; Wohlleben, Wendel; Strauss, Volker; Treumann, Silke; Chaves, Claudilene R.; Gröters, Sibylle; Landsiedel, Robert; Ravenzwaay, Bennard van

doi:10.1016/j.toxlet.2013.11.007

Cited by 17 publications

(10 citation statements)

References 23 publications

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“…Overall, the results of our study are in agreement with other studies investigating QD-induced pulmonary toxicity and injury in that all studies including our own have shown neutrophilic inflammation and pro-inflammatory cytokine induction (Jacobsen et al, 2009; Ma-Hock et al, 2012, 2013; Ho et al, 2013; Roberts et al, 2013). Increased total protein levels in BALF are a valuable measure of alveolar/capillary barrier integrity (Matute-Bello et al, 2011).…”

Section: Discussionsupporting

confidence: 92%

“…QDs have also been shown to penetrate into the outer layers of stratum corneum and epidermis, but not all the way through, porcine skin (Zhang et al, 2008). In contrast, pulmonary exposure to QDs (a potential route of exposure in occupational settings) has been shown to result in neutrophilic and granulomatous inflammation, compromised alveolar-capillary barrier function, DNA damage, and cytotoxicity (Oberdorster et al, 2005; Jacobsen et al, 2009; Ma-Hock et al, 2012, 2013; Ho et al, 2013; Roberts et al, 2013). Furthermore, as observed for in vitro studies, surface coatings (i.e.…”

Section: Introductionmentioning

confidence: 99%

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Susceptibility to quantum dot induced lung inflammation differs widely among the Collaborative Cross founder mouse strains

Scoville

White

Botta

et al. 2015

Toxicology and Applied Pharmacology

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Quantum dots (QDs) are engineered semiconductor nanoparticles with unique physicochemical properties that make them potentially useful in clinical, research and industrial settings. However, a growing body of evidence indicates that like other engineered nanomaterials, QDs have the potential to be respiratory hazards, especially in the context of the manufacture of QDs and products containing them, as well as exposures to consumers using these products. The overall goal of this study was to investigate the role of mouse strain in determining susceptibility to QD-induced pulmonary inflammation and toxicity. Male mice from 8 genetically diverse inbred strains (the Collaborative Cross founder strains) were exposed to CdSe–ZnS core–shell QDs stabilized with an amphiphilic polymer. QD treatment resulted in significant increases in the percentage of neutrophils and levels of cytokines present in bronchoalveolar lavage fluid (BALF) obtained from NOD/ShiLtJ and NZO/HlLtJ mice relative to their saline (Sal) treated controls. Cadmium measurements in lung tissue indicated strain-dependent differences in disposition of QDs in the lung. Total glutathione levels in lung tissue were significantly correlated with percent neutrophils in BALF as well as with lung tissue Cd levels. Our findings indicate that QD-induced acute lung inflammation is mouse strain dependent, that it is heritable, and that the choice of mouse strain is an important consideration in planning QD toxicity studies. These data also suggest that formal genetic analyses using additional strains or recombinant inbred strains from these mice could be useful for discovering potential QD-induced inflammation susceptibility loci.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Susceptibility to quantum dot induced lung inflammation differs widely among the Collaborative Cross founder mouse strains

Scoville

White

Botta

et al. 2015

Toxicology and Applied Pharmacology

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“…Both aspects can be determined after a relatively short exposure period when including specific investigations of the animals. Meanwhile, more than 20 industrially relevant nanomaterials have been tested in the STIS, covering the 13 nanomaterials presented in this study, four carbon-based nanomaterials [34,35], two cadmium-based quantum dots [36,37], one polyacrylate [38], and one pigment [Ma-Hock and co-workers, unpublished observations]. In the following section, the experiences gained with all STIS conducted so far are assessed with the aim of re-evaluating the study design of the STIS and of determining its relevance in predicting nanomaterial effects that develop upon subchronic or chronic exposure.…”

Section: Discussionmentioning

confidence: 99%

Application of short-term inhalation studies to assess the inhalation toxicity of nanomaterials

et al. 2014

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BackgroundA standard short-term inhalation study (STIS) was applied for hazard assessment of 13 metal oxide nanomaterials and micron-scale zinc oxide.MethodsRats were exposed to test material aerosols (ranging from 0.5 to 50 mg/m3) for five consecutive days with 14- or 21-day post-exposure observation. Bronchoalveolar lavage fluid (BALF) and histopathological sections of the entire respiratory tract were examined. Pulmonary deposition and clearance and test material translocation into extra-pulmonary organs were assessed.ResultsInhaled nanomaterials were found in the lung, in alveolar macrophages, and in the draining lymph nodes. Polyacrylate-coated silica was also found in the spleen, and both zinc oxides elicited olfactory epithelium necrosis. None of the other nanomaterials was recorded in extra-pulmonary organs. Eight nanomaterials did not elicit pulmonary effects, and their no observed adverse effect concentrations (NOAECs) were at least 10 mg/m3. Five materials (coated nano-TiO2, both ZnO, both CeO2) evoked concentration-dependent transient pulmonary inflammation. Most effects were at least partially reversible during the post-exposure period.Based on the NOAECs that were derived from quantitative parameters, with BALF polymorphonuclear (PMN) neutrophil counts and total protein concentration being most sensitive, or from the severity of histopathological findings, the materials were ranked by increasing toxic potency into 3 grades: lower toxic potency: BaSO4; SiO2.acrylate (by local NOAEC); SiO2.PEG; SiO2.phosphate; SiO2.amino; nano-ZrO2; ZrO2.TODA; ZrO2.acrylate; medium toxic potency: SiO2.naked; higher toxic potency: coated nano-TiO2; nano-CeO2; Al-doped nano-CeO2; micron-scale ZnO; coated nano-ZnO (and SiO2.acrylate by systemic no observed effect concentration (NOEC)).ConclusionThe STIS revealed the type of effects of 13 nanomaterials, and micron-scale ZnO, information on their toxic potency, and the location and reversibility of effects. Assessment of lung burden and material translocation provided preliminary biokinetic information. Based upon the study results, the STIS protocol was re-assessed and preliminary suggestions regarding the grouping of nanomaterials for safety assessment were spelled out.

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“…24 hours after exposure to aPM 2.5 or filtered air. BALF was collected by slowly instilling and withdrawing 12 ml of cold saline into the left lung 3 times through tracheal intubation52. The BALF was centrifuged (1,500 rpm for 10 min).…”

Section: Methodsmentioning

confidence: 99%

Polydatin protects the respiratory system from PM2.5 exposure

Yan

Wang

Tie

et al. 2017

Sci Rep

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Atmospheric particle is one of the risk factors for respiratory disease; however, their injury mechanisms are poorly understood, and prevention methods are highly desirable. We constructed artificial PM2.5 (aPM2.5) particles according to the size and composition of actual PM2.5 collected in Beijing. Using these artificial particles, we created an inhalation-injury animal model. These aPM2.5 particles simulate the physical and chemical characteristics of the actual PM2.5, and inhalation of the aPM2.5 in rat results in a time-dependent change in lung suggesting a declined lung function, injury from oxidative stress and inflammation in lung. Thus, this aPM2.5-caused injury animal model may mimic that of the pulmonary injury in human exposed to airborne particles. In addition, polydatin (PD), a resveratrol glucoside that is rich in grapes and red wine, was found to significantly decrease the oxidative potential (OP) of aPM2.5 in vitro. Treating the model rats with PD prevented the lung function decline caused by aPM2.5, and reduced the level of oxidative damage in aPM2.5-exposed rats. Moreover, PD inhibited aPM2.5-induced inflammation response, as evidenced by downregulation of white blood cells in bronchoalveolar lavage fluid (BALF), inflammation-related lipids and proinflammation cytokines in lung. These results provide a practical means for self-protection against particulate air pollution.

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Short term inhalation toxicity of a liquid aerosol of glutaraldehyde-coated CdS/Cd(OH)2 core shell quantum dots in rats

Cited by 17 publications

References 23 publications

Susceptibility to quantum dot induced lung inflammation differs widely among the Collaborative Cross founder mouse strains

Susceptibility to quantum dot induced lung inflammation differs widely among the Collaborative Cross founder mouse strains

Application of short-term inhalation studies to assess the inhalation toxicity of nanomaterials

Polydatin protects the respiratory system from PM2.5 exposure

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