Comparative pulmonary toxicity assessment of single-wall carbon nanotubes in rats.

The aim of this study was to evaluate the acute lung toxicity of intratracheally instilled single-wall carbon nanotubes (SWCNT) in rats. The lungs of rats were instilled either with 1 or 5 mg/kg of the following control or particle types: (1) SWCNT, (2) quartz particles (positive control), (3) carbonyl iron particles (negative control), (4) phosphate-buffered saline (PBS) + 1% Tween 80, or (5) graphite particles (lung tissue studies only). Following exposures, the lungs of PBS and particle-exposed rats were assessed using bronchoalveolar lavage (BAL) fluid biomarkers and cell proliferation methods, and by histopathological evaluation of lung tissue at 24 h, 1 week, 1 month, and 3 months postinstillation. Exposures to high-dose (5 mg/kg) SWCNT produced mortality in ~15% of the SWCNT-instilled rats within 24 h postinstillation. This mortality resulted from mechanical blockage of the upper airways by the instillate and was not due to inherent pulmonary toxicity of the instilled SWCNT particulate. Exposures to quartz particles produced significant increases versus controls in pulmonary inflammation, cytotoxicity, and lung cell parenchymal cell proliferation indices. Exposures to SWCNT produced transient inflammatory and cell injury effects. Results from the lung histopathology component of the study indicated that pulmonary exposures to quartz particles (5 mg/kg) produced dose-dependent inflammatory responses, concomitant with foamy alveolar macrophage accumulation and lung tissue thickening at the sites of normal particle deposition. Pulmonary exposures to carbonyl iron or graphite particles produced no significant adverse effects. Pulmonary exposures to SWCNT in rats produced a non-dose-dependent series of multifocal granulomas, which were evidence of a foreign tissue body reaction and were nonuniform in distribution and not progressive beyond 1 month postexposure (pe). The observation of SWCNT-induced multifocal granulomas is inconsistent with the following: (1) lack of lung toxicity by assessing lavage parameters, (2) lack of lung toxicity by measuring cell proliferation parameters, (3) an apparent lack of a dose response relationship, (4) nonuniform distribution of lesions, (5) the paradigm of dust-related lung toxicity effects, (6) possible regression of effects over time. In addition, the results of two recent exposure assessment studies indicate very low aerosol SWCNT exposures at the workplace. Thus, the physiological relevance of these findings should ultimately be determined by conducting an inhalation toxicity study.

Penetration of hard substrates by a fungus employing enormous turgor pressures.

Many fungal pathogens penetrate plant leaves from a specialized cell called an appressorium. The rice blast pathogen Magnaporthe grisea can also penetrate synthetic surfaces such as poly(vinyl chloride). Previous experiments have suggested that penetration requires an elevated appressorial turgor pressure. In the present report we have used nonbiodegradable Mylar membranes, exhibiting a range of surface hardness, to test the proposition that penetration is driven by turgor. Reducing appressorial turgor by osmotic stress inhibited penetration of these membranes. The size of the turgor deficit required to inhibit penetration was a function of the surface hardness. Penetration of the hardest membranes was inhibited by small decreases in appressorial turgor, while penetration of the softer membranes was sensitive only to large decreases in turgor. Similarly, penetration of the host surface was inhibited in a manner comparable to penetration of the hardest Mylar membranes. Indirect measurements of turgor, obtained through osmotically induced collapse of appressoria, indicated that the infection apparatus can generate turgor pressures in excess of 8.0 MPa (80 bars). We conclude that penetration of synthetic membranes, and host epidermal cells, is accomplished by application of the physical force derived from appressorial turgor.