The emergence of engineered nanoscale materials has provided significant advancements in electronic, biomedical, and material science applications. Both engineered nanoparticles and nanoparticles derived from combustion or incidental processes exhibit a range of physical and chemical properties, which have been shown to induce inflammation and oxidative stress in biologic systems. Oxidative stress reflects the imbalance between the generation of reaction oxygen species (ROS) and the biochemical mechanisms to detoxify and repair resulting damage of reactive intermediates. This review examines current research incidental and engineered nanoparticles in terms of their health effects on the lungs and mechanisms by which oxidative stress via physicochemical characteristics influence toxicity or biocompatibility. Although oxidative stress has generally been thought of as an adverse biological outcome, this review will also briefly discuss some of the potential emerging technologies to use nanoparticle-induced oxidative stress to treat disease in a site specific fashion.

Ambient particulate matter (PM) originates from a range of sources and differs in composition with respect to season, time of day, and particle size. In this study, ambient PM samples in the ultrafine and submicrometer fine range were tested for the potential to exacerbate a murine model of allergic airway inflammation when exposure occurs solely during allergic sensitization, but not during subsequent allergen challenge. Temporally resolved and size-segregated PM samples were used to understand how summer or winter, day or night, and ambient ultrafine and submicrometer fine particle size influence PM's ability to exacerbate allergic inflammation. PM was collected in urban Fresno, CA. BALB/c mice were exposed to PM and house dust mite allergen (HDM) via intranasal aspiration on d 1, 3, and 5. HDM challenge occurred on d 12-14, with inflammation assessed 24 h following final challenge. While season or particle size did not predict allergic inflammation, daytime ultrafine and submicrometer fine particles significantly increased total cellular inflammation, specifically lymphocyte and eosinophil infiltration, compared to allergic controls. Further studies examined PM-mediated changes within the lung during the period where allergen sensitization occurred by measuring direct effects of PM on pulmonary oxidative stress and inflammation. Pulmonary levels of heme oxygenase-1 (HO-1), a biomarker of oxidative stress, but not cellular inflammation, demonstrated a remarkable correlation with the degree of allergic inflammation in animals sensitized to allergen and PM concomitantly, suggesting acute PM-mediated HO-1 levels may serve as a predictive indicator of a particle's ability to exacerbate allergic airway inflammation.

Increasingly, evidence suggests a role for a systemic procoagulant state in the pathogenesis of cardiac dysfunction subsequent to inhalation of airborne particulate matter. The authors evaluated blood cell parameters and markers of platelet activation in mice exposed to concentrated ambient particulate matter (CAPs) from the San Joaquin Valley of California, a region with severe particulate matter (PM) pollution episodes. The authors exposed mice to an average of 88.5 microg/m(3) of CAPs in a size range less than 2.5 microm for 6 h/day for 5 days per week for 2 weeks. Platelets were analyzed by flow cytometry for relative size, shape, aggregation, fibrinogen binding, P-selectin, and lysosomal-associated membrane protein-1 (LAMP-1) expression. Serum cytokines were analyzed by bead-based immunologic assays. CAPs-exposed mice had elevations in macrophage inflammatory protein (MIP)-1 alpha, MIP-1 beta, interleukin (IL)-6, IL-10, tumor necrosis factor alpha (TNFalpha), macrophage colony-stimulating factor (M-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), platelet-derived growth factor (PDGF)-bb, and RANTES (regulated upon activation, normally T-expressed, and presumably secreted). Platelets were the only peripheral blood cells that were significantly elevated in number in CAPs-exposed mice. Flow cytometric analysis of unstimulated platelets from CAPs-exposed mice indicated size and shape changes, and platelets from CAPs-exposed animals had a 54% increase in fibrinogen binding indicative of platelet priming. Stimulation of platelets by thrombin resulted in up-regulation of LAMP-1 expression in CAPs-exposed animals and an increased microparticle population relative to control animals. These findings demonstrate a systemic proinflammatory and procoagulant response to inhalation of environmentally derived fine and ultrafine PM and suggests a role for platelet activation in the cardiovascular and respiratory effects of particulate air pollution.

The EPA regulates ambient particulate matter (PM) because substantial associations have been established between PM and health impacts. Presently, regulatory compliance involves broad control of PM emission sources based on mass concentration rather than chemical composition, although PM toxicity is likely to vary depending upon PM physicochemical properties. The overall objective of this study was to help inform source-specific PM emission control regulations. For the first time, source-oriented PM was collected from the atmosphere in Fresno, CA, onto 38 source/size substrates. Mice were exposed via oropharyngeal aspiration to equivalent mass doses [50 μg] of two size fractions: ultrafine (Dp < 0.17μm) and submicron fine (0.17 < Dp < 1 μm) during summer and winter seasons. At 24 hours post-exposure, cellular and biochemical indicators of pulmonary inflammation were evaluated in the bronchoalveolar lavage fluid. Significant inflammatory responses were elicited by vehicle, regional background, and cooking PM sources that were dependent on season and particle size. This is the first study of source-oriented toxicity of atmospheric PM and supports source-specific emissions control strategies.

) and the number of farmworkers is estimated to be between 175,000 to 500,000.While the San Joaquin Valley is one of the world's most productive agricultural regions, it is also frequently in violation of U.S. ambient air-quality concentration standards, particularly those for atmospheric particulate matter (PM) (Velasco 2005), which is defined as liquid or solid material such as soil dust or smoke suspended in the air. Particulate levels for the South Coast Air Basin and the Central Valley in California are the highest recorded in the country, exceeding the national ambient air-quality standards for each season of the year. Workers and residents of the San Joaquin Valley are exposed to airborne particulate matter from a broad range of sources including farming practices such as the tilling of dry soil, agricultural burning, crop harvesting and diesel-powered water pumping. Particle emissions include inorganic compounds from soil lofted by, for example, dairy operations and off-road vehicles, or organic matter from animal feed and disturbed, dried manure.The three parameters -size, composition and distribution -for each classification of particles are sufficiently different that each can produce unique health outcomes following inhalation. Epidemiological studies have shown a strong correlation between the exposure of human populations to particulate matter and acute and chronic health effects, including increased deaths due to cardiovascular illness and emergency room visits related to the severity of asthma symptoms (Sheppard same levels of light brown apple moth control as obtained in New Zealand. Many fruit crops in California already receive control measures for native and introduced leafrollers, and these tactics may prove to be effective for light brown apple moth without a great deal of modification.If the New Zealand experience is any indication, adequate control of this leafroller can be achieved more effectively through a vigorous program of biological control and the use of selective insecticides for other pest species. That approach identified a need to introduce natural enemies to attack light brown apple moth through all stages of development. The focus on introductions to address parasitism gaps, especially those targeting the late larval and pupal stages, proved to be highly effective. Further exploration of natural enemies in New Zealand may yield guidance for possible parasitoid importations to North America.As New Zealand has already found, it is unlikely that any one parasitoid will be so specific that it attacks only light brown apple moth. Therefore, any introduction of natural enemies into California must be preceded by a careful cost-benefit analysis. Light brown apple moth is a polyphagous insect, feeding on many plant species, and some native leafrollers may occupy the same niche. The benefit of suppressing populations of light brown apple moth and allowing reduced use of insecticide must outweigh possible adverse impacts on populations of endemic moths and natural enemies. This is an ...