JoAnn S. Lighty

Bio: JoAnn S. Lighty is an academic researcher from University of Utah. The author has contributed to research in topics: Chemical looping combustion & Combustion. The author has an hindex of 30, co-authored 119 publications receiving 3501 citations. Previous affiliations of JoAnn S. Lighty include Boise State University & Utah State University.

Combustion aerosols: factors governing their size and composition and implications to human health.

Abstract: Particulate matter (PM) emissions from stationary combustion sources burning coal, fuel oil, biomass, and waste, and PM from internal combustion (IC) engines burning gasoline and diesel, are a significant source of primary particles smaller than 2.5 μm (PM2.5) in urban areas. Combustion-generated particles are generally smaller than geologically produced dust and have unique chemical composition and morphology. The fundamental processes affecting formation of combustion PM and the emission characteristics of important applications are reviewed. Particles containing transition metals, ultrafine particles, and soot are emphasized because these types of particles have been studied extensively, and their emissions are controlled by the fuel composition and the oxidant-tem-perature-mixing history from the flame to the stack. There is a need for better integration of the combustion, air pollution control, atmospheric chemistry, and inhalation health research communities. Epidemiology has demonstrated t...

Phase and size distribution of polycyclic aromatic hydrocarbons in diesel and gasoline vehicle emissions.

Abstract: Emission measurements were obtained for a variety of military vehicles at Hill Air Force Base (Ogden, UT) in November 2000 as part of a Strategic Environmental Research and Development Program. Aircraft ground support equipment vehicles using gasoline, diesel, and JP8 fuels were tested using chassis dynamometers under predetermined load. The exhaust from the tested vehicle was passed to a dilution tunnel where it was diluted 30-40 times and collected using Micro-Orifice Uniform Deposit Impactor (MOUDI) fitted with aluminum substrates, an XAD-coated annular denuder, and a filter followed by a solid adsorbent. All MOUDI substrates were analyzed for mass and for organic and elemental (EC) carbon by the thermal/optical reflectance method and for polycyclic aromatic hydrocarbons (PAHs) by GC/MS. Black carbon was measured with a photoacoustic instrument. The denuder and filter/solid adsorbent samples were analyzed for semivolatile PAH. Overall, there is more mass and higher EC contribution when the vehicle is run under higher load in comparison with the low load. However, older vehicles generally show more mass and EC emissions than newer vehicles, and there is a shift toward smaller particle sizes for the low load, which is most pronounced for newer vehicles. The particle-associated semivolatile PAHs and nonvolatile four-through six-ring PAHs are present predominantly on the submicron particles collected on MOUDI stages 0.1-0.18, 0.18-0.32, and 0.32-0.56 microm. For the low-load runs, the distribution of PAHs seems to be shifted toward smaller size particles. The gas-particle phase distribution of semivolatile PAHs depends also on the engine loading. For idle, not only are the more volatile two- and three-ring PAHs, from naphthalene to dimethylphenanthrenes, retained on the denuder portion, but also less volatile four-ring PAHs, such as fluoranthene and pyrene, are retained by the denuder at the 80-90% range, which implies that they are present predominantly in the gas phase. In contrast, for engines under high loads, a much larger portion of three- and four-ring PAHs are partitioned to the particle phase.

Particle characteristics responsible for effects on human lung epithelial cells.

Abstract: Some recent epidemiologic investigations have shown an association between increased incidence of respiratory symptoms and exposure to low levels of particulate matter (PM*) less than 10 microm or less than 2.5 microm in aerodynamic diameter (PM10 and PM2.5, respectively). If particulates are causally involved with respiratory symptoms, it is important to understand which components may be responsible. However, increasing evidence suggests that transition metals present in particles, especially iron, generate reactive oxygen species (ROS) that may be involved in producing some of the observed respiratory symptoms. The hypothesis for this study is twofold: bioavailable transition metals from inhaled airborne particulates catalyze redox reactions in human lung epithelial cells, leading to oxidative stress and increased production of mediators of pulmonary inflammation: and the size, transition metal content, and mineral speciation of particulates affect their ability to cause these effects. This work focused on the relation between physical characteristics of particles (eg, size, bioavailable transition metal content, and mineral speciation) and their ability to generate hydroxyl radicals in cell-free systems and to cause oxidative stress, which results in the synthesis of mediators of pulmonary inflammation in cultured human lung epithelial cells. These relations were studied by comparing size-fractionated, chemically characterized coal fly ash (CFA) produced by combustion of three different coals to obtain milligram quantities of ash. One transition metal, iron, was studied specifically because it is by far the predominant transition metal in CFA. In addition, smaller quantities of particles from gasoline engines, diesel engines, and ambient air were studied. Phosphate buffer soluble fractions from particles from all sources were capable of generating ROS, as measured by production of malondialdehyde (MDA) from 2-deoxyribose. This activity was inhibited over 90% for all particles by the metal chelator N-[5-[3-[(5-aminopentyl)hydroxycarbamoyl]propionamidol-pentyl]-3-[[5-(N-hydroxyacetamido)pentyl]carbamoyl]propionohydroxamic acid (desferrioxamine B, or DF), strongly suggesting that transition metal(s), probably iron, were responsible. Particles from coal or gasoline combustion had greater ability to produce ROS than particles from diesel combustion. Iron was mobilized by citrate (at pH 7.5) from particles of all sources tested; gasoline combustion particles were the only particles not analyzed for iron mobilization because there were not enough particles for the iron mobilization assay. CFA particles were size-fractioned; the amount of iron mobilized by citrate was inversely related to the size of particles and also depended on the source of coal. Iron from the CFA particles was responsible for inducing the iron-storage protein ferritin in cultured human lung epithelial cells (A549 cells). The amount of iron mobilized by citrate was directly proportional to the amount of ferritin induced in the A549 cells. Iron from the CFA was also responsible for inducing the inflammatory mediator interleukin (IL) 8 in A549 cells. Iron existed in several species in the fly ash, but the bioavailable iron was associated with the glassy aluminosilicate fraction, which caused ferritin and IL-8 to be induced in the A549 cells. In crustal dust, another component of urban particulates, iron was associated with oxides and clay but not with aluminosilicates. The crustal dust contained almost no iron that could be mobilized by citrate. Iron could be mobilized from diesel combustion particulates, but at a much lower level than for all other combustion particles. Samples of ambient PM2.5 collected in Salt Lake City over 5-day periods during one month varied widely in the amount of iron that could be mobilized. If bioavailable transition metals (eg, iron) are related to the specific biological responses outlined here, then the potential exists to develop in vitro assays to determine whether particulates of unknown composition and origin can cause effects similar to those observed in this study.

Interleukin-8 levels in human lung epithelial cells are increased in response to coal fly ash and vary with the bioavailability of iron, as a function of particle size and source of coal.

Abstract: Particulate air pollution contains iron, and some of the pathological effects after inhalation may be due to radical species produced by iron-catalyzed reactions. We tested the hypothesis that iron present in coal fly ash (CFA) could induce the expression and synthesis of the inflammatory cytokine interleukin-8 (IL-8). CFA, containing as much as 14% iron, was used as a model combustion source particle. Three coal types were used to generate three size fractions enriched in particles [submicron ( 10 micrometer. Treatment of human lung epithelial (A549) cells for 4 h with CFA from Utah enriched in <1 micrometer particles (20 microgram/cm(2)) resulted in a 2.6-fold increase in mRNA levels for IL-8. IL-8 levels were increased in the medium by as much as 8-fold when cells were treated with the fraction enriched in the smallest size Utah CFA for 24 h. IL-8 production was completely inhibited when the CFA was pretreated with the metal chelator desferrioxamine B, suggesting that a transition metal was responsible for the induction, probably iron. Treatment with a soluble form of iron, ferric ammonium citrate (FAC), mimicked the IL-8 level increase observed with CFA. There was a direct relationship, above a threshold level of bioavailable iron, between the levels of IL-8 and bioavailable iron in A549 cells treated with CFA or FAC. Further, the relationship between IL-8 and bioavailable iron for CFA was indistinguishable from that for FAC. These results strongly suggest that iron can induce IL-8 in A549 cells and that iron was the likely component of CFA that induced IL-8. CFA-induced IL-8 production was inhibited by tetramethylthiourea or dimethyl sulfoxide, suggesting that radical species were involved in the induction. These results demonstrate that iron present in CFA may be responsible for production and release of inflammatory mediators by the lung epithelium through generation of radical species and suggest that iron may contribute to the exacerbation of respiratory problems by particulate air pollution.

Health effects of fine particulate air pollution: lines that connect

Abstract: Efforts to understand and mitigate the health effects of particulate matter (PM) air pollution have a rich and interesting history. This review focuses on six substantial lines of research that have been pursued since 1997 that have helped elucidate our understanding about the effects of PM on human health. There has been substantial progress in the evaluation of PM health effects at different time-scales of exposure and in the exploration of the shape of the concentration-response function. There has also been emerging evidence of PM-related cardiovascular health effects and growing knowledge regarding interconnected general pathophysiological pathways that link PM exposure with cardiopulmonary morbidity and mortality. Despite important gaps in scientific knowledge and continued reasons for some skepticism, a comprehensive evaluation of the research findings provides persuasive evidence that exposure to fine particulate air pollution has adverse effects on cardiopulmonary health. Although much of this research has been motivated by environmental public health policy, these results have important scientific, medical, and public health implications that are broader than debates over legally mandated air quality standards.

Nanomaterials and nanoparticles: Sources and toxicity

Abstract: This review is written with the goal of informing public health concerns related to nanoscience, while raising awareness of nanomaterials toxicity among scientists and manufacturers handling them. We show that humans have always been exposed to nanoparticles and dust from natural sources and human activities, the recent development of industry and combustion-based engine transportation profoundly increasing anthropogenic nanoparticulate pollution. The key to understanding the toxicity of nanoparticles is that their minute size, smaller than cells and cellular organelles, allows them to penetrate these basic biological structures, disrupting their normal function. Among diseases associated with nanoparticles are asthma, bronchitis, lung cancer, neurodegenerative diseases (such as Parkinson`s and Alzheimer`s diseases), Crohn`s disease, colon cancer. Nanoparticles that enter the circulatory system are related to occurrence of arteriosclerosis, and blood clots, arrhythmia, heart diseases, and ultimately cardiac death. We show that possible adverse effects of nanoparticles on human health depend on individual factors such as genetics and existing disease, as well as exposure, and nanoparticle chemistry, size, shape, and agglomeration state. The faster we will understand their causes and mechanisms, the more likely we are to find cures for diseases associated with nanoparticle exposure. We foresee a future with better-informed, and hopefully more cautious manipulation of engineered nanomaterials, as well as the development of laws and policies for safely managing all aspects of nanomaterial manufacturing, industrial and commercial use, and recycling.

Nanomaterials and nanoparticles: Sources and toxicity

Abstract: This review is presented as a common foundation for scientists interested in nanoparticles, their origin, activity, and biological toxicity. It is written with the goal of rationalizing and informing public health concerns related to this sometimes-strange new science of “nano,” while raising awareness of nanomaterials’ toxicity among scientists and manufacturers handling them. We show that humans have always been exposed to tiny particles via dust storms, volcanic ash, and other natural processes, and that our bodily systems are well adapted to protect us from these potentially harmful intruders. The reticuloendothelial system, in particular, actively neutralizes and eliminates foreign matter in the body, including viruses and nonbiological particles. Particles originating from human activities have existed for millennia, e.g., smoke from combustion and lint from garments, but the recent development of industry and combustion-based engine transportation has profoundly increased anthropogenic particulate pollution. Significantly, technological advancement has also changed the character of particulate pollution, increasing the proportion of nanometer-sized particles-“nanoparticles”-and expanding the variety of chemical compositions. Recent epidemiological studies have shown a strong correlation between particulate air pollution levels, respiratory and cardiovascular diseases, various cancers, and mortality. Adverse effects of nanoparticles on human health depend on individual factors such as genetics and existing disease, as well as exposure, and nanoparticle chemistry, size, shape, agglomeration state, and electromagnetic properties. Animal and human studies show that inhaled nanoparticles are less efficiently removed than larger particles by the macrophage clearance mechanisms in the lungs, causing lung damage, and that nanoparticles can translocate through the circulatory, lymphatic, and nervous systems to many tissues and organs, including the brain. The key to understanding the toxicity of nanoparticles is that their minute size, smaller than cells and cellular organelles, allows them to penetrate these basic biological structures, disrupting their normal function. Examples of toxic effects include tissue inflammation, and altered cellular redox balance toward oxidation, causing abnormal function or cell death. The manipulation of matter at the scale of atoms, “nanotechnology,” is creating many new materials with characteristics not always easily predicted from current knowledge. Within the nearly limitless diversity of these materials, some happen to be toxic to biological systems, others are relatively benign, while others confer health benefits. Some of these materials have desirable characteristics for industrial applications, as nanostructured materials often exhibit beneficial properties, from UV absorbance in sunscreen to oil-less lubrication of motors. A rational science-based approach is needed to minimize harm caused by these materials, while supporting continued study and appropriate industrial development. As current knowledge of the toxicology of “bulk” materials may not suffice in reliably predicting toxic forms of nanoparticles, ongoing and expanded study of “nanotoxicity” will be necessary. For nanotechnologies with clearly associated health risks, intelligent design of materials and devices is needed to derive the benefits of these new technologies while limiting adverse health impacts. Human exposure to toxic nanoparticles can be reduced through identifying creation-exposure pathways of toxins, a study that may someday soon unravel the mysteries of diseases such as Parkinson’s and Alzheimer’s. Reduction in fossil fuel combustion would have a large impact on global human exposure to nanoparticles, as would limiting deforestation and desertification. While nanotoxicity is a relatively new concept to science, this review reveals the result of life’s long history of evolution in the presence of nanoparticles, and how the human body, in particular, has adapted to defend itself against nanoparticulate intruders.

Handbook of Chemistry and Physics

Abstract: There is a special reason for reviewing this book at this time: it is the 50th edition of a compendium that is known and used frequently in most chemical and physical laboratories in many parts of the world. Surely, a publication that has been published for 56 years, withstanding the vagaries of science in this century, must have had something to offer. There is another reason: while the book is a standard fixture in most chemical and physical laboratories, including those in medical centers, it is not as frequently seen in the laboratories of physician's offices (those either in solo or group practice). I believe that the Handbook can be useful in those laboratories. One of the reasons, among others, is that the various basic items of information it offers may be helpful in new tests, either physical or chemical, which are continuously being published. The basic information may relate

A technology-based global inventory of black and organic carbon emissions from combustion

Abstract: [1] We present a global tabulation of black carbon (BC) and primary organic carbon (OC) particles emitted from combustion. We include emissions from fossil fuels, biofuels, open biomass burning, and burning of urban waste. Previous ‘‘bottom-up’’ inventories of black and organic carbon have assigned emission factors on the basis of fuel type and economic sector alone. Because emission rates are highly dependent on combustion practice, we consider combinations of fuel, combustion type, and emission controls and their prevalence on a regional basis. Central estimates of global annual emissions are 8.0 Tg for black carbon and 33.9 Tg for organic carbon. These estimates are lower than previously published estimates by 25–35%. The present inventory is based on 1996 fuel-use data, updating previous estimates that have relied on consumption data from 1984. An offset between decreased emission factors and increased energy use since the base year of the previous inventory prevents the difference between this work and previous inventories from being greater. The contributions of fossil fuel, biofuel, and open burning are estimated as 38%, 20%, and 42%, respectively, for BC, and 7%, 19%, and 74%, respectively, for OC. We present a bottom-up estimate of uncertainties in source strength by combining uncertainties in particulate matter emission factors, emission characterization, and fuel use. The total uncertainties are about a factor of 2, with uncertainty ranges of 4.3–22 Tg/yr for BC and 17–77 Tg/yr for OC. Low-technology combustion contributes greatly to both the emissions and the uncertainties. Advances in emission characterization for small residential, industrial, and mobile sources and topdown analysis combining field measurements and transport modeling with iterative inventory development will be required to reduce the uncertainties further. INDEX TERMS: 0305 Atmospheric Composition and Structure: Aerosols and particles (0345, 4801); 0322 Atmospheric Composition and Structure: Constituent sources and sinks; 0345 Atmospheric Composition and Structure: Pollution—urban and regional (0305); 0360 Atmospheric Composition and Structure: Transmission and scattering of radiation; 0365 Atmospheric Composition and Structure: Troposphere—composition and chemistry; KEYWORDS: emission, black carbon, organic carbon, fossil fuel, biofuel, biomass burning