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Abstract Particulate matter (PM) pollution is responsible for hundreds of thousands of deaths worldwide, the majority due to cardiovascular disease (CVD). While many potential pathophysiological mechanisms have been proposed, there is not yet a consensus as to which are most important in causing pollution-related morbidity/mortality. Nor is there consensus regarding which specific types of PM are most likely to affect public health in this regard. One toxicological mechanism linking exposure to airborne PM with CVD outcomes is oxidative stress, a contributor to the development of CVD risk factors including atherosclerosis. Recent work suggests that accelerated shortening of telomeres and, thus, early senescence of cells may be an important pathway by which oxidative stress may accelerate biological aging and the resultant development of age-related morbidity. This pathway may explain a significant proportion of PM-related adverse health outcomes, since shortened telomeres accelerate the progression of many diseases. There is limited but consistent evidence that vehicular emissions produce oxidative stress in humans. Given that oxidative stress is associated with accelerated erosion of telomeres, and that shortened telomeres are linked with acceleration of biological ageing and greater incidence of various age-related pathology, including CVD, it is hypothesized that associations noted between certain pollution types and sources and oxidative stress may reflect a mechanism by which these pollutants result in CVD-related morbidity and mortality, namely accelerated aging via enhanced erosion of telomeres. This paper reviews the literature providing links among oxidative stress, accelerated erosion of telomeres, CVD, and specific sources and types of air pollutants. If certain PM species/sources might be responsible for adverse health outcomes via the proposed mechanism, perhaps the pathway to reducing mortality/morbidity from PM would become clearer. Not only would pollution reduction imperatives be more focused, but interventions which could reduce oxidative stress would become all the more important.

Provides a broad overview of the major natural removal mechanisms that occur in the environment, including chemical transformations, biological degradation, and physical processes. (Author/BB)

Robert F. Phalen Boston, MA: Kluwer Academic Publishers, 2002. 144 pp. ISBN: 1-4020-7225-2, $70.00 cloth. One of the more controversial issues in the field of air pollution concerns public health [...]

In 2012, the WHO classified diesel emissions as carcinogenic, and its European branch suggested creating a public health standard for airborne black carbon (BC). In 2011, EU researchers found that life expectancy could be extended four to nine times by reducing a unit of BC, vs reducing a unit of PM2.5.Only recently could such determinations be made. Steady improvements in research methodologies now enable such judgments. In this Critical Review, we survey epidemiological and toxicological literature regarding carbonaceous combustion emissions, as research methodologies improved over time. Initially, we focus on studies of BC, diesel, and traffic emissions in the Western countries (where daily urban BC emissions are mainly from diesels). We examine effects of other carbonaceous emissions, e.g., residential burning of biomass and coal without controls, mainly in developing countries. Throughout the 1990s, air pollution epidemiology studies rarely included species not routinely monitored. As additional PM2.5.chemical species, including carbonaceous species, became more widely available after 1999, they were gradually included in epidemiological studies. Pollutant species concentrations which more accurately reflected subject exposure also improved models. Natural “interventions” - reductions in emissions concurrent with fuel changes or increased combustion efficiency; introduction of ventilation in highway tunnels; implementation of electronic toll payment systems – demonstrated health benefits of reducing specific carbon emissions. Toxicology studies provided plausible biological mechanisms by which different PM species, e.g., carbonaceous species, may cause harm, aiding interpretation of epidemiological studies. Our review finds that BC from various sources appears to be causally involved in all-cause, lung cancer, and cardiovascular mortality, morbidity, and perhaps adverse birth and nervous system effects. We recommend that the U.S. EPA rubric for judging possible causality of PM2.5.mass concentrations, be used to assess which PM2.5.species are most harmful to public health. Implications:Black carbon (BC) and correlated co-emissions appear causally related with all-cause, cardiovascular, and lung cancer mortality, and perhaps with adverse birth outcomes and central nervous system effects. Such findings are recent, since widespread monitoring for BC is also recent. Helpful epidemiological advances (using many health relevant PM2.5 species in models; using better measurements of subject exposure) have also occurred. “Natural intervention” studies also demonstrate harm from partly combusted carbonaceous emissions. Toxicology studies consistently find biological mechanisms explaining how such emissions can cause these adverse outcomes. A consistent mechanism for judging causality for different PM2.5 species is suggested. A list of acronyms will be found at the end of the article. [ABSTRACT FROM AUTHOR]

Ambient air particulate matter (PM) originates as either primary particles emitted directly into the atmosphere from a specific source or as secondary particles produced from atmospheric chemical reactions between precursor gases or between these gases and primary particles. PM can derive from both natural and anthropogenic sources, resulting in a complex chemical mix. The "fine" size mode of ambient PM, designated as PM2.5, is defined as comprising those particles having aerodynamic diameters below 2.5 μm. While the total mass of PM2.5 has been associated with adverse human health outcomes, the relationship between these and specific chemical components has not been resolved. This article provides a perspective on the current state of the science concerning health effects from a major group of chemical species found within PM2.5, namely common inorganic constituents. The specific chemical classes discussed herein are secondary inorganic species, namely, sulfate, nitrate, and acidity, and generally crustal-derived species, namely, phosphate, sodium, potassium, calcium, magnesium, silicon, and aluminum. The article discusses evidence for adverse health effects from inorganic PM2.5 components within the framework of various caveats surrounding both epidemiology and toxicology assessments. The largest database exists for sulfate, but conclusions that attribute sulfate to health outcomes have not been consistent across all epidemiology studies, and there is a lack of coherence with toxicology studies, which show biological responses only at high levels of exposure. Limited epidemiological and toxicological data for nitrate suggests little or no adverse health effects at current levels. Epidemiological studies specifically identifying crustal components of PM2.5 suggest that they are not likely, by themselves, to produce a significant health risk, and these components do not have unequivocal biological plausibility from toxicological studies for being significant contributors to adverse health outcomes. [ABSTRACT FROM AUTHOR]

Researchers and regulators have often considered preferentially regulating the types of ambient airborne particulate matter (PM) most relevant to human health effects. While few would argue the inherent merits of such a policy, many believe there may not yet be enough information to differentially regulate PM species. New evidence, using increasingly sophisticated methodologies, has become available in the last several years, allowing more accurate assessment of exposure and resultant associations with specific types of PM, or PM derived from different sources. Such new studies may also allow differentiation of effects from different chemical components in the same study against the same health endpoints. This article considers whether this new evidence might be adequate to allow us to "speciate" PM types or sources by severity of health effects. We address this issue with respect to two widespread sources of PM, emissions from motor vehicles and coal-fired power plants. Emissions from less widespread sources, residual oil and steel/coking facilities, are also discussed in order to illustrate how health effects associated with such emissions might instead be associated with more widespread sources when accurate exposure information is unavailable. Based upon evaluation of studies and methodologies which appear to contain the most accurate information on exposure and response to important emissions, including variable local emissions, it is concluded that public health will likely be better protected by reduction of various vehicular emissions than by continued regulation of the total mass of fine PM (PM <2.5 μ m, or PM2.5) as if all PM in this mode is equitoxic. However, the knowledge base is incomplete. Important remaining research questions are identified. [ABSTRACT FROM AUTHOR]

Epidemiological studies of particulate matter (PM) using central area monitors have associated total PM mass, as well as certain individual components of PM, including sulfate, with adverse human health effects. However, some recent studies that used concentrated ambient particles (CAPs) or analyzed the effects of air pollution from different sources or geographic areas suggest that while some particles may be harmful, other particulate species including secondary sulfates may have negligible health effects. Toxicology studies to date also suggest that secondary sulfates pose little health risk. While studies using central-area monitors implicitly assume that all residents of the area are exposed to the same levels of pollution, newer studies find substantial health effects for those in close proximity to major roads. These latter studies recognize that although population exposure to widespread pollutants, such as total PM mass and sulfates, may be relatively uniform over a wide area, exposure to pollutants from local sources is not. While there is an emerging literature associating several adverse health effects with proximity to local pollution sources, the current database provides limited information that allows identification of specific particulate species that may cause little to no harm. In this article, we suggest that ambient secondary sulfates, and eastern North American regional air masses generally, appear to have little adverse impact on public health. This suggestion is based on evidence gleaned from eight avenues of investigation: (1) recent non-central-area monitor studies, including exposure gradient or proximity studies; (2) CAPs studies; (3) studies that examine effects related to different geographic areas or sources; (4) toxicology studies; (5) the limited number of studies that analyze existing central-area monitor data to explicitly examine the health impacts of sulfate and acidity versus PM mass; (6)“modern”area monitor studies with additional capabilities to distinguish among sources of pollution; (7) partial reinterpretation of two pivotal cohort studies; and (8) studies separating effects of secondary sulfates from those of primary metal sulfates. However, uncertainties remain regarding the role that secondary sulfates may play in ambient PM chemistry pathways leading to potentially harmful products, such as the possible effects of secondary organic aerosols that may be the product of acid catalysis of sulfur dioxide. Thus, more targeted study is needed, and some research suggestions are made in this regard. [ABSTRACT FROM AUTHOR]

Respiratory-tract infection, specifically pneumonia, contributes substantially to the increased morbidity and mortality among elderly individuals exposed to airborne particulate matter of < 10 µm diameter (PM[sub 10]). These epidemiological findings suggest that PM[sub 10] may act as an immunosuppressive factor that can undermine normal pulmonary antimicrobial defense mechanisms. To investigate whether, and how, compromised pulmonary immunocompetence might contribute to increased mortality, two sets of laboratory studies were performed. The first examined the effects of a single inhalation exposure to concentrated ambient PM[sub 2.5] (CAPS) from New York City air on pulmonary/systemic immunity and on the susceptibility of exposed aged rats to subsequent infection with Streptococcus pneumoniae. The second set of studies determined whether CAPS exposure, at a concentration approximating or somewhat greater than the promulgated 24-h NAAQS of 65 µg/m³, could exacerbate an ongoing infection. Taken together, results demonstrated that a single exposure of healthy animals to CAPS had little effect on pulmonary immune function or bacterial clearance during subsequent challenge with S. pneumoniae. Alternatively, CAPS exposure of previously infected rats significantly increased bacterial burdens and decreased percentages of lavageable neutrophils and proinflammatory cytokine levels compared to those in infected filtered-air-exposed controls. These studies demonstrate that a single exposure to ambient PM[sub 2.5] compromises a host's ability to handle ongoing pneumococcal infections and support the epidemiological findings of increased pneumonia-related deaths in ambient PM-exposed elderly individuals. [ABSTRACT FROM AUTHOR]

A health hazard to welders is development of lung cancer. It is believed that this is likely due, in part, to the presence in welding fumes of several hexavalent chromium (Cr[VI]) species, whose solubility depends primarily on which process (i.e., manual metal arc verus metal -- inert gas) is used. However, inhalation of Cr alone is uncommon in this setting. Thus, an examination of potential contributions from other coinhalants in creating or enhancing conditions whereby inhaled fume-associated Cr (primarily the insoluble forms) may initiate cancer is critical to increasing our understanding and preventing this particular occupational disease. One major chemical species formed and released during welding is ozone (O[SUB3]). Though implications of adverse pulmonary effects from individual exposure to Cr or O[SUB3] have been investigated, those from simultaneous exposure are unclear. To begin to address whether the carcinogenic potential of insoluble Cr[VI] agents might be enhanced in hosts inhaling mixtures of Cr and O[SUB3] versus Cr alone, analyses of total lung Cr burden, Cr retention in lung epithelium and interstitium, and potential shifts in lung cell distribution of Cr from the cytoplasm to nuclei were undertaken in F-344 rats exposed nose-only (5 h/d, 5 d/wk for up to 48 wk) to an extrapolated occupationally relevant level of Cr (360 μg Cr/m[SUP3] as calcium chromate) alone and in combination with 0.3 ppm O[SUB3]. Overall, there was only a nominal effect from O[SUB3] on Cr retention or on distribution of Cr particles among extracellular sites and within lung cells. However, there were O[SUB3]-related effects upon mechanisms for clearing the Cr from the deep lung, specifically at the levels of particle uptake and postphagocytic/endocytic processing by macrophages. This O[SUB3] exposure-related shift in normal pulmonary clearance might potentially increase the health risk in workers exposed to other insoluble or poorly soluble carcinogenic Cr compounds. [ABSTRACT FROM AUTHOR]

A major health hazard to coal miners is development of emphysema following long-term exposure to coal dust. One mechanism underlying development of emphysema is the oxidation of critical methionine (Met) residues in antiproteolytic factor, α1-antitrypsin (A1AT) resulting in a protease-antiprotease imbalance in the lung. Several studies have documented an association between the incidence and severity of emphysema among miners and their exposure to crystalline silica (i.e., SiO[sub 2]). However, what remains unclear is the role of other co-inhaled nonemphysematogenic nonoxidant inorganic constituent in disease pathogenesis. We hypothesize that in miners, inhaled trivalent chromium (Cr[sup 3+], the only form of Cr in coal) may potentially affect lung A1AT activity in situ via Cr complexing with Met residues, and thereby exacerbate any SiO[sub 2]-induced imbalance. To ascertain if Cr[sup 3+] could, in fact, affect A1AT activity, in vitro studies were done to assess elastase inhibitory activity following A1AT incubation with soluble Cr[sup 3+]. In addition, to determine if Cr[sup 3+] found in the lungs as detoxification products of inhaled hexavalent Cr (Cr[sup 6+]) could affect A1AT in situ, lavages from the lungs of chromate-exposed rats were also analyzed for elastase inhibitory activity. The in vitro results indicate that Cr[sup 3+] ions clearly inhibited A1AT function, with an IC50 of 1.1 mM being estimated under the experimental conditions used. The in vivo results indicate that long-term inhalation (12 wk or longer) of chromate-bearing atmospheres also gave rise to significant (i.e., 50–70%) inhibition of the antielastase activity of A1AT. Together, these results clearly suggest that the Cr[sup 3+] present in coal dusts could potentially act to inhibit A1AT activity in the lungs of miners and thereby promote the emphysematogenicity of SiO[sub 2] or of other emphysematogens present as coconstituents in these dusts. [ABSTRACT FROM AUTHOR]

In addition to developing nations relying almost exclusively upon biomass fuels, such as wood for cooking and home heating, North Americans, particularly in Canada and the northwestern and northeastern sections of the United States, have increasingly turned to woodburning as an alternate method for domestic heating because of increasing energy costs. As a result, the number of households using woodburning devices has increased dramatically. This has resulted in an increase in public exposure to indoor and outdoor woodsmoke-associated pollutants, which has prompted widespread concern about the adverse human health consequences that may be associated with prolonged woodsmoke exposure. This mini-review article brings together many of the human and animal studies performed over the last three decades in an attempt to better define the toxicological impact of inhaled woodsmoke on exposed children and adults; particular attention is given to effects upon the immune system. General information regarding occurrence and woodsmoke chemistry is provided so as to set the stage for a better understanding of the toxicological impact. It can be concluded from this review that exposure to woodsmoke, particularly for children, represents a potential health hazard. However, despite its widespread occurrence and apparent human health risks, relatively few studies have focused upon this particular area of research. More laboratory studies aimed at understanding the effects and underlying mechanisms of woodsmoke exposure, particularly on those individuals deemed to be at greatest risk, are badly needed, so that precise human health risks can be defined, appropriate regulatory standards can be set, and accurate decisions can be made concerning the use of current and new woodburning devices. [ABSTRACT FROM AUTHOR]

The goal of this study was to examine effects from repeated exposure to ozone (O[sub 3]) on immune cells involved in cell-mediated antibacterial responses in the lungs. Rats exposed to 0.1 or 0.3 ppm O[sub 3] for 4 h/day, 5 days/wk, for 1 or 3 wk were analyzed for the ability to clear an intrapulmonary challenge with Listeria monocytogenes or had their lungs processed to obtain pulmonary alveolar macrophages (PAM) and lung-associated lymphocytes for analyses of select cell functions and surface marker expression. The results indicate that repeated inhalation exposure to O[sub 3] affected local cell-mediated immunity (CMI) responses as evidenced by effects on clearance of Listeria. However, this modulation was not consistently dependent on exposure concentration or duration. Short-term repeat exposures had more effect on host resistance than did the more prolonged regimen, with rats exposed to 0.1 ppm O[sub 3] most adversely impacted. Clearance patterns suggest modifications in innate resistance following 1 wk of exposure to 0.1 ppm O[sub 3], but no similar effect following a 3-wk regimen. Exposure to 0.3 ppm O[sub 3] appeared to affect both innate and acquired resistance after a 1-wk regimen, but mainly the former after an additional 2 wk of exposure. We conclude that these two mechanisms of resistance are differentially affected by O[sub 3] and that distinct time- and O[sub 3] concentration-dependent adaptation phenomena evolve for each; that is, in situ adaptation to higher levels of O[sub 3] may occur more readily with acquired than with innate/PAM-dependent resistance. A similar pattern of inconsistent effect on PAM and lung-associated lymphocytes was also evident. For example, while 3-wk exposures had a greater effect on PAM reactive oxygen intermediate ROI production, evidence for a significant effect on antibacterial activity was only notable among PAM from rats exposed for 1 wk. Among lung lymphocytes, while 3-wk exposure to 0.1 ppm O[sub 3] led to a significant increase in CD25 expression, there was no corresponding increase in responsivity to concanavalin A (ConA); only among cells from 1-wk-exposed rats did lymphoproliferative responses increase. Though investigations of altered immune cell cytokine receptor expression/binding activity are ongoing, results herein provide further evidence to support our longstanding hypothesis that some well-documented effects of O[sub 3] exposure on human health are quite likely linked to changes in local immune cell (i.e., PAM and lung-associated lymphocytes) functions, with the latter being related to changes in the capacities of these cells to interact with immunoregulatory cytokines. [ABSTRACT FROM AUTHOR]

While acute exposures to ozone (O[sub 3]) can alter airway responsiveness, effects from long-term exposures at low concentrations are less clear. This study assessed whether such exposures could induce nonspecific hyperresponsiveness in nonatopic (nonsensitized) guinea pigs and/or could exacerbate the pre-existing hyperresponsive state in atopic (sensitized) animals, and whether gender was a factor modulating any effect of O[sub 3]. Responsiveness was measured during and following exposures to 0.1 and 0.3 ppm O[sub 3] for 4 h/day, 4 days/wk for 24 wk in male and female nonsensitized animals, those sensitized to allergen (ovalbumin) prior to initiation of O[sub 3] exposures, and those sensitized concurrently with exposures. Ozone did not produce hyperresponsiveness in nonsensitized animals, but did exacerbate hyperresponsiveness to both specific and nonspecific bronchoprovocation challenges in sensitized animals, an effect that persisted through at least 4 wk after exposures ended. Gender was not a factor modulating response to O[sub 3]. Induced effects on responsiveness were not associated with numbers of eosinophils in the lungs nor with any chronic pulmonary inflammatory response, but were correlated with antigen-specific antibodies in blood. This study supports a role for chronic O[sub 3] exposure in the exacerbation of airways dysfunction in a certain segment of the general population, namely, those demonstrating atopy. [ABSTRACT FROM AUTHOR]

Significant respiratory-tract exposure to insoluble aluminum compounds, such as alumina (aluminum oxide, Al2O3), can occur in occupational settings, yet little is known about the temporal pattern of pulmonary clearance of these materials from the lungs with repeated exposures, and potential subsequent translocation to other organs. This study evaluated the clearance pattern of alumina from the lungs of rats, and burdens in selected extrapulmonary organs (brain, bone, liver, spleen, kidney). Rats were instilled with alumina once weekly for 20 wk. Quantification of retention was performed by measuring aluminum burdens in the lungs and extrapulmonary organs during the exposure period, and then weekly for an additional 19 wk after the exposures ended. Lung burdens of aluminum were found to steadily increase during exposure. Clearance of the material following the end of the exposure regime was extremely slow; only approximately 9% of the amount in the lungs following the 20 weekly exposures was cleared by the end of the postexposure period. This study supports the concept of gradual accumulation and long-term retention of aluminum within the respiratory tract of individuals repeatedly exposed to alumina in occupational settings. [ABSTRACT FROM AUTHOR]

The evaluation of respiratory tract toxicity from airborne materials frequently involves exposure of animals via inhalation. This provides a natural route of entry into the host and, as such, is the preferred method for the introduction of toxicants into the lungs. However, for various reasons, this technique cannot always be used, and the direct instillation of a test material into the lungs via the trachea has been employed in many studies as an alternative exposure procedure. Intratracheal instillation has become sufficiently widely used that the Inhalation Specialty Section of the Society of Toxicology elected to develop this document to summarize some key issues concerning the use of this exposure procedure. Although there are distinct differences in the distribution, clearance, and retention of materials when administered by instillation compared to inhalation, the former can be a useful and cost-effective procedure for addressing specific questions regarding the respiratory toxicity of chemicals, as long as certain caveats are clearly understood and certain guidelines are carefully followed. [ABSTRACT FROM PUBLISHER]

Clearance mechanisms remove inhaled deposited particles from the lungs, by mucociliary transport in conducting airways and to a large extent by alveolar macrophages in the respiratory region. This paper describes the effects of acute exposures to sulphuric acid (H2SO4), nitrogen dioxide (NO2), or ozone (O3) on particle clearance in rabbits. Cells recovered by bronchopulmonary lavage from animals exposed in vivo were also examined. [ABSTRACT FROM PUBLISHER]

Particle deposition patterns were measured in the first five branching generations of replicate hollow casts made from a solid cast of a human tracheobronchial tree. The casts were exposed to radioactively tagged aerosols, having MMADs of approx. 3 and 8 μm, under a series of constant and cyclic inspiratory flow patterns having equivalent mean flow rates. Deposition efficiencies at bifurcation and length subregions of each generation were greater under cyclic flow and these differences were greater for the smaller sized aerosol. [ABSTRACT FROM PUBLISHER]

Male Fisher 344 rats were exposed to 2 mg vanadium(V)/m3 (as ammonium metavanadate NH4VO3, 0.32 μm MMD) atmospheres for 8 hr/day for 4 days in a nose-only exposure system. In exposed rats, lung V burdens increased in a time-dependent fashion. Analysis of lung cells and lavage fluid 24 hr after the final exposure suggested that tissue damage and a strong inflammatory response was elicited; numbers of neutrophil and small macrophages (Mø), as well as levels of lavageable protein and lactate dehydrogenase, were significantly elevated as compared with levels observed with air-exposed rats. Vanadium also affected pulmonary alveolar Mø (PAM) capacities to produce and respond to immunoregulating cytokines. Inducible PAM production of tumor necrosis factor-a was significantly inhibited, as was the ability to increase cell surface Class II/I-A molecule expression in response to interferon-γ (rFN-γ). PAM from V-exposed hosts were also inhibited in their ability to be primed by EFN-γ to produce superoride anion and hydrogen peroxide in response to stimulation with opsonized zy-mosan. These studies indicate that short-term repeated exposure of rats to atmospheric V, at levels encountered in an occupational setting, can alter host pulmonary immunomocompetence, with one major effect occurring at the level of cytokine-related functions. These alterations may be underlying mechanisms for the well-documented increases in bronchopulmonary infections and cancers in workers chronically exposed to V-containing atmospheres. [ABSTRACT FROM AUTHOR]

While ambient acid aerosols are considered a potential respiratory health hazard, the mechanism by which they induce responses in the lungs is not known. Attempts to ascertain these mechanisms using inhalation exposures are complicated by a number of technical difficulties, chief among which are neutralization of inhaled acids by endogenous ammonia and variations in deposition with inhaled particle size. To control for these variables, a novel exposure system allowing experimental evaluation of factors which influence biologic responses to acid sulfate particles was developed. The system consists of two subunits, a generation/delivery component and a cell exposure component. Sulfuric acid aerosols are generated by nebulizing dilute acid solutions. Particles larger than a specified size of interest (based upon the specific exposure conditions desired) are removed, and particles at the desired size and mass concentration are uniformly delivered onto a target cell monolayer. The system is capable of delivering acid particles larger than 0.7 μm (mass median diameter), yet at constant particle mass concentrations. This paper describes the design of the exposure system and its performance characteristics and presents initial results of some biological responses obtained using it. In conjunction with inhalation studies, this exposure system may provide additional insights into mechanisms by which acid aerosols adversely affect the respiratory tract and into the physical characteristics of acid particles which modulate toxicity. [ABSTRACT FROM PUBLISHER]

Examining interspecies differences in response to ambient pollutants is an essential component of risk assessment. The potential hazard to public health from the inhalation of acid sulfate aerosols is of current concern. A significant biological target is the pulmonary macrophage, which provides a primary defense of the respiratory region of the lungs. One essential function of these cells is phagocytosis of particles. This study assessed the effects of acidic environments on the phagocytic activity of pulmonary macrophages obtained by lavage from humans and three species of laboratory animals commonly used in acid aerosol toxicology studies, namely, rats, rabbits, and guinea pigs. Cells were incubated with polystyrene latex particles in media acidified by addition of sulfuric acid. The percentage of cells which were phagocytic, as well as the relative number of particles ingested by these cells, was found to decrease with increasing acidity for all species. The ranking of response in order of decreasing sensitivity to acidic challenge was as follows: guinea pig>rat>rabbit>human. [ABSTRACT FROM PUBLISHER]

A symposium entitled, Health Effects of Atmospheric Acid Aerosols: A Model Problem in Inhalation Toxicology and Air Pollution Risk Assessment, was held at the 30th Annual Meeting of the Society of Toxicology (SOT) in Dallas, Texas. The symposium was sponsored by the Inhalation Toxicology Specialty Section of SOT, and was organized to integrate evidence from various disciplines concerning health effects from acid aerosols in ambient air. [ABSTRACT FROM PUBLISHER]