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With more than 4,000 individual PFAS compounds present in a variety of industrial or consumer products, we are at stage where our ability to measure these compounds far exceeds our understanding of the potential health impacts and our ability to communicate human health risks when the compounds are found in the environment. In a collaboration between North Carolina State and Oregon State Universities, we are currently measuring PFAS in landfill gas from about 25 landfills across the U.S. Michael A. Abraczinskas: PFAS challenges for environmental regulatory agencies This critical review of PFAS exposures in humans is timely and deserves considerable attention due to concerns over toxicity and persistence in the environment. Michael Kleinman: PFOA and PFAS: toxicology and mechanistic considerations Perfluorooctanoic acid (PFOA) and Perfluoroalkyl substances (PFAS), which are used in many commercial applications, are persistent in the environment, do not readily undergo chemical degradation or biotransformation, bioaccumulate and are found, not only in the serum of occupationally exposed workers, but also the blood and tissues of the general population (Kudo and Kawashima [48]; Sanchez Garcia et al. [63]) including children and adolescents (Duffek et al. [25]). Many PFAS and PFOA compounds degrade to acid forms (PFAAs), environmental exposures are often to mixtures of compounds and toxic potential (potency) can vary across the family of compounds. [Extracted from the article]

People in polluted communities are often exposed to both PM and ozone (O3), albeit not always simultaneously; an important question is whether exposure to particles with seasonal compositional differences can influence biological outcomes. We addressed this question using a mouse model of cardiovascular disease by contrasting the health outcomes of exposures to particles formed or aged during periods of relatively high photochemical activity (i.e. spring/summer), which has increased ambient O3 concentrations, with outcomes of exposures to fall/winter particles which are associated with lower O3 concentrations. Electrocardiographs (ECGs) and blood pressures (BPs) were acquired following exposures to concentrated ambient particles (CAPs). ECGs were analyzed to changes in specific waveform parameters and changes in heart rate variability (HRV). Exposures elicited several types of waveform abnormalities that were associated with seasonal differences in particle constituents. Alterations in R-R interval and P-R interval were seen following exposure to summer CAPs but not fall CAPs and differential responses were seen in the corrected Q-T interval following the two seasonal exposures. Measures of HRV increased after exposure to summer CAPs compared to air-exposed controls but not following the winter CAPs exposure. There were chemical differences with respect to the organic constituents in ambient particles between summer and fall aerosol. The oxygen to carbon ratios (O:C) were generally higher in the spring and summer than in the fall, consistent with seasonal differences in atmospheric photochemical activity. Seasonal differences in atmospheric photochemical activity can modify ambient aerosol composition and can alter biological responses in the cardiovascular system. The results from this study confirm that ambient photochemical activity can alter the toxicity of ambient PM. Regional and seasonal differences in PM2.5 composition should be important considerations when evaluating the effects of PM exposure on cardiovascular health. Implications: Particles formed during periods of high photochemical activity (e.g. spring/summer) elicit more adverse cardiovascular health effects than particles formed during periods of low photochemical activity (e.g. fall/winter). Seasonal differences in atmospheric photochemical activity modified ambient aerosol composition and worsened cardiovascular responses. These results can inform regulatory agencies and may help design air quality regulations for PM2.5 that consider seasonal and regional variations. [ABSTRACT FROM AUTHOR]

Waterpipe smoking is becoming more popular worldwide and there is a pressing need to better characterize the exposure of smokers to chemical compounds present in the mainstream smoke. We report real-time measurements of mainstream smoke for carbon monoxide, volatile organic compounds and nanoparticle size distribution and chemical composition using a custom dilution flow tube. A conventional tobacco mixture, a dark leaf unwashed tobacco, and a nicotine-free herbal tobacco were studied. Results show that carbon monoxide is present in the mainstream smoke and originates primarily from the charcoal used to heat the tobacco. Online measurements of volatile organic compounds in mainstream smoke showed an overwhelming contribution from glycerol and its decomposition products. Gas phase analysis also showed that very little filtration of the gas phase products is provided by the percolation of mainstream smoke through water. Waterpipe smoking generated high concentrations of 4–100 nm nanoparticles, which were mainly composed of sugar derivatives and especially abundant in the first 10 min of the smoking session. These measured emissions of volatiles and particles are compared with those from a reference cigarette (3R4F) and represent the equivalent of the emission of one or more entire cigarettes for a single puff of hookah smoke. Considerations related to the health impacts of waterpipe smoking are discussed. [ABSTRACT FROM AUTHOR]

Each year, the general public and wildland firefighters in the US are exposed to smoke from wildland fires. As part of an effort to characterize health risks of breathing this smoke, a review of the literature was conducted using five major databases, including PubMed and MEDLINE Web of Knowledge, to identify smoke components that present the highest hazard potential, the mechanisms of toxicity, review epidemiological studies for health effects and identify the current gap in knowledge on the health impacts of wildland fire smoke exposure. Respiratory events measured in time series studies as incidences of disease-caused mortality, hospital admissions, emergency room visits and symptoms in asthma and chronic obstructive pulmonary disease patients are the health effects that are most commonly associated with community level exposure to wildland fire smoke. A few recent studies have also determined associations between acute wildland fire smoke exposure and cardiovascular health end-points. These cardiopulmonary effects were mostly observed in association with ambient air concentrations of fine particulate matter (PM2.5). However, research on the health effects of this mixture is currently limited. The health effects of acute exposures beyond susceptible populations and the effects of chronic exposures experienced by the wildland firefighter are largely unknown. Longitudinal studies of wildland firefighters during and/or after the firefighting career could help elucidate some of the unknown health impacts of cumulative exposure to wildland fire smoke, establish occupational exposure limits and help determine the types of exposure controls that may be applicable to the occupation. [ABSTRACT FROM AUTHOR]

The article presents comments on several articles related to the issues of air quality and climate change. Professor Michael T. Kleinman discusses hydrofluorocarbons and the health aspects of multiple air pollutants that contribute to fine particles and ozone. Howard J. Feldman tackles the link between climate change and pollutant buildup. J. Jason West elaborates on the interconnections between air pollution and climate change.

Graph: Michael T. Kleinman Graph: Eric D. Stevenson Per- and polyfluoroalkyl substances (PFAS) are a complex class of chemical contaminants that include perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS), all of which are compounds that are extremely stable and persistent in the environment. Although the exact mechanisms are not fully understood, PFAS toxicity can cause increased oxidative stress, changes in gene expression, and immune suppression, all of which have been described as key characteristics of carcinogens that affect humans; thus, PFAS may pose significant risks as toxic contaminants and carcinogens. The discussants - Michael Abraczinska, Xuelian Bai, Morton Barlaz, Virginia Guidry, and Alex Lan - will provide different perspectives, and may agree or disagree with the conclusions and recommendations of the Critical Review and with one another. [Extracted from the article]

The article discusses the 2014 Critical Review discussion by the Air and Waste Management Association in the U.S. The discussion was centered on relationships between air pollution and human health, with an emphasis on an important component of regulated particulate matter (PM) PM2.5 and PM10 exposure. The discussants include Daniel S. Greenbaum, Ronald E. Wyzga, and Michael T. Kleinman.

Motor vehicle exhaust emissions are known to exacerbate asthma and other respiratory diseases. Several studies have demonstrated significant associations between living near highly trafficked roadways and increased incidence of asthma and increased severity of asthma-related symptoms, medication usage, and physician visits. This study tested the hypotheses that (1) exposure to particulate matter (PM) near a heavily trafficked Los Angeles freeway would enhance inflammatory and allergic responses in ovalbumin (OVA)-sensitized BALB/c mice compared to sensitized, clean air controls, and (2) there would be differences in response at two distances downwind of heavily traveled freeways because of greater toxicity of PM closest to the freeway. An ambient particle concentrator was used to expose ovalbumin (OVA)-treated BALB/c mice to purified air, to concentrated fine ambient particles, and to concentrated ultrafine airborne particles (CAPs) at 2 distances, 50 m and 150 m, downwind of a roadway that is impacted by emissions from both heavy-duty diesel and light duty gasoline vehicles. Tissues and biological fluids from the mice were analyzed after exposures for 5 days/wk in 2 consecutive weeks. The biomarkers of allergic or inflammatory responses that were assessed included cytokines released by Type 2 T-helper cells (interleukin [IL]-5 and IL-13), OVA-specific immunoglobulin E (IgE), OVA-specific immunoglobulin G1 (IgG1), and pulmonary infiltration of polymorphonuclear leukocytes and eosinophils. IL-5 and IgG1 were significantly increased in mice exposed to CAPs 50 m downwind of the road, compared to responses in mice exposed to purified air, providing evidence of allergic response. No significant increases in allergy-related responses were observed in mice exposed to CAPs 150 m downwind of the road. The biological responses at the 50-m site were significantly associated with organic and elemental carbon components of fine and ultrafine particles (p ≤ .05). The primary source of these contaminants at the roadway sites was motor vehicle emissions, suggesting that particulate matter from motor vehicle fuel combustion could exert adjuvant effects and promote the development of allergic airway diseases. [ABSTRACT FROM AUTHOR]

A factorial design study was performed to examine the acute effects of inhaled acid particles alone and in mixtures with ozone to test the hypothesis that acid particles and ozone would act synergistically. Sprague-Dawley rats were exposed nose-only for a single 4-h period to all 9 possible combinations of purified air and 2 concentrations each of O 3 (0.3 and 0.6 ppm) and submicrometer (0.3 µ m mass median diameter [MMD]) sulfuric acid aerosols H 2 SO 4 (0.5 and 1.0 mg/m 3 ). Respiratory-tract injury and impairment of alveolar macrophage functions were evaluated. Two-way analyses of variance were used to test for significance of main effects and statistical interactions, and Tukey multiple comparison tests were used to test the significance of differences between group mean values. Addition of H 2 SO 4 to O 3 -containing atmospheres resulted in significant H 2 SO 4 concentration-dependent reductions in O 3 -induced inflammatory responses, and H 2 SO 4 , alone and in combination with O 3 , depressed some functions of innate immunity. DNA synthesis in nasal, tracheal, and lung tissue following pollutant exposure, which is an index of injury or killing of epithelial cells, was significantly increased by O 3 but not by H 2 SO 4 when administered alone, compared to purified air. When administered with O 3 , H 2 SO 4 did not reduce the effects of O 3 on DNA synthesis in the trachea or the lung, but did reduce the DNA synthesis response to O 3 in the nose. No significant changes in antibody-directed Fc receptor (FcR) binding of sheep red blood cells by alveolar macrophages were observed, but macrophage phagocytic activity was significantly reduced by the pollutant exposures. In summary, the results of this study indicate significant interactions between O 3 and H 2 SO 4 in concurrent exposures; however, the findings do not support the hypothesis that O 3 and H 2 SO 4 act synergistically in rats after single 4-h exposures. [ABSTRACT FROM AUTHOR]

A mobile whole-body exposure system was developed for exposing mice to concentrated ambient particulate matter smaller than 2.5 μm in mass median aerodynamic diameter (MMAD). Each 20-L exposure cage was designed to hold 9 mice within individual compartments. This allowed for transport and subsequent exposure. Airflow mixing and the potential for stagnant areas within the compartments were modeled using computational fluid dynamic modeling (CFD). CFD analysis showed no stagnant areas and good mixing throughout the exposure cage. The actual performance of the exposure system was determined for 0.5 to 2.0 μm diameter aerosols by measuring (1) uniformity of aerosol distribution and (2) particle deposition in the tracheobronchial and pulmonary regions of mice exposed in the system. A 0.6-μm MMAD (GSD = 2.0) cigarette smoke aerosol was used to experimentally measure the uniformity of aerosol distribution to the nine individual compartments. The average data from three runs showed no statistically significant difference among individual compartments. Particle deposition efficiency in adult male BALB/c mice was measured after exposure (30 min) in the system using monodisperse fluorescent polystyrene latex particles (0.5, 1, and 2 μm aerodynamic diameter). The measured deposition efficiency in this mobile exposure system for the combined tracheobronchial and pulmonary regions of the adult male BALBc mice was 21% for 0.5 μm, 11% for 1.0 μm, and 6.5% for 2.0 μm particles. These deposition efficiencies are similar to those reported for mice exposed in a nose-only exposure system, which indicates that particle losses to animal fur and exposure system surfaces were acceptable. [ABSTRACT FROM AUTHOR]

The U.S. EPA has tightened control of fine particles primarily by limiting maximum 24 h average airborne concentrations. The present investigation used real-time monitoring to record short-term PM excursions and literature evaluation to determine whether PM levels reached in excursions might be health significant. Data recorded in Birmingham, AL, Penticton, British Columbia, and Zeebrugge, Belgium revealed numerous excursions, one reaching 2,000 mu g/M[sup 3]. Toxicology and clinical studies involving brief exposures to particle levels in the range of observed excursions elicited adverse effects in both animals and humans. The area of lung surface developing lesions was elevated in rats breathing the same 4 h dose of aerosols when the 4 h average rate of aerosol delivery included a short-term (greater than or equal to 5 min) burst (greater than or equal to 50%) above the average dose rate. Elevations were observed with each of two aerosols tested. The magnitude of the effect was higher with one of the two aerosols, whose dose rate included four excursions rather than just one excursion. Symptom severity in asthmatics was associated with PM elevations, but the strength of the association depended upon the PM averaging time: the strength of the PM association with symptom severity increased as the PM averaging time varied from 24 h to 8 h to 1 h. Three hundred people were overcome after wind lofted particles into the air during a 4 day outdoor music festival in Queen Creek, AZ in April 1997. More research is necessary, but evidence presented here suggests that greater risk reduction might be achievable via controlling 1 h and 24 h PM averages than via tightening control of 24 h averages without controlling the 1 h average. [ABSTRACT FROM AUTHOR]

Healthy young adult (300 g) Sprague-Dawley rats were exposed for 1-day or 5-day periods, nose only, to purified air (CA) or four different pollutant atmospheres. Pollutant atmospheres included (a) 0.2 ppm ozone; (b) 0.4 ppm O3; (c) a low concentration mixture of ozone and sulfuric acid-coated carbon particles (0.2 ppm, 100 mug/m3 and 50 mug/ m3, respectively); and (d) a high-concentration O3 and sulfuric acid-coated carbon particle mixture (0.4 ppm, 500 mug/m3 and 250 mug/m3, respectively). Following 1-day exposures to the high O3 concentration, significant ( p .05) decreases were observed in respiratory tidal volumes and significant increases were observed in lung inflammatory response. Following 5-day exposures to 0.4 ppm O3, tidal volumes and lung inflammation were not significantly different from those seen in CA controls. In contrast, following 5-day exposures to the high-concentration O3-particle mixture, lung inflammation was increased significantly relative to that seen after 1-day high concentration mixture exposure or after CA exposure. Macrophage Fc-receptor binding, an important immunological function of macrophages, was significantly depressed after 5-day exposures to either the high- or low-concentration O3-particle mixtures compared to 1-day exposures or to CA. Thus, at the concentrations tested, repeated exposures to O3 produced diminished responses in breathing pattern changes and lung parenchymal injuries compared to acute, single exposures. This diminution was not observed after exposures to mixtures of acidic particles plus ozone. We conclude that mixtures of ozone and acidic particles may alter adaptive mechanisms that have been reported by us and others after repeated exposures to ozone alone. [ABSTRACT FROM AUTHOR]

Provides information on a study which examined the effects of carbon monoxide and hypoxemia on men with stable angina pectoris residing at near sea level. Background of the study; Design and method; Results and discussion; Conclusions.

Examines the effects of exposure to inhaled carbon monoxide at sea level and simulated high altitudes on the incidence of cardiac ectopy in subjects with coronary artery disease. Characteristics of subjects at time of entry into study; Incidence of ectopy among subjects; Incidence of ventricular ectopy that occurred at blood oxygen saturation levels of 98% and 90%.

Examines the effect of carbon monoxide exposure in subjects with stable angina pectoris. Performance of graded exercise test following exposure; Increase of blood carboxyhemoglobin levels; Reduction of oxygen uptake.

Examines the effects of air pollutant exposure on the pulmonary and respiratory systems. Identification of pollutants; Comparison of effects from exposure to sodium chloride against a mixture of sodium chloride plus irritant particles and gases; Implications of pollutant concentrations for existence of respiratory symptoms.