Abstract  This publication briefly reviews the impact of increasing atmospheric carbon dioxide and tropospheric ozone on global climate change, and the response of forest trees to these atmospheric pollutants and their interactions; points out the need for large-scale field experiments to evaluate the response of plants to these environmental stresses; and describes the development, operational parameters, experimental methods, and the potential research scope of the aspen Free-air Carbon dioxide and ozone Enrichment (FACE) project.

Abstract  Higher temperatures caused by increasing greenhouse gas concentrations are predicted to exacerbate photochemical smog if precursor emissions remain constant. We perform a statistical analysis of 21 years of ozone and temperature observations across the rural eastern U.S. The climate penalty factor is defined as the slope of the ozone/temperature relationship. For two precursor emission regimes, before and after 2002, the climate penalty factor was consistent across the distribution of ozone observations. Prior to 2002, ozone increased by an average of ~3.2 ppbv/°C. After 2002, power plant NOx emissions were reduced by 43%, ozone levels fell ~10%, and the climate penalty factor dropped to ~2.2 ppbv/°C. NOx controls are effective for reducing photochemical smog and might lessen the severity of projected climate change penalties. Air quality models should be evaluated against these observations, and the climate penalty factor metric may be useful for evaluating the response of ozone to climate change.

Abstract  Isoprene epoxydiols (IEPOX), formed from the photooxidation of isoprene under low-NOx conditions, have recently been proposed as precursors of secondary organic aerosol (SOA) on the basis of mass spectrometric evidence. In the present study, IEPOX isomers were synthesized in high purity (> 99%) to investigate their potential to form SOA via reactive uptake in a series of controlled dark chamber studies followed by reaction product analyses. IEPOX-derived SOA was substantially observed only in the presence of acidic aerosols, with conservative lower-bound yields of 4.7-6.4% for β-IEPOX and 3.4-5.5% for δ-IEPOX, providing direct evidence for IEPOX isomers as precursors to isoprene SOA. These chamber studies demonstrate that IEPOX uptake explains the formation of known isoprene SOA tracers found in ambient aerosols, including 2-methyltetrols, C5-alkene triols, dimers, and IEPOX-derived organosulfates. Additionally, we show reactive uptake on the acidified sulfate aerosols supports a previously unreported acid-catalyzed intramolecular rearrangement of IEPOX to cis- and trans-3-methyltetrahydrofuran-3,4-diols (3-MeTHF-3,4-diols) in the particle phase. Analysis of these novel tracer compounds by aerosol mass spectrometry (AMS) suggests that they contribute to a unique factor resolved from positive matrix factorization (PMF) of AMS organic aerosol spectra collected from low-NOx, isoprene-dominated regions influenced by the presence of acidic aerosols.

Abstract  The in vitro study was aimed to determine the effect of ozone on periodontopathogenic microorganisms. Ozone was generated for 6 s-2 × 24 s (corresponding to 0.56 mg-2 × 2.24 mg of ozone) against 23 mainly anaerobic periodontopathogenic species. Agar diffusion test was used as a screening method. Then, the killing activity was tested in a serum-free environment and with 25% v/v inactivated serum. Further, the effect of ozone on bactericidal activity of native serum was analyzed against Fusobacterium nucleatum, Porphyromonas gingivalis, and Aggregatibacter actinomycetemcomitans. Agar diffusion test showed a high efficacy of ozone against microorganisms, especially against Porphyromonas gingivalis. This result was confirmed by the killing tests; most of the strains in a concentration of 10(5) were completely eliminated after twofold 18-s application of ozone. Only four of the six potentially "superinfecting" species (Staphylococcus aureus, Enterococcus faecalis, Enterobacter cloacae, Candida albicans) survived in part. Addition of heat-inactivated serum reduced the killing rate of ozone by 78% after 6-s and by 47% after twofold 18-s exposures; no strain was completely eradicated after any application of ozone. The bactericidal effect of native serum was enhanced after application of ozone; no effect was visible on the included A. actinomycetemcomitans strain which was found to be completely resistant to the bactericidal action of serum. In conclusion, (a) ozone has a strong antibacterial activity against putative periodontopathogenic microorganisms, and (b) the bactericidal effect is reduced in the presence of serum. Ozone may have potential as an adjunctive application to mechanical treatment in periodontitis patients.

Abstract  Antioxidants in respiratory mucus protect the underlying airway epithelium from damage by ozone (O(3)), a common outdoor air pollutant. To understand O(3)-antioxidant interactions and the variation of these interactions among individuals, in vitro assays are needed to measure the total antioxidant capacity of airway lavage fluid, a convenient source of (diluted) mucous samples. Here, we compare the oxygen radical absorbance capacity (ORAC), a general method that uses peroxyl radicals as a reactive substance, to the recently developed ozone specific antioxidant capacity (OZAC), a procedure that directly employs O(3). For prepared model mucous antioxidant solutions containing uric acid, ascorbic acid or glutathione, the ORAC and OZAC methods yielded comparable antioxidant capacities. The addition of EDTA or DETAPAC, necessary to prevent auto-oxidation of test solutions during the ORAC assay, unpredictably altered ORAC measurements. EDTA did not have a significant effect on OZAC measurements in either prepared uric acid or ascorbic acid solutions. When assessing antioxidant capacities of nasal lavage samples, the ORAC and OZAC assays were no longer comparable. Because the OZAC of nasal lavage samples was positively related to measured uric acid concentrations whereas the ORAC data were not, the OZAC method appears to provide more realistic mucous antioxidant capacities than the ORAC method.

Abstract  There is growing concern that exposure to air pollutants during pregnancy affects health outcomes in the offspring due to alterations in the development of immune and other homeostatic processes. To assess the risks of maternal inhalation exposure to ozone (O(3)), timed pregnant BALB/c mice were exposed to different concentrations of O(3) (0, 0.4, 0.8, and 1.2 ppm) for 4 h/day for 10 days during gestation (GD9-GD18), and pulmonary inflammation and immune responses were assessed in the offspring at 6 weeks-of-age. Maternal O(3) exposure reduced the number of productive dams by 25% at the highest O(3) concentration (1.2 ppm) and decreased the rate of weight gain in the offspring. Delayed-type hypersensitivity responses to bovine serum albumin were suppressed in the female offspring by maternal exposure to the two highest concentrations of O(3), whereas humoral immune responses to sheep red blood cells were not altered in either sex. Maternal exposure to 1.2 ppm O(3) increased lactate dehydrogenase (LDH) activity in bronchoalveolar lavage fluid (BALF) of the offspring but did not affect the number of inflammatory cells or levels of total protein, IFN-γ, IL-17, and IL-4 cytokines in BALF, or CD4(+), CD8(+), CD25(+), and TCRβ(+)CD1d(+) T-cells in the spleen. Offspring born from air-exposed dams sensitized early in life (postnatal day [PND] 3) to ovalbumin (OVA) antigen and then challenged as adults developed eosinophilia, elevated levels of LDH activity and total protein in BALF, and increased pulmonary responsiveness to methacholine, compared with animals sensitized at PND42. Maternal O(3) exposure in the 1.2 ppm O(3) group decreased BALF eosinophilia and serum OVA-specific IgE in the female offspring sensitized early in life but did not affect development of allergic airway inflammation by offspring sensitized late in life. In summary, maternal exposure to O(3) affected reproductive outcome and produced modest decreases in immune function and indicators of allergic lung disease in surviving offspring.

Abstract  The transcription factor Forkhead box O3 (Foxo3) has a critical role in suppressing the expansion of antigen-specific effector T-cell populations; hence, Foxo3 is a potential target for enhancing the antitumor immunity of cancer vaccines. In this report, we evaluated the potential of RNA interference (RNAi)-mediated silencing of Foxo3 in antigen-presenting cells as an adjuvant for HER2/neu DNA cancer vaccines. Bicistronic plasmids expressing the N-terminal extracellular domain of human HER-2/neu and the Foxo3 short hairpin RNA (hN'-neu-Foxo3 shRNA) or the scrambled control (hN'-neu-scramble shRNA) were subcutaneously injected into mice by gene gun administration to elicit antitumor immunity against p185neu-overexpressing MBT-2 bladder tumor cells. We found that mice treated with hN'-neu-Foxo3 shRNA showed greater reductions in tumor growth and longer survival times than mice treated with hN'-neu-scramble shRNA, indicating that the silencing of Foxo3 enhanced the antitumor efficacy of the HER-2/neu cancer vaccine. Cytotoxicity analyses further revealed that the Foxo3 shRNA-enhanced antitumor effect was associated with significant increases in the number of functional CD8(+) T cells and in the levels of cytotoxic T lymphocytes activity. Interleukin-6 was induced by hN'-neu-Foxo3 shRNA treatment but did not have a critical role in the antitumor effect of the hN'-neu-Foxo3 shRNA vaccine. Moreover, in vivo lymphocyte depletion analyses confirmed that the antitumor efficacy of the hN'-neu-Foxo3 shRNA vaccine depended on functional CD8(+) T cells. Finally, Foxo3 suppression was shown to markedly improve the effect of the HER-2/neu DNA vaccine in limiting the growth and lung metastases of MBT-2 cells. Overall, these results support RNAi-mediated silencing of Foxo3 as an effective strategy to enhance the therapeutic antitumor effect of HER-2/neu DNA vaccines against p185neu-positive tumors.

Abstract  The formation of secondary organic aerosol (SOA) produced from α-pinene, linalool, and limonene by ozonolysis was examined using a dynamic chamber system that allowed the simulation of ventilated indoor environments. Experiments were conducted at typical room temperatures and air exchange rates. Limonene ozonolysis produced the highest SOA mass concentrations and linalool the lowest with α-pinene being intermediate. Simplified empirical modeling simulations were conducted to provide insights into reaction chemistry. Assessment of variability of particle-bound reactive oxygen species (ROS) may be important in the understanding of health effects associated with particulate matter. The ROS intensities defined as ROS/SOA mass were found to be moderately correlated with the SOA densities. Greater ROS intensities were observed for the cases where ozone was in excess. ROS intensities approached a relatively constant value in the region where ozone was in deficit. The estimated initial ROS half-life time was approximately 6.5 h at room temperature suggesting the time sensitivity of ROS measurements. The ROS formed from terpenoid ozonolysis could be separated into three categories: short-lived/high reactive/volatile, semivolatile/relatively stable and nonvolatile/low reactive species based on ROS measurements under various conditions. Such physical characterization of the ROS in terms of reactivity and volatility provides some insights into the nature of ROS.

Abstract  Human and animal toxicology has had a profound impact on our historical and current understanding of air pollution health effects. Early animal toxicological studies of air pollution had distinctively military or workplace themes. With the discovery that ambient air pollution episodes led to excess illness and death, there became an emergence of toxicological studies that focused on industrial air pollution encountered by the general public. Not only did the pollutants investigated evolve from ambient mixtures to individual pollutants but also the endpoints and outcomes evaluated became more sophisticated, resulting in our present state of the science. Currently, a large toxicological database exists for the effects of particulate matter and ozone, and we provide a focused review of some of the major contributions to the biological understanding for these two "criteria" air pollutants. A limited discussion of the toxicological advancements in the scientific knowledge of two hazardous air pollutants, formaldehyde and phosgene, is also included. Moving forward, the future challenge of air pollution toxicology lies in the health assessment of complex mixtures and their interactions, given the projected impacts of climate change and altered emissions on ambient conditions. In the coming years, the toxicologist will need to be flexible and forward thinking in order to dissect the complexity of the biological system itself, as well as that of air pollution in all its varied forms.

Abstract  O2', O3', O5'-tri-acetyl-N(6)-(3-hydroxylaniline)adenosine (WS070117), a new structure-type lipid regulator, is being developed in pre-clinical study. In order to monitor drug kinetics it is essential to understand pre-analytical factors that may affect drug assay. In vitro stability and metabolism were investigated using high-performance liquid chromatography (HPLC) method in this study. The hydrolysis products were identified by HPLC-mass spectrometry (MS)/MS method. The esterases involved in WS070117 hydrolysis was assigned via inhibition rate assay. It was found that WS070117 was chemically unstable in alkaline solutions compared to acidic and near neutral solutions. Enzymatic hydrolysis was even more rapid. Hydrolytic rate constants differ between species, being 4.24, 5.96 × 10(-3) and 6.85 × 10(-2) min(-1) in rat, dog and human plasma at 37°C, respectively. The hydrolysis was catalyzed by plasma esterase because NaF (sodium fluoride: a general esterase inhibitor) inhibited WS070117 hydrolysis and metabolite production. Hydrolysis was fast in rat plasma and was catalysed by carboxylesterase and butyrylcholinesterase. In dog plasma, carboxylesterase, butyrylcholinesterase and paraoxonase were mainly responsible. Butyrylcholinesterase was the major esterase involved in WS070117 hydrolysis in human plasma. The WS070117 hydrolysis in plasma proceeded by gradual loss of acetyl groups. The knowledge of in vitro drug stability and metabolic pathways identified in this study will be essential for future pre-clinical and clinical pharmacokinetics studies.

Abstract  Context: Ozone exposure triggers airway inflammatory responses that may be influenced by biologically active purine metabolites. Objective: To examine the relationships between airway purine metabolites and established inflammatory markers of ozone exposure, and to determine if these relationships are altered in individuals with atopy or asthma. Materials and methods: Mass spectrometry was utilized to measure concentrations of purine metabolites (adenosine monophosphate [AMP], adenosine, hypoxanthine, uric acid) and non-purine metabolites (taurine, urea, phenylalanine, tyrosine) in induced sputum obtained from 31 subjects with normal lung function (13 healthy controls, eight atopic nonasthmatics, and 10 atopic asthmatic [AA]) before and 4 h after ozone exposure. Results: At baseline, the purines AMP and hypoxanthine correlated with multiple inflammatory markers including neutrophil counts and the cytokines interleukin (IL)-6, IL-8, tumor necrosis factor alpha (TNF-α), and IL-1β (r ranged from 0.41 to 0.66, all P < 0.05). Following ozone exposure, these purines remained correlated with IL-6, IL-8, and TNF-α (r = 0.37-0.68). However, AMP and hypoxanthine increased significantly post ozone exposure in atopic nonasthmatics but not in AA. In contrast, the non-purine metabolite taurine correlated with baseline neutrophil counts (r = 0.56) and IL-6 (r = 0.53) and was elevated post-exposure in both atopic cohorts. Discussion and conclusions: The purine metabolites AMP and hypoxanthine are correlated with multiple inflammatory markers at baseline and after ozone exposure. However, changes in these purine metabolites after ozone appear to differ from other inflammatory markers, with less response in AA relative to atopic nonasthmatics. Purine metabolites may play a role in the signaling responses to ozone, but these responses may be altered in subjects with asthma.

Abstract  Summary:  Ozone (O(3) ) and endotoxin are common environmental contaminants that cause asthma exacerbation. These pollutants have similar phenotype response characteristics, including induction of neutrophilic inflammation, changes in airway macrophage immunophenotypes, and ability to enhance response to inhaled allergen. Evoked phenotyping studies of volunteers exposed to O(3) and endotoxin were used to identify the response characteristics of volunteers to these pollutants. New studies support the hypotheses that similar innate immune and oxidant processes modulate response to these agents. These include TLR4 and inflammasome-mediated signaling and cytokine production. Innate immune responses are also impacted by oxidative stress. It is likely that continued discovery of common molecular processes which modulate response to these pollutants will occur. Understanding the pathways that modulate response to pollutants will also allow for discovery of genetic and epigenetic factors that regulate response to these pollutants and determine risk of disease exacerbation. Additionally, defining the mechanisms of response will allow rational selection of interventions to examine. Interventions focused on inhibition of Toll-like receptor 4 and inflammasome represent promising new approaches to preventing pollutant-induced asthma exacerbations. Such interventions include specific inhibitors of innate immunity and antioxidant therapies designed to counter the effects of pollutants on cell signaling.

Abstract  Asthma is a known risk factor for acute ozone-associated respiratory disease. Ozone causes an immediate decrease in lung function and increased airway inflammation. The role of atopy and asthma in modulation of ozone-induced inflammation has not been determined.

We sought to determine whether atopic status modulates ozone response phenotypes in human subjects.

Fifty volunteers (25 healthy volunteers, 14 atopic nonasthmatic subjects, and 11 atopic asthmatic subjects not requiring maintenance therapy) underwent a 0.4-ppm ozone exposure protocol. Ozone response was determined based on changes in lung function and induced sputum composition, including airway inflammatory cell concentration, cell-surface markers, and cytokine and hyaluronic acid concentrations.

All cohorts experienced similar decreases in lung function after ozone. Atopic and atopic asthmatic subjects had increased sputum neutrophil numbers and IL-8 levels after ozone exposure; values did not significantly change in healthy volunteers. After ozone exposure, atopic asthmatic subjects had significantly increased sputum IL-6 and IL-1beta levels and airway macrophage Toll-like receptor 4, Fc(epsilon)RI, and CD23 expression; values in healthy volunteers and atopic nonasthmatic subjects showed no significant change. Atopic asthmatic subjects had significantly decreased IL-10 levels at baseline compared with healthy volunteers; IL-10 levels did not significantly change in any group with ozone. All groups had similar levels of hyaluronic acid at baseline, with increased levels after ozone exposure in atopic and atopic asthmatic subjects.

Atopic asthmatic subjects have increased airway inflammatory responses to ozone. Increased Toll-like receptor 4 expression suggests a potential pathway through which ozone generates the inflammatory response in allergic asthmatic subjects but not in atopic subjects without asthma.

Abstract  Salicylic acid (SA), a ubiquitous phenolic phytohormone, is involved in many plant physiological processes including stomatal movement. We analysed SA-induced stomatal closure, production of reactive oxygen species (ROS) and nitric oxide (NO), cytosolic calcium ion ([Ca²+](cyt)) oscillations and inward-rectifying potassium (K+(in)) channel activity in Arabidopsis. SA-induced stomatal closure was inhibited by pre-treatment with catalase (CAT) and superoxide dismutase (SOD), suggesting the involvement of extracellular ROS. A peroxidase inhibitor, SHAM (salicylhydroxamic acid) completely abolished SA-induced stomatal closure whereas neither an inhibitor of NADPH oxidase (DPI) nor atrbohD atrbohF mutation impairs SA-induced stomatal closures. 3,3'-Diaminobenzidine (DAB) and nitroblue tetrazolium (NBT) stainings demonstrated that SA induced H₂O₂ and O₂⁻ production. Guard cell ROS accumulation was significantly increased by SA, but that ROS was suppressed by exogenous CAT, SOD and SHAM. NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) suppressed the SA-induced stomatal closure but did not suppress guard cell ROS accumulation whereas SHAM suppressed SA-induced NO production. SA failed to induce [Ca²+](cyt) oscillations in guard cells whereas K+(in) channel activity was suppressed by SA. These results indicate that SA induces stomatal closure accompanied with extracellular ROS production mediated by SHAM-sensitive peroxidase, intracellular ROS accumulation and K+(in) channel inactivation.

Abstract  Isothiocyanates (ITCs) are degradation products of glucosinolates in crucifer plants and have repellent effect on insects, pathogens and herbivores. In this study, we report that exogenously applied allyl isothiocyanate (AITC) induced stomatal closure in Arabidopsis via production of reactive oxygen species (ROS) and nitric oxide (NO), and elevation of cytosolic Ca(2+) . AITC-induced stomatal closures were partially inhibited by an inhibitor of NADPH oxidase and completely inhibited by glutathione monoethyl ester (GSHmee). AITC-induced stomatal closure and ROS production were examined in abscisic acid (ABA) deficient mutant aba2-2 and methyl jasmonate (MeJA)-deficient mutant aos to elucidate involvement of endogenous ABA and MeJA. Genetic evidences have demonstrated that AITC-induced stomatal closure required MeJA priming but not ABA priming. These results raise the possibility that crucifer plants produce ITCs to induce stomatal closure, leading to suppression of water loss and invasion of fungi through stomata.

Abstract  #Studying long-term effects of ozone on perennial plant communities in situ is difficult because of the need for large observation plots and long exposure times, and because of confounding effects of altered microclimatic conditions in most systems. A novel free-air fumigation system was designed for multi-year exposures of semi-natural grassland plots to either ambient or elevated ozone concentrations at a Swiss sub-alpine site. The system operates by releasing ozone-enriched air from either one of two 120 sectors, placed in each of the two main wind directions. Ozone-enriched air is rapidly mixed with ambient air behind a small transparent windscreen mounted at canopy height around the 7-m diameter circular plots. Ozone generation and dispensing during daylight hours is PC controlled and depends upon wind speed, wind direction and ambient ozone. In 2001, from April to October fumigation was possible during 85% of the time. The ozone-enrichment factor (EF, [O3]enriched/[O3]control) in ozone plots relative to control plots averaged 1.48 (±0.24 SD), and EF was highest with winds of around 2 m s-1. The seasonal cumulative ozone exposure (AOT40) at canopy level was 5 ppm h in the control and 30 ppm h in the ozone-treated plots, with less than 10% variation between replicates, and 13 ppm h in ambient air at 2 m. Variation in ozone across the plot-diameter was <5% for 24-h mean concentrations, but differed by a maximum of 20% in terms of AOT40. There was no difference in microclimatic conditions between experimental plots and ambient conditions. It is concluded that the system is suitable for long-term ozone experiments at relatively low running costs, but that the variation in ozone distribution across the plots may lead to systematic differences in cumulative exposure over longer periods of time which need to be taken into account when relating exposure to biological effects.

Abstract  An ozone (O3) exposure study was conducted in Nashville, TN, using passive O3 samplers to measure six weekly outdoor, indoor, and personal O3 exposure estimates for a group of 10- to 12-yr-old elementary school children. Thirty-six children from two Nashville area communities (Inglewood and Hendersonville) participated in the O3 sampling program, and 99 children provided additional timeactivity information by telephone interview. By design, this study coincided with the 1994 Nashville/Middle Tennessee Ozone Study conducted by the Southern Oxidants Study, which provided enhanced continuous ambient O3 monitoring across the Nashville area. Passive sampling estimated weekly average outdoor O3 concentrations from 0.011 to 0.030 ppm in the urban Inglewood community and from 0.015 to 0.042 ppm in suburban Hendersonville. The maximum 1- and 8-hr ambient concentrations encountered at the Hendersonville continuous monitor exceeded the levels of the 1- and 8-hr metrics for the O3 National Ambient Air Quality Standard. Weekly average personal O3 exposures ranged from 0.0013 to 0.0064 ppm (7-31% of outdoor levels). Personal O3 exposures reflected the proportional amount of time spent in indoor and outdoor environments. Air-conditioned homes displayed very low indoor O3 concentrations, and homes using open windows and fans for ventilation displayed much higher concentrations. Implications: This study demonstrates the usefulness of passive O3 sampling technology in measuring long-term outdoor/indoor/personal exposures. The test subjects did well in following simple directions concerning accurate exposure assessment and in keeping time-activity diaries. Personal O3 exposure, in between the extremes of higher outdoor and lower indoor exposures, is a function of time spent outdoors. Clearly, those children spending more time outdoors are subject to higher O3 exposures than are their more housebound peers. Continuous State and Local Air Monitoring System O3 monitoring results substantially overestimate weeklong indoor and personal O3 exposure. Centrally air-conditioned indoor environments confer a substantial degree of protection from ambient O3 levels.

Abstract  In a previous panel study in Paris, France, detrimental effects of moderately high levels of winter air pollution on the symptoms and lung function of asthmatic children were demonstrated. A new study was conducted, with the aim of assessing the short-term effects of photo-oxidant and particulate air pollution on childhood asthma during spring and early summer in Paris. Eighty-two medically diagnosed asthmatic children were followed up for 3 months. Outcomes included the incidence and prevalence of asthma attacks, nocturnal cough, supplementary use of beta2-agonists, symptoms of airway irritation, and peak expiratory flow (PEF) value and its variability. The statistical methods controlled for the lack of independence between daily health outcomes, temporal trends and pollen and weather conditions. Black smoke and nitrogen dioxide (NO2) were associated with increases in the occurrence of nocturnal cough and respiratory infections. Ozone (O3) was associated with an increase in the occurrence of asthma attacks and respiratory infections and with changes in lung function, as shown by an increase in PEF variability and a decrease in PEF. Statistically significant interactions were demonstrated between O3 and temperature and between O3 and pollen count for asthma attacks. O3 levels had a greater effect on additional bronchodilator use and on irritations of the eyes, nose and throat on days on which no steroids were used. Particulate matter was associated with eye irritation only. This study showed that, although within international air quality standards, the prevailing levels of photo-oxidant and particulate pollution in spring and early summer had measurable short-term effects on children with mild-to-moderate asthma.

Abstract  Electrocardiogram and arterial blood pressure of elastase-treated emphysematous rats (E rats) and saline-treated control rats (S rats) were recorded continuously during exposure to either 1 ppm ozone (O3) for 3 hr or 0.5 ppm O3 for 6 hr. The heart rates (HRs) of both groups decreased to about 50 and 65% of the initial levels at the end of 1 ppm and 0.5 ppm O3 exposure, respectively. Mean arterial blood pressures (MAPs) also decreased to about 76 and 82%, respectively. There was no significant difference in these responses between E and S rats, although the levels of HRs and MAPs of the E rats were always a little lower than those of the S rats. Another group of E and S rats was continuously exposed to 0.2 ppm O3 for 4 weeks. The HRs of both E and S groups decreased to about 81 and 88% of the initial levels on the first day, respectively, although they recovered completely by the third day. No significant difference in the variation of HRs during exposure was noted between E and S rats. However the HR responses of these rats to a challenge exposure of 0.8 ppm O3 for 1.5 hr appeared to be different. That is, S rats were more tolerant of the challenge exposure to O3 for 1.5 hr than the E rats.

Abstract  In exposure-response modeling, a major concern is the numerical definition of exposure in relating crop loss to O3, yet few indices have been considered. This paper addresses research in which plant growth was regressed for soybean, wheat, cotton, corn, and sorghum against 613 numerical exposure indices using the Box-Tidwell model. When the minimum sum of squared errors criterion was used, optimum performance was not attained for any single index; however, near optimum performances were achieved by two censored cumulative indices and from a class of indices called the generalized, phenologically weighted, cumulative impact indices (GPWCIs). The top-performing GPWCIs accumulated concentrations, used sigmoid weighting schemes emphasizing O3 concentrations of 0.06 ppm (118 microg m(-3)) or higher, and had phenological weighting schemes with greatest weight occurring 20 to 40 days prior to crop maturity. These findings indicate that (1) peak concentrations are important, but lower concentrations should be included in the calculations, (2) increased plant sensitivity occurs between flowering and maturity, and (3) plants respond to cumulative exposure impact.

Abstract  The objective of this study is to compare the use of several indices of exposure in describing the relationship between O3 and reduction in agricultural crop yield. No attempt has been made to determine which exposure-response models best fit the data sets examined. Hourly mean O3 concentration data, based on two-three measurements per hour, were used to develop indices of exposure from soybean and winter wheat experiments conducted in open-top chambers at the Boyce Thompson Institute, Ithaca, New York NCLAN field site. The comparative efficacy of cumulative indices (i.e. number of occurrences equal to or above specific hourly mean concentrations, sum of all hourly mean concentrations equal to or above a selected level, and the weighted sum of all hourly mean concentrations) and means calculated over an experimental period to describe the relationship between exposure to O3 and reductions in the yield of agricultural crops was evaluated. None of the exposure indices consistently provided a best fit with the Weibull and linear models tested. The selection of the model appears to be important in determining the indices that best describe the relationship between exposure and response. The focus of selecting a model should be on fitting the data points as well as on adequately describing biological responses. The investigator should be careful to couple the model with data points derived from indices relevant to the length of exposure. While we have used a small number of data sets, our analysis indicates that exposure indices that weight peak concentrations differently than lower concentrations of an exposure regime can be used in the development of exposure-response functions. Because such indices may have merit from a regulatory perspective, we recommend that additional data sets be used in further analyses to explore the biological rationale for various indices of exposure and their use in exposure-response functions.

Abstract  Recently, a stainless-steel air pollution chamber was acquired in this laboratory, and data were obtained in a study that convincingly demonstrated that chamber and face-mask inhalation methods of exposing young adult subjects for 6.6 h to nearly identical total inhaled O3 doses at 0.12 ppm produced very similar pulmonary function, symptoms, and exercise ventilatory pattern responses. However, the results of a 6.6-h face-mask exposure to 0.08 ppm O3, compared to some previous chamber exposure study results, revealed several small incongruities that may be due primarily to high individual subject "noise" in responses to a relatively low O3 exposure. To resolve these differences, it was the primary purpose of this study to compare chamber exposure responses to those elicited via face-mask exposure to 0.08 ppm O3 for 6.6 h with subjects serving as their own controls. Two types of O3 exposure patterns were used: (1) the usual square-wave profile, and (2) an acute triangular profile, in which O3 concentration was increased each hour from 0.03 ppm to 0.15 ppm during h 4 and then decreased each hour to 0.05 ppm (mean = 0.08 ppm). Thirty young adults (15 of each gender) served as subjects. The two exposure methods (i.e., face mask and chamber) yielded near identical total inhaled O3 doses in both the square-wave and triangular exposure profiles, and produced very similar postexposure pulmonary function, symptoms, and exercise ventilatory pattern responses. However, pulmonary function and symptoms responses became statistically significant from preexposure at the end of h 4 (when [O3] = 0.15 ppm) in the triangular protocols, but not until h 6 in the square-wave protocols. These results support previous evidence that O3 concentration has a greater singular effect in the total inhaled O3 dose than do VE and exposure duration.