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At least 19 recordsLinked to original sources
PubMed1998

Methods development for epidemiologic investigations of the health effects of prolonged ozone exposure. Part II. An approach to retrospective estimation of lifetime ozone exposure using a questionnaire and ambient monitoring data (California sites).

An extensive body of data supports a relation between acute exposures to ambient ozone and the occurrence of various acute respiratory symptoms and changes in measures of lung function. In contrast, relatively few data are available on the human health effects that result from long-term exposure to ambient ozone, Current efforts to study long-term ozone-related health effects are limited by the methods available for ascertaining lifetime exposures to ozone. The present feasibility study was undertaken as part of the Health Effects Institute's Environmental Epidemiology Planning Project (Health Effects Institute 1994) to (1) determine whether, in the context of an epidemiologic study, reliable estimates can be obtained for lifetime exposures to ozone by combining estimates from lifetime residential histories, typical activity patterns during life, and residence-specific ambient ozone monitoring data; (2) identify the minimum data required to produce reliable estimates of lifetime exposure; and (3) analyze the relations between various estimates of lifetime ozone exposure and measures of lung function. A convenience sample of 175 first-year students at the University of California, Berkeley, who lived all of their lives in selected areas of California (the Los Angeles Basin or the San Francisco Bay Area), were studied on two occasions (test and retest or test sessions 1 and 2), five to seven days apart. Residential and lifestyle data were obtained from a questionnaire: residence-based ambient ozone exposure values were assigned by interpolation of ambient ozone monitoring data to residential locations. Estimated lifetime exposure was based on average ozone levels between 10 a.m. and 6 p.m. and hours of exposure to ozone concentrations greater than 60 parts per billion (ppb). "Effective" lifetime exposure to ozone was based on a weighted average of estimated time spent in different ambient ozone environments as determined by different combinations of activity data. Pulmonary function was evaluated with flows and volumes from maximum expiratory flow-volume curves and slope of phase III of the single-breath nitrogen washout (SBNW) curves. Although the test-retest reliability of the residential history was acceptably high only for first and second residences, most of the unreliability for other residences came from residences occupied for relatively short durations. Therefore, the test-retest reliability of estimated lifetime exposure to ozone was high, with intraclass correlations greater than 0.90 for all approaches evaluated. Multiple, linear regression analyses showed a consistently negative relation between estimates of lifetime exposure to ozone and flows that reflect the physiology of pulmonary small airways. No relation was observed between lifetime ozone exposure and forced expiratory volume or the slope of phase III, and the relation between lifetime exposure and forced expiratory volume in one second was inconsistent. The results of the flow measures were unaffected by the method used to estimate lifetime exposure and gave effect estimates that were nearly identical. The data from this study indicate that useful and reproducible estimates of lifetime ozone exposure can be obtained in epidemiologic studies by using a residential history. However, the total burden of ozone to which the subjects were exposed cannot be determined accurately from such data. Nonetheless, the estimates so obtained appear to be associated with alterations in pulmonary function that are consistent with the predicted site of maximum effect of ozone in the human lung.

Air Pollution↗
PubMed1998

Methods development for epidemiologic investigations of the health effects of prolonged ozone exposure. Part III. An approach to retrospective estimation of lifetime ozone exposure using a questionnaire and ambient monitoring data (U.S. sites).

Methods are needed for retrospective estimation of long-term ozone exposures in epidemiologic studies. The overall objective of this study was to evaluate whether data from available U.S. ozone monitoring sites are useful for estimating lifetime ozone exposures of young adults (for example, college students). Several aspects of this question were evaluated. First, we applied and (compared several spatial interpolation methods to a set of long-term average ozone data from all U.S. monitoring sites in operation from 1981 through 1990. Interpolation methods included simple and weighted averages, linear regression, and, in an exploratory way, kriging. The comparison of methods was carried out for five different metrics of ozone concentration: the daily one-hour maximum (MAX1) and eight-hour maximum (MAX8), the average ozone concentrations between 10 a.m. and 6 p.m. (MID8) and between 10 a.m. and 10 p.m. (MID12), and the sum of all hourly ozone concentrations greater than or equal to 60 parts per billion (ppb) (SUM06). We also tested whether interpolations were improved by modeling the influence of covariates such as population density, elevation, and weather on ozone concentrations. We analyzed the reliability of a set of newly developed questions about past activity levels among a group of 52 freshmen students at Yale University. This was done by analyzing the agreement between answers to the same questionnaire administered two times, one month apart (test and retest), to the same students. Finally, we combined the interpolation models with residential history information obtained by questionnaire to derive long-term ozone exposure estimates for a group of 200 Yale freshmen. Results of our study showed that the density of available monitoring sites appears to be adequate for estimating spatial patterns of long-term average ambient ozone concentrations. A simple regression-based interpolation on the three nearest sites produced consistently good results. Including covariates in the interpolation models did not substantially improve the estimates. The largest estimation errors occurred for areas where ozone concentrations were highest. The newly developed activity history questions exhibited fair to moderate reliability, The results of this work imply that reasonably precise estimates of long-term ambient ozone concentrations for use in large-scale epidemiologic studies can be achieved by interpolating ozone concentrations between available U.S. monitoring sites. This study did not address the issues of whether and how retrospective data on factors that modify exposure or dose (e.g., indoor/outdoor penetration of ozone and time outdoors) can be used to derive estimates of long-term personal ozone exposures and contribute to the assessment of received dose.

Air Pollution↗
PubMed1997

Effects of ozone on normal and potentially sensitive human subjects. Part II: Airway inflammation and responsiveness to ozone in nonsmokers and smokers.

Exposure to ozone at levels near the National Ambient Air Quality Standard causes respiratory symptoms, changes in lung function, and airway inflammation. Although ozone-induced changes in lung function have been well characterized in healthy individuals, the relationship between airway inflammation and changes in pulmonary function have not been prospectively examined. The purpose of this study was to determine whether individuals who differ in, lung function responsiveness to ozone also differ in susceptibility to airway inflammation and injury. A secondary goal was to determine whether ozone exposure induces airway inflammation in smokers, a population known to have airway inflammation and an increased burden of toxic oxygen species. Healthy nonsmokers (n = 56) and smokers (n = 34) were exposed to 0.22 parts per million (ppm)* ozone for 4 hours, with intermittent exercise, for the purpose of selecting ozone "responders" (decrement in forced expiratory volume in 1 second [FEV1] > 15%) and "nonresponders" (decrement in FEV1 < 5%). Selected subjects then were exposed twice to ozone (0.22 ppm for 4 hours with exercise) and once to air (with the same exposure protocol), each pair of exposures separated by at least 3 weeks, in a randomized, double-blind fashion. Nasal lavage (NL) and bronchoalveolar lavage (BAL) were performed immediately after one ozone exposure and 18 hours after the other, and either immediately or 18 hours after the air exposure. Indicators of airway effects in lavage fluid included changes in inflammatory cells, proinflammatory cytokines, protein markers of epithelial injury and repair, and generation of toxic oxygen species. In the classification exposure, fewer smokers than nonsmokers were responsive to ozone (11.8% vs. 28.6%, respectively); an insufficient number of smoker-responders were identified to study as a separate group. In the BAL study, all groups developed a similar degree of airway inflammation, consisting of increases in interleukins 6 and 8 (maximal immediately after exposure), and increases in polymorphonuclear leukocytes (PMNs), lymphocytes, and mast cells (maximal 18 hours after exposure). The increase in PMNs was inversely correlated with age (p = 0.013), but gender, nonspecific airway responsiveness, and allergy history were not predictive of inflammation. Alveolar macrophage production of toxic oxygen species decreased after ozone exposure in nonsmokers; however, not in smokers. Findings from nasal lavage did not mirror lower airway inflammatory responses in these studies. We conclude that, in response to ozone exposure, smokers experienced smaller decrements in lung function and fewer symptoms than nonsmokers; however, the intensity of the airway inflammatory response was independent of smoking status or airway responsiveness to ozone. Furthermore, the burden of toxic oxygen species following ozone exposure was greater for smokers than for nonsmokers. Subjects were young, healthy, and able to sustain exercise; the results may not be representative of nonsmokers or smokers in general. Nevertheless, the findings indicate that measuring symptoms and spirometric changes is not sufficient to assess the potential risks associated with ozone exposure.

Adolescent↗
PubMed2001

Characterization of raw water for the ozone application measuring ozone consumption rate.

This study was conducted to illustrate an ideal method for characterizing natural waters for ozonation processes in drinking water treatment plants. A specific instrument designed with the flow injection analysis (FIA) technique enabled us to measure accurately the ozone decomposition rate, which was found to consist of two stages: the instantaneous ozone consumption stage and the slower ozone decay stage. The ozone consumption rate was measured at the initial and secondary stages by determining certain parameters called the instantaneous ozone demand (ID) and the pseudo first-order decay rate constant (k(c)). Using the OH*-probe, the yield of OH* per consumed ozone was also measured to determine its potential to produce OH* for the oxidation of micropollutants during the ozonation process. The ozone consumption of the ID values was significant in most natural waters, and substantial amounts of OH* were found to generate during the instantaneous ozone consumption stage. This study also investigated the effects of particulates, ozone doses, and sequential ozone injection on ozone decomposition kinetics and OH* formation yield.

Algorithms↗
PubMed2003

Impact of ozone mini-holes on the heterogeneous destruction of stratospheric ozone.

A comprehensive study of ozone mini-holes over the mid-latitudes of both hemispheres is presented, based on model simulations with the coupled climate-chemistry model ECHAM4.L39(DLR)/CHEM representing atmospheric conditions in 1960, 1980, 1990 and 2015. Ozone mini-holes are synoptic-scale regions of strongly reduced total ozone, directly associated with tropospheric weather systems. Mini-holes are supposed to have chemical and dynamical impacts on ozone levels. Since ozone levels over northern mid-latitudes show a negative trend of approximately -4%/decade and since it exists a negative correlation between total column ozone and erythemally active solar UV-radiation reaching the surface it is important to understand and assess the processes leading to the observed ozone decline. The simulated mini-hole events are validated with a mini-hole climatology based on daily ozone measurements with the TOMS (total ozone mapping spectrometer) instrument on the satellite Nimbus-7 between 1979 and 1993. Furthermore, possible trends in the event frequency and intensity over the simulation period are assessed. In the northern hemisphere the number of mini-hole events in early winter decreases between 1960 and 1990 and increases towards 2015. In the southern hemisphere a positive trend in mini-hole event frequency is detected between 1960 and 2015 in spring associated with the increasing Antarctic Ozone Hole. Finally, the impact of mini-holes on the stratospheric heterogeneous ozone chemistry is investigated. For this purpose, a computer-based detection routine for mini-holes was developed for the use in ECHAM4.L39(DLR)/CHEM. This method prevents polar stratospheric cloud formation and therefore heterogeneous ozone depletion inside mini-holes. Heterogeneous processes inside mini-holes amount to one third of heterogeneous ozone destruction in general over northern mid- and high-latitudes during winter (January-April) in the simulation.

Atmosphere↗
PubMedDate not supplied

Toxicology and carcinogenesis studies of ozone and ozone 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone in Fischer-344/N rats.

The purpose of this study was to evaluate the toxicity and potential carcinogenicity or cocarcinogenicity of ozone exposure in rats. Fischer-344/N (F-344/N) rats were exposed 6 hr/day, 5 days/wk, to 0, 0.12, 0.5, or 1.0 ppm ozone by inhalation for 2-yr and lifetime exposures. The cocarcinogenicity study included subcutaneous administration of 0, 0.1, or 1.0 mg/kg body weight of 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) and inhalation of 0 or 0.5 ppm ozone to male rats. NNK was administered by subcutaneous injections 3 times per week for the first 20 wk with ozone inhalation exposure. The ozone inhalation exposure was for 2 yr (104 wk), including the first 20 wk of NNK treatment and continuing for 84 wk after the last NNK injection. Ozone exposure caused a concentration-related increase in inflammation of the centriacinar region of the lung. There was also increased fibrosis and an extension of the bronchiolar epithelium in these centriacinar regions to involve the proximal alveoli. There was no increased incidence of neoplasms at any site, including the lung, that was associated with ozone exposure. Rats administered 1.0 mg/kg body weight NNK alone had an increased incidence of bronchiolar/alveolar neoplasms, but this effect was not enhanced by ozone exposure. Ozone exposure for 2 yr and lifetime was associated with site-specific toxic alterations in the nasal passage and lung similar to those previously described for short-term exposures. While there was significant attenuation of the pulmonary lesions as compared to short-term exposures, lesions persisted in the lifetime study and there was evidence of a mild progressive fibrosis. We conclude that under the conditions of these studies: (a) ozone exposure is not carcinogenic to either male or female F-344/N rats, (b) ozone does not enhance the incidence of pulmonary neoplasms in F-344/N rats exposed to a known pulmonary carcinogen (NNK), and (c) mild site-specific toxic lesions characteristic of ozone exposure persist in the nasal passage and lung throughout the lifetime of the rat with continued ozone exposure.

Administration, Inhalation↗
PubMed2003

A national ozone biomonitoring program--results from field surveys of ozone sensitive plants in northeastern forests (1994-2000).

Ozone biomonitoring is a detection and monitoring technique that involves documenting ozone-induced visible injury to known ozone-sensitive species under conditions of ambient exposure. The USDA Forest Service administers a long-term, nationwide ozone biomonitoring program to address public and scientific concerns about ozone impacts on forest health. A systematic grid is used as the basis for biomonitoring site locations. At each site, trained field crews evaluate a maximum of thirty plants of up to six species and record the amount and severity of leaf-injury on individual plants. Injury from ozone was found more often on biomonitoring sites in the eastern Unites States than in the interior or west-coast areas. Further results from the northeast reveal that in any year, there is a higher percentage of ozone-injured plants with more severe symptoms in areas with relatively high ozone concentrations than in areas with relatively low ozone. In very dry years (e.g., 1999) the percentage of injured plants and injury severity estimates are both sharply reduced even though ambient ozone exposures are high. These findings demonstrate that biomonitoring data provide meaningful evidence of when high ozone concentrations during the growing season have biological significance. Any assessment of ozone stress in the forest environment must include both biomonitoring (i.e., plant response) and air quality data to be complete.

Air Pollutants↗
PubMedDate not supplied

Longitudinal distribution of ozone absorption in the lung: effects of nitrogen dioxide, sulfur dioxide, and ozone exposures.

Investigators used an ozone bolus inhalation method to study the effects of continuous exposure to ozone, nitrogen dioxide, and sulfur dioxide on ozone absorption in the conducting airways of human lungs. Healthy, young nonsmokers (6 males, 6 females) were exposed on separate days for 2 h to air containing 0.36 ppm nitrogen dioxide, 0.75 ppm nitrogen dioxide, 0.36 ppm sulfur dioxide, or 0.36 ppm ozone. Every 30 min, the subject interrupted exposure for approximately 5 min, during which he or she orally inhaled five ozone boluses-each in a separate breath. Investigators targeted penetration of the boluses distal to the lips in the 70-130-ml range, which corresponded to the lower conducting airways. The authors computed the change in absorption resulting from exposure (delta lambda) by comparing the amount of each ozone bolus that was absorbed with a corresponding value obtained prior to exposure. Results indicated that ozone exposure caused delta lambda to decrease relative to air exposure (p < .01), whereas both nitrogen dioxide and sulfur dioxide exposures caused an increase in delta lambda that was not significantly different from air exposure. This resulted, at least in part, to an artifact caused by preexposure to ozone boluses. The authors concluded that exposure of the lower conducting airways to nitrogen dioxide or sulfur dioxide increased their capacity to absorb ozone because more of the biochemical substrates that are normally oxidized by ozone were made available. During continuous ozone exposure, this excess of substrate is depleted and the absorption of ozone boluses decreases.

Absorption↗
PubMed2001

The 1996 Paso del Norte Ozone Study: analysis of meteorological and air quality data that influence local ozone concentrations.

The 1996 Paso del Norte Ozone Study and subsequent data analyses were implemented to develop an understanding of the chemical and physical processes which lead to high concentrations of ozone in the Paso del Norte study area which includes El Paso County, Texas, Sunland Park, New Mexico, and Ciudad Juárez, Mexico. Both the data and data analysis results are being used to support photochemical grid modeling. El Paso County and Sunland Park fail to meet the National Ambient Air Quality Standard (NAAQS) for ozone, and neighboring Ciudad Juárez fails to meet the Mexican ambient standard for ozone. This paper summarizes the measurement campaigns of the 1996 Paso del Norte Ozone Study and the findings and conclusions that arose from subsequent data analyses. Data analyses showed that high ozone concentrations resulted from a combination of conditions, including high surface temperatures, strong sunlight with few clouds, light surface winds and high concentrations of ozone precursors at ground level in the morning, and slow convective boundary layer (CBL) growth. Synoptic-scale meteorological conditions observed during high ozone episodes included an aloft high-pressure system and aloft warming. Aloft carryover of ozone and ozone precursors did not significantly contribute to high concentrations of ozone at the surface.

Air Movements↗
PubMed1991

Noninvasive determination of respiratory ozone absorption: development of a fast-responding ozone analyzer.

We developed a chemiluminescent ozone analyzer and constructed an ozone bolus generator with the eventual goal of using a bolus-response method to measure noninvasively the longitudinal distribution of ozone absorption in human lungs. Because the analyzer will be used to sample gases within a single breath, it must have a sufficiently rapid response to monitor changes in ozone concentration during a four-second breathing period, yet its sampling flow must be small enough that it does not interfere with quiet respiratory flows of 300 mL/sec. Our analyzer, which is based on the chemiluminescent reaction between 2-methyl-2-butene and ozone, has favorable performance characteristics: a 90 percent step-response time of 110 msec; a linear calibration from 0.03 to 10 parts per million (ppm)2 with a sensitivity of 2.3 nA/ppm; a signal-to-noise ratio of 30 evaluated at 0.5 ppm; and a minimum detection limit of 0.017 ppm. At an airflow corresponding to quiet breathing, the ozone generator is capable of producing single boluses with a peak ozone fraction as high as 4 ppm, but containing only 0.35 micrograms of ozone dispersed over a small volume of 19 mL. To test the combination of ozone analyzer and bolus generator, we performed bolus-response experiments at steady airflows of 50 to 200 mL/sec in excised pig and sheep tracheas. In spite of the small surface area available for radial diffusion, we found that 25 to 50 percent of the ozone introduced into the trachea was absorbed. By comparing the mathematical moments of the bolus input and the response curves to the predictions of a diffusion theory, we computed an absorption coefficient (K). The values of K increased with increasing airflow, implying that ozone absorption is limited by diffusion processes in the airway lumen as well as in the surrounding tissue.

Absorption↗
PubMed1995

Reactive absorption of ozone by aqueous biomolecule solutions: implications for the role of sulfhydryl compounds as targets for ozone.

The rates of reactive absorption of ozone by various biomolecule solutions were measured. At pH 7, the ability of various biomolecules to reactively absorb ozone was in the following sequence: thiosulfate > ascorbate > cysteine approximately methionine > glutathione. The rates of reactive absorption under a variety of conditions were then analyzed using a mathematical model in order to estimate the reaction rate constants for the various ozone-biomolecule reactions. Compared to the ozone-methionine rate constant, the relative rate constants for thiosulfate, ascorbate, cysteine, and glutathione reactions were 18 +/- 2, 12 +/- 1, 1.1 +/- 0.1, and 0.62 +/- 0.03, respectively. Using an ozone-methionine reaction rate constant of 4 x 10(6) M-1 s-1, the rate constants for thiosulfate, ascorbate, cysteine, and glutathione were 7.2 x 10(7), 4.8 x 10(7), 4.4 x 10(6), and 2.5 x 10(6) M-1 s-1, respectively. Competitive studies using tryptophan as a standard ozone target were consistent with these rate constants. Compared to tryptophan, the relative ozone reaction rate constants for methionine, cysteine, and glutathione were 0.77 +/- 0.08, 0.88 +/- 0.19, and 0.42 +/- 0.01, respectively. These relative rate constants refer to ozone consumption rather than biomolecule consumption, so they may be compared with the relative rate constants obtained from reactive absorption. In addition, various inconsistencies in the literature regarding the rates of the ozone-cysteine and the ozone-glutathione reactions were reviewed.

Absorption↗
PubMedDate not supplied

Upregulation of phosphoinositide 3-kinase and protein kinase B in alveolar macrophages following ozone inhalation. Role of NF-kappaB and STAT-1 in ozone-induced nitric oxide production and toxicity.

Inhalation of toxic doses of ozone causes lung injury and inflammation in humans and experimental animals. Using a rodent model of ozone toxicity, we have previously demonstrated that macrophages recruited to the lung following exposure to this oxidant contribute to the pathogenesis of tissue injury. In the present studies we analyzed potential mechanisms regulating alveolar macrophage activity following ozone inhalation and the role of inflammatory mediators in toxicity. Treatment of mice with ozone (0.8 ppm, 3 h) resulted in increased expression of inducible nitric oxide synthase (iNOS) protein and production of nitric oxide (NO) and peroxynitrite by alveolar macrophages. In contrast, these effects were not observed in macrophages from transgenic mice with a targeted disruption of the gene for iNOS, or in mice overexpressing superoxide dismutase. Moreover, ozone toxicity, as measured by bronchoalveolar lavage protein levels and nitrotyrosine staining of the lung was prevented in both of these transgenic mouse strains. The promoter/enhancer region of the iNOS gene contains binding sites for the transcription factors NF-kappaB and STAT-1 which regulate the activity of the gene. Ozone inhalation resulted in a rapid and prolonged activation of NF-kappaB in alveolar macrophages. Phosphoinositide 3-kinase (PI 3-K) and its down stream target, protein kinase B (PKB), which are known to regulate NF-kappaB activity, also increased in alveolar macrophages following ozone inhalation. These data, together with our findings that inhibitors of PI 3-K block NO production, suggest that these proteins are important in controlling expression of iNOS. Furthermore, the fact that macrophages from NF-kappaB p50 knockout mice did not generate reactive nitrogen intermediates and that these mice were protected from ozone induced toxicity demonstrate the importance of the NF-kappaB signaling pathway in lung injury. We also found that STAT-1 nuclear binding activity and STAT-1 protein expression were upregulated in macrophages from ozone treated animals. Taken together, these data suggest that biochemical signaling pathways that control the expression of genes critical for the inflammatory process play a role in ozone toxicity.

Administration, Inhalation↗
PubMedDate not supplied

Initial field evaluation of the Harvard active ozone sampler for personal ozone monitoring.

Assessing personal exposure to ozone has only been feasible recently with the introduction of passive ozone samplers. These devices are easy to use, but changes in air velocity across their collection surfaces can affect performance. The Harvard active ozone sampler (AS) was developed in response to problems with the passive methods. This active sampler has been tested extensively as a microenvironmental sampler. To test for personal sampling, 40 children attending summer day-camp in Riverside, California wore the active ozone sampler for approximately 2.6 h on July 19 and 21, 1994, when ozone concentrations were about 100 ppb and 140 ppb, respectively. The children spent 94-100% of the sampling period outside, staying within a well-defined area while participating in normal camp activities. Ambient ozone concentrations across this area were monitored by two UV photometric ozone monitors. The active sampler was worn in a small backpack that was also equipped with a passive ozone sampler. Device precision, reported as the percent difference between duplicate pairs of samplers, was +/- 3.7% and +/- 4.2% for the active and passive samplers, respectively. The active sampler measured, on average, 94.5 +/- 8.2% of the ambient ozone while the passive samplers measured, on average, 124.5 +/- 18.8%. The samplers were worn successfully for the entire sampling period by all participating children.

Air Pollutants↗
PubMed2002

Forecasting peak daily ozone levels--I. A regression with time series errors model having a principal component trigger to fit 1991 ozone levels.

This research was motivated by the need to warn the population of Milwaukee, WI, on high-ozone days. A statistical model for the peak daily 1-hr ozone level is proposed. A Regression with Time Series Errors (RTSE) model, which includes a principal component (PC) trigger, is the basis for forecasting the peak daily 1-hr ozone level. The RTSE model, with a PC trigger, is first employed to estimate daily peak ozone measured at the University of Wisconsin, Milwaukee-North (UWM-N), during the 1991 ozone season. The RTSE model uses peak daily temperature, morning vector average wind direction, and the PC trigger as predictor variables. The PC trigger was designed to summarize atmospheric circumstances when peak ozone was greater than 100 parts per billion (ppb). It is verified that the RTSE model, with a PC trigger, significantly improves the prediction of peak daily ozone, particularly peak ozone greater than 100 ppb. In comparison with the RTSE model without the PC trigger, the RTSE model with a PC trigger raised the R2 from 0.680 to 0.809. It is suggested that the RTSE model, with the PC trigger, is an adequate statistical model that has the potential for real-time ozone forecasting.

Air Pollutants↗
PubMed1983

Preexposure to low ozone concentrations does not diminish the pulmonary function response on exposure to higher ozone concentrations.

To determine whether persons repeatedly exposed to low ozone concentrations would demonstrate a diminished responsivity, as a result of adaptation or desensitization, when subsequently exposed to a higher ozone concentration, we performed the following study. Respiratory sensitivity (pulmonary function response) to 2 h of exposure to 0.42 or 0.50 ppm ozone (acute exposure) was determined 3 months before or 6 to 8 wk after the study. Twenty-one subjects (8 men, 13 women) were exposed for 2 h or 5 consecutive days to filtered air, 0.20, 0.20, 0.20, and 0.42 to 0.50 ppm ozone, respectively. There were no significant differences between the responses of men and women to ozone. Subjects were divided into a sensitive group (greater than 20% drop in FEV1) and a nonsensitive group (less than 10% drop in FEV1) on the basis of their responses to the acute exposure. Neither the overall group nor the nonsensitive group showed a significant response to 0.20 ppm. Sensitive subjects (n = 9) showed small but significant decreases in FEV1 on exposure to 0.20 ppm. The predominant finding was that the 3 days of preexposure to 0.20 ppm ozone had no effect on the response to 0.42 or 0.50 ppm ozone on the fourth day (when compared with the previous acute exposure to 0.42 or 0.50 ppm). We conclude that subjects repeatedly (3 times) exposed to a low (0.20 ppm) concentration of ozone do not demonstrate a pulmonary function adaptation or desensitization on a subsequent exposure to a higher (0.42 or 0.50 ppm) ozone concentration.

Adaptation, Physiological↗
PubMed1995

The cascade mechanism to explain ozone toxicity: the role of lipid ozonation products.

Ozone is so reactive that it can be predicted to be entirely consumed as it passes through the first layer of tissue it contacts at the lung/air interface. This layer includes the lung lining fluid (tracheobronchial surface fluid and alveolar and small airway lining fluid) and, where the lung lining fluid is thin or absent, the membranes of the epithelial cells that line the airways. Therefore, the biochemical changes that follow the inhalation of ozone must be relayed into deeper tissue strat by a cascade of ozonation products. Lipid ozonation products (LOP) are suggested to be the most likely species to act as signal transduction molecules. This is because unsaturated fatty acids are present in the lipids in both the lung lining fluid and in pulmonary cell bilayers, and ozone reacts with unsaturated fatty acids to produce ozone-specific products. Further, lipid ozonation products are finite in number, have structures that are predictable from the Criegee ozonation mechanism, and are small, diffusible, stable (or metastable) molecules. Preliminary data show that individual LOP cause the activation of specific lipases, which trigger the release of endogenous mediators of inflammation.

Animals↗
PubMed2001

Ozone predictions in Atlanta, Georgia: analysis of the 1999 ozone season.

Ozone prediction has become an important activity in many U.S. ozone nonattainment areas. In this study, we describe the ozone prediction program in the Atlanta metropolitan area and analyze the performance of this program during the 1999 ozone-forecasting season. From May to September, a team of 10 air quality regulators, meteorologists, and atmospheric scientists made a daily prediction of the next-day maximum 8-hr average ozone concentration. The daily forecast was made aided by two linear regression models, a 3-dimensional air quality model, and the no-skill ozone persistence model. The team's performance is compared with the numerical models using several numerical indicators. Our analysis indicated that (1) the team correctly predicted next-day peak ozone concentrations 84% of the time, (2) the two linear regression models had a better performance than a 3-dimensional air quality model, (3) persistence was a strong predictor of ozone concentrations with a performance of 78%, and (4) about half of the team's wrong predictions could be prevented with improved meteorological predictions.

Air Pollution↗
PubMed1998

Relationship of inhaled ozone concentration to acute tracheobronchial epithelial injury, site-specific ozone dose, and glutathione depletion in rhesus monkeys.

Acute pulmonary epithelial injury produced by short-term exposure to ozone varies by site within the tracheobronchial tree. To test whether this variability is related to the local dose of ozone at the tissue site or to local concentrations of glutathione, we exposed adult male rhesus monkeys for 2 h to filtered air or to 0.4 or 1.0 ppm ozone generated from 18O2. Following exposure, lungs were split into lobes and specimens were selected by microdissection so that measurements could be made on airway tissue of similar branching history, including trachea, proximal (generation one or two) and distal (generation six or seven) intrapulmonary bronchi, and proximal respiratory bronchioles. One half of the lung was lavaged for analysis of extracellular components. In monkeys exposed to filtered air, the concentration of reduced glutathione (GSH) varied throughout the airway tree, with the proximal intrapulmonary bronchus having the lowest concentration and the parenchyma having the highest concentration. Exposure to 1.0 ppm ozone significantly reduced GSH only in the respiratory bronchiole, whereas exposure to 0.4 ppm increased GSH only in the proximal intrapulmonary bronchus. Local ozone dose (measured as excess 18O) varied by as much as a factor of three in different airways of monkeys exposed to 1.0 ppm, with respiratory bronchioles having the highest concentration and the parenchyma the lowest concentration. In monkeys exposed to 0.4 ppm, the ozone dose was 60% to 70% less than in the same site in monkeys exposed to 1.0 ppm. Epithelial disruption was present to some degree in all airway sites, but not in the parenchyma, in animals exposed to 1.0 ppm ozone. The mass of mucous and ciliated cells decreased in all airways, and necrotic and inflammatory cells increased. At 0.4 ppm, epithelial injury was minimal, except in the respiratory bronchiole, where cell loss and necrosis occurred, and was 50% that found in monkeys exposed to 1.0 ppm ozone. We conclude that there is a close association between site-specific O3 dose, the degree of epithelial injury, and glutathione depletion at local sites in the tracheobronchial tree.

Animals↗