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PubMed2006

The effect of exercise on nasal uptake of ozone in healthy human adults.

The nose may help protect the lower respiratory tract from the effects of ambient ozone by scrubbing ozone from inspired air. Reductions in both nasal resistance and nitric oxide production with exercise may influence the efficiency of ozone uptake in the nose. Nasal ozone uptake was measured in 10 healthy volunteers before and after 15 min of moderate bicycle exercise. Ozone (0.2 parts/million) was pulled through both nostrils and out of the mouth at a constant flow while the subjects closed their epiglottises. Nasal uptake of ozone was determined by comparing the ozone concentration entering the nostrils to that exiting the mouth. Average preexercise uptake of ozone was 56 +/- 7.8 and 37 +/- 4.9% at 10 and 20 l/min, respectively. These averages did not significantly differ from those immediately postexercise (55 and 37%). Nasal ozone uptake increased significantly (P < 0.001) with decreasing flow rate, but intersubject variability in uptake could not be predicted by nasal volume or cross-sectional areas (as measured by acoustic rhinometry) or endogenous nitric oxide production. However, the percent change in ozone uptake after exercise, within an individual, was correlated with both 1) percent change in nasal volume (r = 0.70 at 10 l/min) and 2) percent change in the rate of volumetric expansion between the nasal valve and turbinates (r = 0.82 at 10 l/min). These results may be useful for assessing human risk associated with ozone exposure during exercise.

Adaptation, Physiological↗
PubMedDate not supplied

Neuronal nitric oxide synthase is associated with airway obstruction in BALB/c mice exposed to ozone.

BACKGROUND: The functional role of nitric oxide (NO) and the various nitric oxide synthase (NOS) isoforms in asthma is controversial. OBJECTIVE: To investigate the role of NO in mice exposed to ozone, three known isoforms of NOS [inducible NOS (iNOS), neuronal NOS (nNOS), and endothelial NOS (eNOS)] were studied. METHODS: The expression of iNOS, nNOS, and eNOS was determined in lung by Western blot analysis after exposure to filtered air and ozone (0.12, 0.5, 1 or 2 ppm) for 3 h. Using barometric whole-body plethysmography and increase in enhanced pause (P(enh)) as an index of airway obstruction, we measured airway responses to ozone exposure. Bronchoalveolar lavage (BAL) was performed. Nitrate and nitrite were measured using a modified Griess reaction. RESULTS: The nitrate concentration in BAL fluid, which indicates the in vivo generation of NO in airways, from the ozone-exposed group was significantly greater than that from the group exposed to filtered air (631.0 +/- 86.4 vs. 152.1 +/- 16.9 micromol/l, p < 0.05). The nitrate concentration in BAL fluid was increased more in mice exposed to 2-ppm ozone than that in mice exposed to filtered air or 0.12-, 0.5-, or 1-ppm ozone. Increases in P(enh) after exposure to ozone or filtered air were significantly higher in the ozone-exposed groups than in the group exposed to filtered air (p < 0.01). Increases in P(enh) were dependent on the ozone concentration. Although the protein levels of eNOS and iNOS determined were within normal levels, the amount of nNOS protein was markedly elevated in airway tissue homogenates of the group exposed to 2-ppm ozone. CONCLUSION: These findings demonstrate that the nNOS isoform may be involved in airway obstruction in mice exposed to ozone.

Airway Obstruction↗
PubMed1993

Effects of ozone and neutrophils on function and morphology of the isolated rat lung.

Since whole-animal studies suggest that neutrophils play a role in ozone-induced impairment of pulmonary function and increases in airway reactivity, this study was designed to study more precisely the interaction of neutrophils and ozone using the isolated perfused rat lung. Sprague-Dawley rat lungs (n = 60) were ventilated for 3 h with 95% air and 5% CO2 alone or mixed with 1 ppm ozone and perfused with buffer alone or with neutrophils (8 x 10(7)). RL, Cdyn, Ppa, airway reactivity to methacholine, lung/body weight, bronchoalveolar lavage fluid (BALF) protein concentration, and airway lesions were analyzed using a two-way GLM or Kruskal-Wallis test (p < or = 0.05 significant). Both ozone and neutrophils increased RL and decreased Cdyn. Ozone but not neutrophils increased airway reactivity to methacholine. Neutrophils but not ozone increased lung weight/body weight and BALF protein concentration. Ozone damaged airway epithelium. In distal bronchioles, neutrophils enhanced this damage. We conclude that (1) ozone impaired pulmonary function, increased airway reactivity, and damaged airway epithelium without causing measurable microvascular leak; (2) neutrophils impaired pulmonary function, probably a result of microvascular leak, but did not change airway reactivity or damage airway epithelium; and (3) neutrophils had no effect on ozone-induced airway reactivity but had an additive effect on ozone-induced pulmonary function impairment and a synergistic effect on ozone-induced airway epithelial injury.

Animals↗
PubMed1981

Threshold concentration of ozone causing an increase in bronchial reactivity in humans and adaptation with repeated exposures.

To determine the lowest concentration of ozone that causes an increase in bronchial reactivity to histamine and to determine whether adaptation to this effect of ozone develops with repeated exposures, we studied 19 healthy adult subjects. Bronchial reactivity was assessed by measuring the rise in specific airway resistance (delta SRaw) produced by inhalation of 10 breaths of histamine aerosol (1.6% solution). In 5 subjects, bronchial reactivity was determined at 9:00 and 11:30 A.M. on 4 consecutive days without exposure to ozone (Group I). In 7 other subjects (Group II), bronchial reactivity was assessed at 9:00 and 11:30 A.M. on 3 consecutive days, and subjects were exposed to 0.2 ppm of ozone from 9:30 to 11:30 A.M. on the third day. Seven additional subjects (Group III) had bronchial reactivity assessed in a similar fashion for 2 days and then again on 3 consecutive days of 2-h exposures to 0.4 ppm of ozone. Pre-exposure bronchial reactivity of the groups was the same, and no change in bronchial reactivity occurred in the group tested repeatedly but not exposed to ozone. An increase in delta SRaw provoked by histamine was noted after the first exposure to 0.4 ppm but not to 0.2 ppm of ozone (p less than 0.025). With 3 repeated 2-h exposures to 0.4 ppm on consecutive days, however, the delta SRaw produced by histamine progressively decreased, returning to pre-exposure values after the third exposure. Our results indicate that the threshold concentration of ozone causing an increase in bronchial reactivity in healthy human subjects is between 0.2 and 0.4 ppm, and that adaptation to this effect of ozone develops with repeated exposures. The threshold concentration of ozone identified in other studies as causing changes in symptoms, lung volumes, or airway resistance was also between 0.2 and 0.4 ppm, and the time course of the development of tolerance to ozone in these other studies was similar to hat observed in our study. We propose that the appearance of symptoms, changes in pulmonary function, and the increase in bronchial reactivity may be caused by a change in the activity of afferent nerve endings in the airway epithelium.

Adaptation, Physiological↗
PubMed1991

[Changes of procoagulant and fibrinolytic activities in the alveoli of rats exposed to ozone].

The purpose of this study was to evaluate the role of ozone, a reactive product of environmental photochemical oxidation, in the development of pulmonary fibrosis. Male Wistar rats were exposed continuously to 0.5 ppm ozone for 1,4,7 and 14 days, and alveolar macrophages and lavage fluid obtained by bronchoalveolar lavage were examined. The results were as follows: 1) The total protein content in the lavage fluid was significantly increased compared to the control at 1 to 7 days by ozone exposure. Both alveolar macrophage and neutrophil counts increased in response to ozone exposure. However, approximately 90% of the free cells recovered were alveolar macrophages throughout the exposure period. 2) The plasminogen activator (PA) activity released from alveolar macrophages did not change in the group exposed for 1 day. But the activities were significantly high in the groups exposed for 4 to 14 days. 3) The PA activity of the lavage fluid showed a marked increase on the 1st day of ozone exposure, and subsequently decreased rapidly. However, the significantly increased activity was maintained throughout the exposure period. 4) In contrast, the procoagulant (PC) activity was unchanged on the 1st day of ozone exposure but the activity increased significantly on the 4th day, and was maintained at a high level until the 14th day. 5) The elastase inhibitory capacity (EIC) of the lavage fluid was significantly increased compared to the control by ozone exposure, but this difference was not seen throughout the exposure period when the EIC was corrected for the total protein content in the lavage fluid. These results revealed that both PA and PC activities increased in the alveolar fluid of rats exposed to 0.5 ppm ozone. The transition in the respective activities suggested that the fibrinolytic pathway in the alveoli was enhanced early in the exposure to ozone, while the coagulation pathway was enhanced later. This imbalance in coagulation homeostasis may be important in the regulation of fibrotic responses in the lungs of rats exposed to ozone. These findings are in agreement with morphological reports indicating that ozone exposure initially damaged the alveoli and later caused pulmonary fibrosis.

Animals↗
PubMed1979

Asthma and respiratory irritants (ozone).

Asthmatics appear to be more susceptible to the effects of air pollutants than nonasthmatics. The present studies were undertaken to examine the effects of exposing asthmatics to ozone concentrations that occur in the environment. Seventeen well-documented male and female asthmatics have been exposed for 2 hr in an environmental chamber to 0.25 ppm of ozone on one occasion (ozone) and to air on another occasion (air). Effects were assessed by measurements of pulmonary function obtained prior to (0 hr), every half-hour during and at the end of all exposures (2 hr). Paired t-test analysis of lung volumes, forced expiratory volume in 1 sec (FEV1.0), and maximum expiratory flow rates at 50% of vital capacity (V50%VC) showed no significant changes (p greater than 0.05) when the following comparisons were made: 0 hr air vs 0 hr ozone, 0 hr air vs. 2 hr air, 0 hr ozone vs. 2 hr ozone, 2 hr air vs. 2 hr ozone. There was variability in severity of asthma and pulmonary function status; most subjects were taking some form of medication at the time of study. Some asthmatics showed no change or improvement with both air and ozone and others developed greater reductions in pulmonary function with ozone than with air. Approximately one-third of the asthmatics demonstrated greater changes in V50%VC with exposure to 0.25 ppm of ozone relative to air exposure. These studies indicate that acute exposures to ozone at realistic concentrations in the environment can produce adverse responses in some asthmatics.

Adult↗
PubMedDate not supplied

Toxicity of ozonated animal manure to the house fly, Musca domestica.

Swine manure slurries were ozonated at a dosage of 1 g/L and tested for their toxicity to the house fly (Musca domestica). The observed toxicity of ozonated swine manure was consistent and independent of origin of the swine manure. A dose (dilution) response curve was performed. A 50% dilution in the ozonated swine manure slurry resulted in 90% reduction in toxicity. Neither the synthetic nor ozonated synthetic swine manure, both of which contained higher concentrations of formaldehyde and three other unidentified carbonyl compounds than the ozonated swine manure, were toxic to the flies. Ozonated swine manure slurry was centrifuged and passed through a 0.45-microm filter. The liquid phase was as toxic as the unfiltered slurry; as such, the toxicant appears to be present in liquid phase. Neither ammonia, hydrogen sulfide, formaldehyde, nor other simple aldehydes appeared to be the toxic agent. The toxic agent appears to be a polar chemical compound and is concentrated in the urine. Several possible compounds have been identified. The toxicity of untreated and ozonated manure slurries from different livestock was compared. Six animal manure slurries (beef and dairy cattle, horse, poultry, sheep, and swine) were ozonated (dosage of 1 g/L) and tested for toxicity to the house fly. Ozonated dairy cattle manure slurry showed 78% mortality after 72 h, whereas ozonated swine manure slurry achieved a 100% mortality rate in 48 h. Neither the unozonated dairy nor swine manure slurries, nor any of the other raw or ozonated manure slurries, were toxic to the flies.

Animals↗
PubMedDate not supplied

Taurine protects rat bronchioles from acute ozone exposure: a freeze fracture and electron microscopic study.

Dietary taurine has been shown to protect rat and hamster lung epithelia from acute oxidant injury. One of the earliest morphologic criteria of oxidant injury is the alteration of tight junctions of the peripheral lung airways. In the present study, we have used this criteria to evaluate whether taurine was capable of protecting rat lungs from ozone exposure. Rats were treated for 10 days with 50% taurine in their drinking water, prior to exposure to 2 ppm of ozone for 3 hours. The lungs from rats pretreated with taurine and exposed to ozone were compared to untreated rats exposed to ozone and air-exposed controls. At 2, 6, 12, 24, 48, and 72 hours after exposure to air or ozone, rats were anesthetized and the lungs perfusion-fixed through the right side of the heart with a solution of glutaraldehyde and paraformaldehyde. Light microscopy revealed the typical, mild inflammatory cell infiltrate beginning at 6 hours after ozone exposure in bronchioles, alveolar ducts, and surrounding alveoli which was absent in the lungs of animals treated with taurine. Electron microscopic analysis of thin sections indicated alterations in tight junctions which was confirmed by tracer studies using ruthenium red and lanthanum. Alterations in airway epithelium tight junctions were seen 2 and 6 hours after ozone treatment and only in the 2-hour tissues from animals pretreated with taurine prior to ozone exposure. Freeze-fracture replicas from all exposure groups by electron microscopy revealed that only the 2- and 6-hour groups showed alterations in tight junctions. The alterations were characterized by decreased number of fibrils and breaks in the fibrils. Rats treated with taurine and exposed to ozone exhibited these alterations focally at 2 hours exposure and no changes were noted at 6 hours post ozone exposure. These data confirmed previous findings that injury induced by ozone is transient and that taurine protects the bronchioles from this form of oxidant injury.

Animals↗
PubMed1999

Application of ozone for enhancing the microbiological safety and quality of foods: a review.

Ozone (O3) is a strong antimicrobial agent with numerous potential applications in the food industry. High reactivity, penetrability, and spontaneous decomposition to a nontoxic product (i.e., O2) make ozone a viable disinfectant for ensuring the microbiological safety of food products. Ozone has been used for decades in many countries and recently, the generally recognized as safe (GRAS) status of this gas has been reaffirmed in the United States. Ozone, in the gaseous or aqueous phases, is effective against the majority of microorganisms tested by numerous research groups. Relatively low concentrations of ozone and short contact time are sufficient to inactivate bacteria, molds, yeasts, parasites, and viruses. However, rates of inactivation are greater in ozone demand-free systems than when the medium contains oxidizable organic substances. Susceptibility of microorganisms to ozone also varies with the physiological state of the culture, pH of the medium, temperature, humidity, and presence of additives (e.g., acids, surfactants, and sugars). Ozone applications in the food industry are mostly related to decontamination of product surface and water treatment. Ozone has been used with mixed success to inactivate contaminant microflora on meat, poultry, eggs, fish, fruits, vegetables, and dry foods. The gas also is useful in detoxification and elimination of mycotoxins and pesticide residues from some agricultural products. Excessive use of ozone, however, may cause oxidation of some ingredients on food surface. This usually results in discoloration and deterioration of food flavor. Additional research is needed to elucidate the kinetics and mechanisms of microbial inactivation by ozone and to optimize its use in food applications.

Bacteria↗
PubMed2000

Bactericidal properties of ozone and its potential application as a terminal disinfectant.

The efficacy of ozone as a terminal disinfectant was evaluated under laboratory conditions. Different microorganisms of importance to the food industry were inoculated onto stainless steel squares and incubated at various temperatures and relative humidities for up to 4 h. Survival of microorganisms from these controls was compared with identically incubated squares exposed to ozone. Exposure of the contaminated surfaces to ozone (2 ppm for 4 h) resulted in a reduction in microbial viability that ranged, depending on organism type, from 7.56 to 2.41 log values. For all the microorganisms tested, this loss in viability was significantly greater (P < 0.05) than that observed in the absence of ozone. Gram-negative bacteria were more sensitive to ozone than gram-positive organisms; bacteria were more sensitive than the yeast strain tested. Exposure to ozone (2 ppm for 4 h) in the presence of ultra-high temperature (UHT) milk resulted in a reduction in bacterial viability that ranged from 5.64 to 1.65 log values. In most cases, this reduction was significantly less (P < 0.05) than that achieved in the absence of organic material, although still significantly greater (P < 0.05) than that observed in the absence of ozone. The presence of a meat-based broth reduced the effectiveness of ozone to a greater extent, although the number of surviving gram-negative organisms was still significantly less (P < 0.05) than in the absence of ozone. Less than 1 log unit of yeast cells was destroyed when exposed to ozone in the presence of UHT milk or meat-based broth. Results of this investigation suggest that if applied after adequate cleaning ozone could be used as an effective disinfectant.

Animals↗
PubMed2006

Effect of ozonated water treatment on microbial control and on browning of iceberg lettuce (Lactuca sativa L.).

We examined the effect of ozonated water treatment on microbial control and quality of cut iceberg lettuce (Lactuca sativa L.). Fresh-cut lettuce was washed in ozonated water (3, 5, and 10 ppm) for 5 min at ambient temperature. The native bacterial population on the lettuce declined in response to a rise in ozone concentration. However, there was no further bacterial reduction (1.4 log CFU/g) above 5 ppm ozone. Although ozonated water treatment increased the phenylalanine ammonia lyase (PAL) activity of the lettuce stored at 10 degrees C compared with the water wash treatment after 1 day of storage, the concentration of ozone did not affect PAL activity. The a* value of the residue of the lettuce methanol extracts, which reflects the extent of browning, increased dramatically in lettuce treated with 10 ppm ozonated water compared with other treatments. Treatment with 3 or 5 ppm ozonated water resulted in more rapid changes in the a* value than after the water treatment. The combined treatment of hot water (50 degrees C, 2.5 min) followed by ozonated water (5 ppm, 2.5 min) had the same bactericidal effect as treatment with ozonated water (5 ppm, 5 min) or sodium hypochlorite (NaOCl, 200 ppm, 5 min), giving a reduction in bacteria numbers of 1.2 to 1.4 log CFU/g. The ascorbic acid content of the lettuce was not affected by these treatments. The combined treatment of hot water followed by ozonated water greatly inhibited PAL activity for up to 3 days of storage at 10 degrees C. Treatment with this combination greatly suppressed increases in the a* value, thus retarding the progress of browning compared with other treatments throughout the 6-day storage. NaOCl treatment also inhibited browning for up to 3 days of storage. Bacterial populations on the lettuce treated with sanitizers were initially reduced but then showed rapid growth compared with that of the water wash treatment, which did not reduce bacterial counts initially.

Consumer Product Safety↗
PubMed2002

Ozone-induced modulation of airway hyperresponsiveness in guinea pigs.

Although acute exposure to ozone (03*) has been shown to influence the severity and prevalence of airway hyperresponsiveness, information has been lacking on effects due to long-term exposure at relatively low exposure concentrations. The goals of this study were to determine whether long-term repeated ozone exposures could induce nonspecific hyperresponsiveness in normal, nonatopic (nonsensitized) animals, whether such exposure could exacerbate the preexisting hyperresponsive state in atopic (sensitized) animals, or both. The study was also designed to determine whether gender modulated airway responsiveness related to ozone exposure. Airway responsiveness was measured during and after exposure to 0.1 and 0.3 ppm ozone for 4 hours/day, 4 days/week for 24 weeks in normal, nonsensitized guinea pigs, in guinea pigs sensitized to an allergen (ovalbumin) prior to initiation of ozone exposures, and in animals sensitized concurrently with ozone exposures. Both male and female animals were studied. Ozone exposure did not produce airway hyperresponsiveness in nonsensitized animals. Ozone exposure did exacerbate airway hyperresponsiveness to specific and nonspecific bronchoprovocation in both groups of sensitized animals, and this effect persisted at least 4 weeks after the end of the exposures. Although the overall degree of airway responsiveness did differ between genders (males had more responsive airways than did females), the airway response to ozone exposure did not differ between the two groups. Ozone-induced effects upon airway responsiveness were not associated with the number of pulmonary eosinophils or with any chronic pulmonary inflammatory response. Levels of antigen-specific antibodies increased in sensitized animals, and a significant correlation was observed between airway responsiveness and antibody levels. The results of this study provide support for a role of ambient ozone exposure in exacerbation of airway dysfunction in persons with atopy.

Acute Disease↗
PubMed2004

The tropospheric ozone problem.

Derived from measurements it has been concluded that in the last hundred years the ground-based ozone concentration has risen by about a factor of two. Models also show a doubling of the tropospheric ozone content due to human activities. It is very likely that mean ozone concentration will further increase. In contrast, episodes with excess ozone levels ("summer smog") have become rare in Central Europe during the last five years. This controversial finding is explained by the reduction of NOx (being the "catalyst" in ozone formation) as well as of reactive ozone precursors like non-methane volatile organic compounds (NMVOC) due to catalytic converters in motor cars. On the other hand, a further increase of methane emissions and probably carbon monoxide is responsible for regional and even global background increase of ozone. The principal formation mechanisms are well understood, despite some open questions concerning the contribution of specified organic substances, especially from biogenic sources. Less known, however, are chemical sinks, especially heterogeneous processes. A better knowledge of these processes may influence the global ozone budget by up to 30% and the regional/local even more. The key question considering ozone abatement is that for determining precursors in time and space. Air quality control has also to consider the question of ozone impact on vegetation, animals and man. Moreover, ozone also contributes to the greenhouse effect. Air pollution control, based on ecological and economic principles, needs a complex understanding of the atmosphere and its interaction with the biosphere. Measures should not be focused on single pollutants, but on impacts, which always have complex causes. Only quantified impacts with consequences unaccepted by society may be a problem.

Oxidants, Photochemical↗
PubMed1991

Leukocyte-mediated epithelial injury in ozone-exposed rat lung.

Both epithelial injury and inflammation are characteristic findings in the centriacinar regions of the lungs of rats exposed to ozone. In humans such effects could lead to long-term lung damage and disease. In animals, neoplastic change in the lungs after exposure to ozone has been described previously. The possible relationships between inflammatory cell recruitment, epithelial injury, and hyperplasia, with special regard to the important role of repair processes in leading to increased incidence of tumors in some species, have been addressed in the present study. We have previously described that leukocytes from lungs inflamed by different agents can injure epithelial cells in vitro. We have suggested that this leukocyte-mediated epithelial injury could enhance epithelial turnover in ozone-exposed lungs and so enhance the likelihood of tumor development. We, therefore, set out to test the hypothesis that bronchoalveolar leukocytes from ozone-exposed lungs can injure epithelial cells in vitro. PVG rats were exposed to 0.2, 0.4, 0.6, and 0.8 parts per million2 (ppm) ozone for seven hours per day for up to four days. On the morning following the last exposure, bronchoalveolar lavage was used to sample the bronchoalveolar leukocytes and the following parameters were assessed: total number, differential leukocyte count, production of oxidants, ability to degrade fibronectin, and ability to injure epithelial cells. In addition to these parameters, which were measured at all concentrations and time points in limited experiments, we also assessed macrophage size in short-term culture and inflammation in histological sections of lungs. Total number of lavageable cells was not affected by ozone inhalation. However, the percentage of macrophages decreased with ozone treatment and the percentage of neutrophils increased on days 1 and 2 at 0.6 and 0.8 ppm ozone. There was no significant effect of ozone exposure on the ability of neutrophils to degrade fibronectin or injure epithelial cells. Production of superoxide anion in response to stimulation with phorbol myristate acetate was significantly decreased by exposure to 0.6 ppm ozone, as described in previous studies. Macrophages from the lungs of rats exposed to ozone were larger than control macrophages.

Animals↗
PubMed1994

Consequences of prolonged inhalation of ozone on Fischer-344/N rats: collaborative studies. Part II: Mechanical properties, responses to bronchoactive stimuli, and eicosanoid release in isolated large and small airways.

Acute exposure to ozone has been shown to have deleterious effects on pulmonary function in normal humans and in all animal species studied to date. The goal of this study was to determine whether near-lifetime exposure to ozone alters the mechanical properties, the pharmacologic responses, or both, of airways isolated from F344/N rats, and to relate these properties to airway wall structure. Segments from approximately fourth-generation airways (representing large airways) and eighth-generation airways (representing small airways) were isolated from rats of both genders that had been exposed for six hours per day, five days per week to 0, 0.12, 0.5, or 1.0 parts per million (ppm)* ozone for 20 months. Using in vitro techniques, the airways were mounted on myographs and several parameters of airway function were evaluated. These included relationships between (1) passive tension and internal circumference of the airways, (2) active tension and internal circumference of the airways, and (3) responses of the airways to bronchoactive stimuli. The effects on these relationships of epithelial damage caused by lumenal abrasion of selected airway segments also were evaluated. Wall and smooth muscle areas were measured in these airways, and responses obtained from mechanical and pharmacologic studies were related to these morphological parameters. Eicosanoid levels were measured in media surrounding airway explants to determine whether near-lifetime exposure to ozone alters production of these important modulators of airway function. The relation between passive tension and internal circumference found in large and small airways was exponential in nature and unaffected by ozone exposure. The relation between active tension and internal circumference of isolated airways produced a curve characterized by active tension that increased with increasing circumference. This result reached a maximum and then decreased as the circumference increased further. The curve describing this relationship did not change after ozone exposure. The maximum effect was evident at the same point on each airway's passive tension and internal circumference relationship. Wall and smooth muscle areas measured in large airways were not affected by ozone exposure. The wall area increased, however, in small airways isolated from males after exposure to 0.5 ppm ozone. In addition, smooth muscle area increased in small airways isolated from rats exposed to 0.5 ppm ozone; this effect of ozone did not vary with gender. No differences in maximum active stress (active tension normalized to smooth muscle area) were detected in large airways after ozone exposure.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Oxidant and acid aerosol exposure in healthy subjects and subjects with asthma. Part II: Effects of sequential sulfuric acid and ozone exposures on the pulmonary function of healthy subjects and subjects with asthma.

These studies were undertaken to evaluate pulmonary responses of humans sequentially exposed to acidic aerosols and ozone at levels that could reasonably be encountered in actual environmental exposures. Subjects first were exposed to sulfuric acid (H2SO4) aerosol to sensitize the airways to ozone. The exposure protocols were designed to provide more quantitative information about the threshold levels of ozone that produce adverse biological effects and to provide exposure-response data on ozone. Two groups of 30 nonsmoking volunteers of both sexes, between the ages of 18 and 45 years, were recruited. The healthy study population comprised 16 men and 14 women with an average age of 28 years and no airway hyperreactivity. The second group comprised 10 men and 20 women comparable in age to the control group, but with allergic asthma and positive skin tests. The study examined an exposure-response relationship using three levels of ozone ranging from below the current standard to one and one-half times the ambient air quality standard (0.08, 0.12, and 0.18 ppm* [parts per million]) with preexposure 24 hours earlier to H2SO4 (100 micrograms/m3) or sodium chloride (NaCl) (control) aerosol in a 45-m3 environmental chamber. The study used an incomplete block design in which each subject was exposed to four of the six paired experimental atmospheres. Both the selection of paired exposures and the order in which they were presented were randomized. The exposure protocol required nine days: Day 1, training and baseline preexposure measurements; Day 2, the first of the three-hour particle (H2SO4 or NaCl) exposures; Day 3 (24 hours after Day 2), ozone exposure at 0.08, 0.12, or 0.18 ppm for three hours; Day 4 (two to four weeks later), exposure to the same ozone concentration as on Day 4. After at least another two weeks, Days 6, 7, 8, and 9 repeated Days 2, 3, 4, and 5 using a second ozone concentration. All three-hour exposures included several predetermined periods of exercise and pulmonary function measurements. To examine for delayed effects, pulmonary function tests were measured two and four hours after exposure on the ozone days. Data were analyzed over the time course of exposure and by exposure level of ozone at each time point to reveal dose-response relationships more closely. The main findings of the study are as follows. No significant symptomatic or physiologic effects of exposure to either aerosol or ozone on lung function were found for the healthy group.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1993

[Can ozone administration activate the tissue metabolism?--A study on brain metabolism during hypoxic hypoxia].

As it was thought that the tissue metabolism could be activated by administration of ozone, the influence of ozone on cerebral metabolism was studied under hypoxic condition. Ozone 1.5% was obtained from an ozonizer which separates the ozone from oxygen. Objects were 30 mature rabbits and they inhaled 3% oxygen in 97% nitrogen (PaO2 17-19 mmHg) by spontaneous respiration through a tracheostomy cannula. Objects were divided into three groups. Control rabbits inhaled only anoxic gases without ozone administration. Although the oxygen group also inhaled anoxic gases, pure oxygen was administered through an A-V shunt, previously made on femoral artery and vein, with an oxygenator, named Nichidai style (counter-current-exchange method). Similarly, the ozone group was given ozone with the oxygenator via A-V shunt. In each group, survival time as well as ATP, ADP, AMP and lactic acid lipo-peroxide in brain were examined. After the administration of ozone, survival time was prolonged significantly, compared with the control group (P < 0.005). Equally, ATP and energy charge in the brain were well maintained (P < 0.005) and the lactate production was inhibited significantly (P < 0.005). These results indicate that oxidizing effect of ozone will be beneficial to maintain energy charge in brain tissue during hypoxia. Further, ozone might activate the energy metabolism in animal tissues.

Animals↗
PubMed1996

Comparison of outdoor and classroom ozone exposures for school children in Mexico City.

To evaluate methods of reducing exposure of school children in southwest Mexico City to ambient ozone, outdoor ozone levels were compared to indoor levels under three distinct classroom conditions: windows/doors open, air cleaner off; windows/doors closed, air cleaner off; windows/doors closed, air cleaner on. Repeated two-minute average measurements of ozone were made within five minutes of each other inside and outside of six different school classrooms while children were in the room. Outdoor ozone two-minute average levels varied between 64 and 361 ppb; mean outdoor levels were above 160 ppb for each of the three conditions. Adjusting for outdoor relative humidity, for a mean outdoor ozone concentration of 170 ppb, the mean predicted indoor ozone concentrations were 125.3 (+/- 5.7) ppb with windows/doors open; 35.4 (+/- 4.6) ppb with windows/doors closed, air cleaner on. The mean predicted ratios of indoor to outdoor ozone concentrations were 0.71 (+/- 0.03) with windows/doors open; 0.18 (+/- 0.02) ppb with windows/doors closed, air cleaner off; and 0.15 (+/- 0.02) ppb with windows/doors closed, air cleaner on. As outdoor ozone concentrations increased, indoor ozone concentrations increased more rapidly with windows and doors open than with windows and doors closed. Ozone exposure in Mexican schools may be significantly reduced, and can usually be kept below the World Health Organization (WHO) guideline of 80 ppb, by closing windows and doors even when ambient ozone levels reach 300 ppb or more.

Air Pollution↗