Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ozone”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources
PubMed2001

Tropical tropospheric ozone and biomass burning.

New methods for retrieving tropospheric ozone column depth and absorbing aerosol (smoke and dust) from the Earth Probe-Total Ozone Mapping Spectrometer (EP/TOMS) are used to follow pollution and to determine interannual variability and trends. During intense fires over Indonesia (August to November 1997), ozone plumes, decoupled from the smoke below, extended as far as India. This ozone overlay a regional ozone increase triggered by atmospheric responses to the El Niño and Indian Ocean Dipole. Tropospheric ozone and smoke aerosol measurements from the Nimbus 7 TOMS instrument show El Niño signals but no tropospheric ozone trend in the 1980s. Offsets between smoke and ozone seasonal maxima point to multiple factors determining tropical tropospheric ozone variability.

Aerosols↗
PubMed2005

Effect of elevated tropospheric ozone on the structure of bacterial communities inhabiting the rhizosphere of herbaceous plants native to Germany.

Current elevated concentrations of ozone in the atmosphere, as they are observed during summer seasons, can cause severe effects on plant vegetation. This study was initiated to analyze whether ozone-stressed plants also transfer signals below ground and thereby alter the bacterial community composition in their rhizospheres. Herbaceous plants, native to Germany, with tolerance (Anthoxanthum odoratum, Achillea millefolium, Poa pratensis, Rumex acetosa, and Veronica chamaedrys) and sensitivity (Matricaria chamomilla, Sonchus asper, and Tanacetum vulgare) to ozone, raised in the greenhouse, were exposed in open-top chambers to two different ozone regimes, i.e., "summer stress" and a normal ozone background. DNA of bacterial cells from the rhizospheres was directly extracted, and partial sequences of the 16S rRNA genes were PCR amplified with primers targeting the following phylogenetic groups: Bacteria, alpha-Proteobacteria, Actinobacteria, and Pseudomonas, respectively. The diversity of the amplified products was analyzed by genetic profiling based on single-strand conformation polymorphism (SSCP). Neither the tolerant nor the sensitive plants, the latter with visible above-ground damage, showed ozone-induced differences in any of the SSCP profiles, with the single exception of Actinobacteria-targeted profiles from S. asper. To increase the stress, S. asper was germinated and raised in the continuous presence of an elevated level of ozone. SSCP profiles with Bacteria-specific primers combined with gene probe hybridizations indicated an ozone-related increase in a Xanthomonas-related 16S rRNA gene and a decrease in the respective gene from the plant plastids. The fact that only this latter unrealistic scenario caused a detectable effect demonstrated that ozone stress has a surprisingly small effect on the structural diversity of the bacterial community in rhizospheres.

Actinobacteria↗
PubMed2004

Ozone-induced production of nitric oxide and TNF-alpha and tissue injury are dependent on NF-kappaB p50.

Ozone-induced lung injury is associated with increased production of reactive nitrogen intermediates and TNF-alpha, which have been implicated in the pathogenic process. Generation of these mediators is regulated in part by transcription factors, e.g., NF-kappaB and CCAAT/enhancer-binding protein (C/EBP). The present studies used NF-kappaB p50 knockout mice to assess the role of this transcription factor protein in ozone-induced inflammatory mediator production and toxicity. Treatment of wild-type (WT) mice with ozone (0.8 ppm, 3 h) resulted in a rapid increase in NF-kappaB binding activity in alveolar macrophages that peaked after 6-12 h. This response was attenuated in NF-kappaB p50(-)/(-) mice. In WT mice, but not NF-kappaB p50(-)/(-) mice, C/EBP was also markedly increased in macrophages following ozone inhalation. Ozone also induced changes in the mobility of C/EBP in gel shift assays, suggesting alterations in the transcription factor complex that may be important in controlling inflammatory gene expression. Whereas macrophages from WT mice produced increased quantities of nitric oxide and TNF-alpha following ozone inhalation, this was not observed in cells from NF-kappaB p50(-)/(-) mice. Ozone-induced decreases in expression of the anti-inflammatory cytokine IL-10 were also prevented in NF-kappaB p50(-)/(-) mice. In WT mice, ozone inhalation caused an increase in bronchoalveolar lavage protein, a marker of tissue damage. This was not evident in NF-kappaB p50(-)/(-) mice. There was also no evidence of peroxynitrite-mediated lung injury in these mice. These findings demonstrate that NF-kappaB and possibly C/EBP signaling are important in ozone-induced production of reactive nitrogen intermediates and TNF-alpha and in tissue injury.

Animals↗
PubMed2005

The changing role of eosinophils in long-term hyperreactivity following a single ozone exposure.

Ozone hyperreactivity over 24 h is mediated by blockade of inhibitory M(2) muscarinic autoreceptors by eosinophil major basic protein. Because eosinophil populations in the lungs fluctuate following ozone, the contribution of eosinophils to M(2) dysfunction and airway hyperreactivity was measured over several days. After one exposure to ozone, M(2) function, vagal reactivity, smooth muscle responsiveness, and inflammation were measured in anesthetized guinea pigs. Ozone-induced hyperreactivity to vagal stimulation persisted over 3 days. Although hyperreactivity one day after ozone is mediated by eosinophils, AbVLA-4 did not inhibit either eosinophil accumulation in the lungs or around the nerves or prevent hyperreactivity at this time point. Two days after ozone, eosinophils in BAL, around airway nerves and in lungs, were decreased, and neuronal M(2) receptor function was normal, although animals were still hyperreactive to vagal stimulation. Depleting eosinophils with AbIL-5 prevented hyperreactivity, thus eosinophils contribute to vagal hyperreactivity by mechanisms separate from M(2) receptor blockade. Three days after ozone, vagal hyperreactivity persisted, eosinophils were again elevated in BAL in lungs and around nerves, and M(2) receptors were again dysfunctional. At this point, airway smooth muscle was also hyperresponsive to methacholine. Eosinophil depletion with AbIL-5, AbVLA-4, or cyclophosphamide protected M(2) function 3 days after ozone and prevented smooth muscle hyperreactivity. However, vagal hyperreactivity was significantly potentiated by eosinophil depletion. The site of hyperreactivity, muscle or nerve, changes over 3 days after a single exposure to ozone. Additionally, the role of eosinophils is complex; they mediate hyperreactivity acutely while chronically may be involved in repair.

Animals↗
PubMed1992

Exposure of surfactant protein A to ozone in vitro and in vivo impairs its interactions with alveolar cells.

This study focused on the question of whether exposure of surfactant protein A (SP-A) to ozone affected properties of this protein that may be involved in regulating alveolar type II cell and alveolar macrophage functions. In vitro exposure of human or canine SP-A to ozone reduced the ability of this protein to inhibit phorbol-ester induced secretion of [3H]phosphatidylcholine by alveolar type II cells in culture. Ozone-exposed human SP-A showed a decreased ability to enhance phagocytosis of herpes simplex virus and to stimulate superoxide anion production by alveolar macrophages. Experiments with elastase showed that ozone-exposed canine SP-A was more susceptible to proteolysis. A conformational change of the protein could underlie this phenomenon. Surfactant isolated from ozone-exposed rats (0.4 ppm ozone for 12 h) was also less able to stimulate superoxide anion production by alveolar macrophages than surfactant from control rats, which suggested that SP-A in vivo was also susceptible to ozone. The results of this study suggest that SP-A-alveolar cell interactions can be inhibited by ozone exposure, which may contribute to the toxicity of ozone in the lungs.

Animals↗
PubMed1983

Time course of airway hyperresponsiveness induced by ozone in dogs.

To better understand the mechanism of ozone-induced airway hyperresponsiveness we determined the time course of the ozone effect in dogs. To do this we assessed airway responsiveness before ozone exposure and then at 1 h, 1 day, and 1 wk after ozone exposure. To assess responsiveness we anesthetized the dogs and obtained dose-response curves of increasing concentrations of acetylcholine or histamine aerosols delivered to the airways vs. pulmonary resistance. Ozone exposures were carried out with the dogs awake and at rest in an exposure chamber for 2 h breathing either through the nose and mouth at a level of 2.2 ppm or through a tracheostomy at a level of 1.0 ppm. For both acetylcholine and histamine and for both routes of ozone delivery airway responsiveness increased most markedly at 1 h after ozone, increased to a lesser degree 1 day later, and returned to control levels by 1 wk. The results are similar to our previous studies in humans that showed that ozone-induced hyperresponsiveness occurs shortly after exposure and is rapidly reversible and suggest that the ozone effect is linked to an acute inflammatory response in the airways.

Acetylcholine↗
PubMed1987

Role of the parasympathetic nervous system in airway hyperresponsiveness after ozone inhalation.

Airway hyperresponsiveness develops in dogs after ozone inhalation. This study examined the role of the parasympathetic nervous system in ozone-induced airway hyperresponsiveness in dogs. Dose-response curves to acetylcholine (n = 8) and histamine (n = 4) were measured before and after exposure to ozone (3 ppm for 30 min). The provocative concentration of each agonist was measured on two randomly assigned days separated by at least 1 wk. On one day a control experiment was performed, and on the other day the dogs were pretreated with the ganglionic blocker hexamethonium bromide in doses that block ganglionic transmission. The acetylcholine provocative concentration decreased on the control day from 5.5 mg/ml (%SE 1.8) before ozone to 0.5 mg/ml (%SE 2.0) after ozone (P less than 0.0001). After pretreatment with hexamethonium the acetylcholine provocative concentration decreased from 9.0 mg/ml (%SE 1.8) before ozone to 1.0 mg/ml (%SE 2.0) after ozone (P = 0.002). The results were similar when histamine was used as the agonist. Therefore, ganglionic blockade does not prevent airway hyperresponsiveness after ozone inhalation, and a parasympathetic reflex mechanism is not responsible for airway hyperresponsiveness after ozone inhalation in dogs.

Acetylcholine↗
PubMed2006

Pulmonary responses to acute ozone exposure in fasted mice: effect of leptin administration.

Leptin is a satiety hormone that also has proinflammatory effects, including augmentation of ozone-induced pulmonary inflammation. The purpose of this study was to determine whether reductions in endogenous levels of leptin can attenuate pulmonary responses to ozone. To reduce serum leptin, we fasted mice overnight before ozone exposure. Fasting caused a marked reduction in serum leptin to approximately one-sixth the levels observed in fed mice, and continuous infusion of leptin via Alzet micro-osmotic pumps restored serum leptin to, but not above, fed levels. Ozone exposure (2 ppm for 3 h) caused a significant, approximately 40% increase in pulmonary resistance (P < 0.01) and increased airway responsiveness in fasted but not in fed mice. The increased effect of ozone on pulmonary mechanics and airway responsiveness in fasted mice was not observed when leptin was restored via continuous infusion. Ozone exposure caused pulmonary inflammation, as evident by increases in bronchoalveolar lavage cells, protein, and soluble tumor necrosis factor receptors. There was no effect of fasting status on ozone-induced changes in the bronchoalveolar lavage inflammatory profile, and leptin treatment did not alter these responses. Our results indicate that fasting augments ozone-induced changes in pulmonary mechanics and airway responsiveness in mice. These effects of fasting are the result of declines in serum leptin. The mechanistic basis for this protective effect of leptin in fasted mice remains to be determined but is not related to effects on ozone-induced inflammation.

Airway Resistance↗
PubMed2005

Ozone therapy on rats submitted to subtotal nephrectomy: role of antioxidant system.

Chronic renal failure (CRF) represents a world health problem. Ozone increases the endogenous antioxidant defense system, preserving the cell redox state. The aim of this study is to evaluate the effect of ozone/oxygen mixture in the renal function, morphology, and biochemical parameters, in an experimental model of CRF (subtotal nephrectomy). Ozone/oxygen mixture was applied daily, by rectal insufflation (0.5 mg/kg) for 15 sessions after the nephrectomy. Renal function was evaluated, as well as different biochemical parameters, at the beginning and at the end of the study (10 weeks). Renal plasmatic flow (RPF), glomerular filtration rate (GFR), the urine excretion index, and the sodium and potassium excretions (as a measurement of tubular function) in the ozone group were similar to those in Sham group. Nevertheless, nephrectomized rats without ozone (positive control group) showed the lowest RPF, GFR, and urine excretion figures, as well as tubular function. Animals treated with ozone showed systolic arterial pressure (SAP) figures lower than those in the positive control group, but higher values compared to Sham group. Serum creatinine values and protein excretion in 24 hours in the ozone group were decreased compared with nephrectomized rats, but were still higher than normal values. Histological study demonstrated that animals treated with ozone showed less number of lesions in comparison with nephrectomized rats. Thiobarbituric acid reactive substances were significantly increased in nephrectomized and ozone-treated nephrectomized rats in comparison with Sham group. In the positive control group, superoxide dismutase (SOD) and catalase (CAT) showed the lowest figures in comparison with the other groups. However, ozone/oxygen mixture induced a significant stimulation in the enzymatic activity of CAT, SOD, and glutathione peroxidase, as well as reduced glutathione in relation with Sham and positive control groups. In this animal model of CRF, ozone rectal administrations produced a delay in the advance of the disease, protecting the kidneys against vascular, hemorheological, and oxidative mechanisms. This behavior suggests ozone therapy has a protective effect on renal tissue by downregulation of the oxidative stress shown in CRF.

Animals↗
PubMedDate not supplied

PACAP reverses airway hyperresponsiveness induced by ozone exposure in guinea pigs.

BACKGROUND: We previously demonstrated that pituitary adenylate cyclase activating peptide (PACAP) inhibits airway smooth muscle contraction and plasma extravasation. OBJECTIVE: We thus hypothesized that PACAP may regulate airway responsiveness through these effects and examined the effects of exogenously applied PACAP on the airway hyperresponsiveness induced by ozone exposure. METHODS: Ozone exposure was carried out in awake, spontaneously breathing guinea pigs using 3 ppm for 2 h. Airway responsiveness to histamine was determined before and 30 and 90 min after the termination of ozone exposure for 2 h in anesthetized animals. Extravasation of Evans blue was measured before and 90 min after the termination of ozone exposure. Either PACAP (10(-6) mol/kg) or vehicle was administered intravenously 60 min after exposure. The airway responsiveness was expressed as the concentration of histamine required to produce a 200% increase in total pulmonary resistance (PC(200)). RESULTS: Ozone exposure caused a significant decrease in PC(200) (n = 5, p < 0.05) 30 min after ozone exposure which persisted 90 min thereafter, thus suggesting that ozone caused airway hyperresponsiveness. PACAP significantly suppressed the increase in airway hyperresponsiveness induced by ozone 90 min after exposure (n = 5, p < 0.05). In contrast, this peptide did not have any effect on plasma extravasation. CONCLUSION: We thus conclude that PACAP decreases ozone-induced airway responsiveness, and, therefore, intravenously administered PACAP may be useful in reversing airway hyperresponsiveness.

Animals↗
PubMedDate not supplied

Antioxidant responsiveness in BALB/c mice exposed to ozone.

BACKGROUND: A single, acute exposure to ozone has been shown to modify the antioxidant defense mechanism in the respiratory tract. OBJECTIVE: The aim of this study was to evaluate the effects of ozone exposure on antioxidant response in BALB/c mice. METHODS: We measured enhanced pause of breathing (Penh) as a marker of airway obstruction using barometric whole-body plethysmography before and after ozone exposure [groups (n = 6): filtered air, 0.12 ppm, 0.5 ppm, 1 ppm, 2 ppm] for 3 h. Antioxidant levels were measured using high-performance liquid chromatography with electrochemical detection in bronchoalveolar lavage (BAL) fluid and lung tissue homogenates. RESULTS: Malondialdehyde concentrations in lung tissue homogenates were significantly increased in the group exposed to 2-ppm ozone compared to the filtered air group. Uric acid and gamma-tocopherol concentrations in BAL fluid were significantly increased in the ozone exposure group compared to the filtered air group (p < 0.01). Uric acid concentrations were increased in a concentration-dependent manner according to ozone concentration to which the animals were exposed. Increases in Penh after ozone exposure were significantly higher in an ozone concentration-dependent manner. The proportion of neutrophils in BAL fluid was significantly higher in the group exposed to 2 ppm than in the filtered air and the group exposed to 0.12 ppm (p < 0.01, respectively). The level of ascorbate correlated with the level of gamma-tocopherol. CONCLUSION: These findings suggest that antioxidant responses may serve as a protective mechanism against a range of oxidants in BALB/c mice exposed to ozone.

Administration, Inhalation↗
PubMed1994

Ozone increases atrial natriuretic peptides in heart, lung and circulation of aged vs. adult animals.

Ozone can cause pulmonary edema and simultaneously decrease blood pressure. Atrial natriuretic peptides may mediate both of these affects since they increase pulmonary capillary permeability and are potent vasodilating peptides. To examine this possibility and determine if aged animals respond differently to ozone, adult (4-6 months old) and aged (24-26 months old) Fischer 344 rats were exposed to ozone (0.5 parts per million) for 8 h. Ozone increased atrial natriuretic peptides recognized by the proANF 1-30, proANF 31-67, and atrial natriuretic factor (ANF) radioimmunoassays in lung from 3.7 +/- 0.2, 3.5 +/- 0.1, and 3.0 +/- 0.2 ng/g of lung, respectively, to 9.7 +/- 1.0, 9.2 +/- 0.4, and 13.3 +/- 2.7 ng/g in adult rats (n = 6) and from 3.6 +/- 0.1, 3.5 +/- 0.1, and 3.2 +/- 0.1 ng/g of lung of aged rats (n = 6) to 10.2 +/- 0.3, 10.0 +/- 0.2, and 12.6 +/- 0.2 ng/g. Ozone increased the content of these peptides in the heart 2- to 5-fold from 266 +/- 25, 226 +/- 22, and 288 +/- 40 ng/g of heart to 716 +/- 26, 471 +/- 14, and 1,473 +/- 235 ng/g in the same adult animals and from 495 +/- 17, 483 +/- 22, and 501 +/- 18 ng/g to 903 +/- 16,879 +/- 21, and 1,489 +/- 31 ng/g of heart in the aged animals. Ozone also doubled the concentration of these atrial natriuretic peptides in the circulatory system. This study demonstrates that ozone increases atrial natriuretic peptides in the lung, heart, and circulation of equal magnitude in aged versus adult animals, indicating an equal response to ozone with aging. This study further suggests that atrial natriuretic peptides may mediate the decreased blood pressure and pulmonary edema observed with ozone exposure.

Aging↗
PubMed1997

Interaction of ozone and allergen challenges on bronchial responsiveness and inflammation in sensitised guinea pigs.

BACKGROUND: Environmental pollutants such as ozone may interact with airway responses to allergen in sensitised individuals. METHODS: We examined the effects of a single exposure to ozone (1 ppm for 1 h) on bronchial responsiveness to acetylcholine (ACh) aerosol 3 and 24 h after single ovalbumin (OA) challenge in OA-sensitised anaesthetised guinea pigs. Broncho-alveolar lavage (BAL) was performed and protein content and differential cell counts were determined. RESULTS: Ozone increased bronchial responsiveness at 3 h but not at 24 h, while OA alone had no effect. At 3 h after ozone, OA induced further, but non-significant increases in bronchial responsiveness to ACh, but at 24 h after ozone, there was enhanced responsiveness. Neutrophil counts in BAL fluid increased at 3 and 24 h after exposure to ozone alone, but there were no further increases with ozone followed by OA exposure. Protein concentration was significantly increased in the ozone and OA groups at 3 and 24 h (163.4 +/- 25.6 and 128.7 +/- 7.4 mg/ml, respectively) compared to 54.0 +/- 18.1 mg/ml in the control group (p < 0.02 and p < 0.01, respectively). CONCLUSION: Our data demonstrate an interaction of OA with ozone exposure on bronchial responsiveness; one underlying mechanism could be through damage at the endothelial-epithelial barrier.

Acetylcholine↗
PubMed1994

Respiratory responses to repeated prolonged exposure to 0.12 ppm ozone.

Repeated exposure to high concentrations of ozone results first in augmentation (typically on the second day) and then attenuation of pulmonary response in humans. To determine the effects of repeated prolonged low-concentration ozone exposure, we exposed 17 healthy nonsmoking male subjects to 0.12 ppm ozone for 6.6 h on 5 consecutive days. Subjects were also exposed once to filtered air. Volunteers exercised at a ventilation of approximately 39 L/min for 50 min of each hour during the exposure. Spirometry, plethysmography, and symptom responses were obtained before, during, and after each exposure. Nasal lavage and aerosol bolus dispersion were obtained before and after exposure. Spirometry decreased and symptoms increased on the first day. Responses were less on the second day compared with those on the first day, and they were absent compared with control values on the subsequent 3 days of ozone exposure. Percent change in FEV1 after ozone exposure compared with that after air exposure averaged -12.79, -8.73, -2.54, -0.6, +0.18% for Days 1 to 5 of ozone exposure, respectively. FEV1 responses ranged from a zero to 34% decrease on Days 1 and 2. After each exposure, we determined the ratio of SRaw after inhaling a fixed dose of methacholine to SRaw after inhaling saline aerosol, as an index of airway responsiveness. Airway responsiveness was significantly increased after each ozone exposure. The mean ratios were 2.22, 3.67, 4.55, 3.99, 3.24, and 3.74 for filtered air and ozone Days 1 to 5, respectively. Symptoms of cough and pain on deep inspiration increased significantly on ozone Day 1 only.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Effect of a leukotriene B4 receptor antagonist SC-53228 on ozone-induced airway hyperresponsiveness and inflammation in dogs.

The importance of the potent neutrophil chemoattractant leukotriene (LT)B4 in causing ozone-induced bronchoconstriction, airway inflammation, and airway hyperresponsiveness in dogs was studied using the LTB4-receptor antagonist SC-53228. Seven dogs from random sources were studied three times, at least 2 wk apart. On each occasion, acetylcholine (Ach) airway responsiveness was measured before and 1 h after ozone (3 ppm, 30 min) or dry air inhalation, followed by a bronchoalveolar lavage (BAL). On the first day, dogs were treated with SC-53228 (0.4 mg/kg intravenously) followed by a continuous intravenous infusion of 1.2 mg/kg/h before ozone inhalation. On the other two days, diluent was infused followed by ozone or dry air inhalation. Cell counts were measured in BAL and cell activation was measured by spontaneous and by phorbol myristate acetate-stimulated (PMA) (2.4 mumol/L) oxygen radical release, measured from washed BAL cells (4 x 10(6) cells) by lucigenin-enhanced chemiluminescence. Ozone inhalation caused bronchoconstriction and airway hyperresponsiveness. SC-53228 inhibited the ozone-induced airway hyperresponsiveness (p = 0.006), but not the bronchoconstriction. Spontaneous (p = 0.004) and PMA-stimulated (p = 0.04) lucigenin-enhanced chemiluminescence were increased after ozone inhalation. The ozone-induced increases in PMA-stimulated chemiluminescence were significantly attenuated by treatment with SC-53228 (p = 0.04). These results suggest that LTB4 is involved in the pathogenesis of ozone-induced airway hyperresponsiveness, possibly through activation of airway inflammatory cell.

Acetylcholine↗
PubMed1999

Ozone exposure increases aldehydes in epithelial lining fluid in human lung.

We hypothesized that exposure of healthy humans to ozone causes both ozonation and peroxidation of lipids in lung epithelial lining fluid. Twelve smokers and 15 nonsmokers (eight lung function "responders" and seven "nonresponders") were exposed once to air and twice to 0. 22 ppm ozone for 4 h with exercise in an environmental chamber, with each exposure separated by at least 3 wk. Bronchoalveolar lavage (BAL) was performed immediately after one ozone exposure and 18 h after the other ozone exposure. BAL fluid was analyzed for the aldehyde products of ozonation and lipid peroxidation, nonanal (C9) and hexanal (C6), as well as total protein, albumin, and immunoglobulin M as markers of changes in epithelial permeability. Ozone exposure resulted in a significant early increase in C9 (p = 0. 0001), with no statistically significant relationship between increases in C9 and lung function changes, airway inflammation, or changes in epithelial permeability. Increases in C6 levels were not statistically significant (p = 0.16). Both C9 and C6 levels returned to baseline by 18 h after exposure. These studies confirm that exposure to ozone with exercise, at concentrations relevant to urban outdoor air, results in ozonation of lipids in the airway epithelial lining fluid of humans.

Adolescent↗
PubMed1978

Health effects of ozone exposure in asthmatics.

To investigate whether ambient air quality standards for ozone adequately protect high-risk populations, we assessed pulmonary and biochemical responses of 22 asthmatic volunteers to 2-hour controlled exposures to ozone at concentrations approximating 0.2 ppm, with secondary stresses of heat and intermittent exercise. All subjects had physician-diagnosed asthma; clinically, they covered a range from minimal wheezing to persistent marked abnormality in forced expiratory performance. Control experiments included repeated sham exposures (to purified air with no ozone added) as well as brief exposures to the odor of ozone followed by purified air. No meaningful changes in forced expiratory measures, lung volumes, or single-breath N2 indices were found after ozone exposure relative to control. Symptoms, scored semiquantitatively, increased slightly but not significantly with exposure to ozone. Small but significant (P is less than 0.05) group mean blood biochemical changes occurred with exposure to ozone; these included increased glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities, increased erythrocyte fragility, and decreased concentration of reduced glutathione. Hemoglobin concentration and acetylcholinesterase activity decreased with ozone and decreased to a lesser extent in control studies. Concentrations of ozone readily attainable in smog episodes thus appear to be capable of affecting blood biochemistry in at least some asthmatic persons, in the absence of obvious adverse pulmonary responses. Whether the biochemical effects represent harm to health or a normal response to stress remains to be determined.

Acetylcholinesterase↗
PubMed1984

Indomethacin inhibits the airway hyperresponsiveness but not the neutrophil influx induced by ozone in dogs.

To determine whether oxygenation products of arachidonic acid may be involved in the airway hyperresponsiveness induced by ozone exposure, we studied whether ozone-induced hyperresponsiveness could be inhibited by the prostaglandin synthetase inhibitor, indomethacin, in dogs. Airway responsiveness was assessed with dose-response curves of acetylcholine aerosol versus pulmonary resistance in 2 sets of experiments: in one set, 5 dogs were given no indomethacin treatment and were studied both before and after ozone exposure (3.0 ppm, 2 h); in another set, the same dogs were studied before indomethacin treatment or ozone exposure and then during treatment (1 mg/kg every 12 h for 4 days) both before and after ozone exposure. On each occasion, we also determined the number of neutrophils in biopsies of the airway epithelium. When the dogs were not treated with indomethacin, ozone caused a marked increase in responsiveness to acetylcholine and a marked increase in the number of neutrophils in the airway epithelium. When the dogs were given indomethacin, responsiveness was no different during treatment than before treatment, but more importantly, responsiveness did not increase significantly after they were exposed to ozone. Interestingly, indomethacin treatment did not affect either the baseline number of epithelial neutrophils before ozone exposure or the increase in the number of neutrophils after exposure. The results suggest that oxygenation products of arachidonic acid that are sensitive to inhibition by indomethacin play a role in ozone-induced hyperresponsiveness without affecting the influx of neutrophils.

Animals↗