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Selecting ozone exposure statistics for determining crop yield loss from air pollutants.

Numerous ozone exposure statistics were calculated using hourly ozone data from crop yield loss experiments previously conducted for alfalfa, fresh market and processing tomatoes, cotton, and dry beans in an ambient ozone gradient near Los Angeles, California. Exposure statistics examined included peak (maximum daily hourly) and mean concentrations above specific threshold levels, and concentrations during specific time periods of the day. Peak and mean statistics weighted for ozone concentration and time period statistics weighted for hour of the day were also determined. Polynomial regression analysis was used to relate each of 163 ozone statistics to crop yield. Performance of the various statistics was rated by comparing residual mean square (RMS) values. The analyses demonstrated that no single statistic was best for all crop species. Ozone statistics with a threshold level performed well for most crops, but optimum threshold level was dependent upon crop species and varied with the particular statistics calculated. The data indicated that daily hours of exposure above a critical high-concentration threshold related well to crop yield for alfalfa, market tomatoes, and dry beans. The best statistic for cotton yield was an average of all daily peak ozone concentrations. Several different types of ozone statistics performed similarly for processing tomatoes. These analyses suggest that several ozone summary statistics should be examined in assessing the relationship of ambient ozone exposure to crop yield. Where no clear statistical preference is indicated among several statistics, those most biologically relevant should be selected.

Journal Article↗

The relationship between foliar injury, nitrogen metabolism, and growth parameters in ozonated soybeans.

A single 12 h ozone exposure peaking at 0.20 ppm proved phytotoxic to greenhouse-grown 'Cutler 71' soybeans at each growth stage tested from V5 to R6. Visible injury occurred within 40 h on the unifoliodate leaves and middle-aged and older trifoliolates while the younger leaves were free from toxicity symptoms. In some instances visible injury was accompanied by a decrease in chlorophyll and an increase in leaf diffusive resistance. Although nitrogen fixation was not significantly altered except at early pod formation (R3), and nitrate reductase activity was significantly reduced only if the ozone exposure occurred at the time of maximal enzyme activity (V5), nitrogen content of the leaves was reduced by ozone treatment. Shoot dry weight was not affected 40 h after ozone treatment, but root dry weight was significantly reduced. Plants grown with supplemental NO(3)(-) were more sensitive to ozone than those dependent on fixed nitrogen. At plant maturity, there was no evidence of an ozone effect on shoot, root, or seed dry weight, NO(3)(-) -grown plants showed a significant increase in growth and yield over N(2)(-) plants; but no ozone effect was observed, despite the increased foliar sensitivity. Multiple ozone exposures at growth stages V3, R1 and R3 exacerbated the effects noted with a single episode and also reduced nitrogenase activity (reflected in specific and total nodule activity) and shoot and root dry weight. At plant maturity, there was again no evidence of a significant effect of multiple ozone treatment on shoot dry weight or seed yield although root weight remained low. The results would tend to support the hypothesis that older leaves of soybean do not make a significant contribution to seed yield. Although they may be injured by ozone during the reproductive phases of growth, seed yield may not be affected if the younger O(3)-tolerant leaves remain functional.

Journal Article↗

Efficacy and fumigation characteristics of ozone in stored maize.

This study evaluated the efficacy of ozone as a fumigant to disinfest stored maize. Treatment of 8.9tonnes (350bu) of maize with 50ppm ozone for 3d resulted in 92-100% mortality of adult red flour beetle, Tribolium castaneum (Herbst), adult maize weevil, Sitophilus zeamais (Motsch.), and larval Indian meal moth, Plodia interpunctella (Hübner) and reduced by 63% the contamination level of the fungus Aspergillus parasiticus Speare on the kernel surface. Ozone fumigation of maize had two distinct phases. Phase 1 was characterized by rapid degradation of the ozone and slow movement through the grain. In Phase 2, the ozone flowed freely through the grain with little degradation and occurred once the molecular sites responsible for ozone degradation became saturated. The rate of saturation depended on the velocity of the ozone/air stream. The optimum apparent velocity for deep penetration of ozone into the grain mass was 0.03m/s, a velocity that is achievable in typical storage structures with current fans and motors. At this velocity 85% of the ozone penetrated 2.7m into the column of grain in 0.8d during Phase 1 and within 5d a stable degradation rate of 1ppm/0.3m was achieved. Optimum velocity for Phase 2 was 0.02m/s. At this velocity, 90% of the ozone dose penetrated 2.7m in less than 0.5d. These data demonstrate the potential usefulness of using ozone in managing stored maize and possibly other grains.

Journal Article↗

Spatial distribution of tropospheric ozone in western Washington, USA.

We quantified the distribution of tropospheric ozone in topographically complex western Washington state, USA (total area approximately 6000 km(2)), using passive ozone samplers along nine river drainages to measure ozone exposure from near sea level to high-elevation mountain sites. Weekly average ozone concentrations were higher with increasing distance from the urban core and at higher elevations, increasing a mean of 1.3 ppbv per 100 m elevation gain for all mountain transects. Weekly average ozone concentrations were generally highest in Cascade Mountains drainages east and southeast of Seattle (maximum=55-67 pbv) and in the Columbia River Gorge east of Portland (maximum=59 ppbv), and lowest in the western Olympic Peninsula (maximum=34 ppbv). Higher ozone concentrations in the Cascade Mountains and Columbia River locations downwind of large cities indicate that significant quantities of ozone and ozone precursors are being transported eastward toward rural wildland areas by prevailing westerly winds. In addition, temporal (week to week) variation in ozone distribution is synchronous within and between all drainages sampled, which indicates that there is regional coherence in air pollution detectable with weekly averages. These data provide insight on large-scale spatial variation of ozone distribution in western Washington, and will help regulatory agencies optimize future monitoring networks and identify locations where human health and natural resources could be at risk.

Journal Article↗

Seedling insensitivity to ozone for three conifer species native to Great Smoky Mountains National Park.

Field symptoms typical of ozone injury have been observed on several conifer species in Great Smoky Mountains National Park, and tropospheric ozone levels in the Park can be high, suggesting that ozone may be causing growth impairment of these plants. The objective of this research was to test the ozone sensitivity of selected conifer species under controlled exposure conditions. Seedlings of three species of conifers, Table Mountain pine (Pinus pungens), Virginia pine (Pinus virginiana), and eastern hemlock (Tsuga canadensis), were exposed to various levels of ozone in open-top chambers for one to three seasons in Great Smoky Mountains National Park in Tennessee, USA. A combination of episodic profiles (1988) and modified ambient exposure regimes (1989-92) were used. Episodic profiles simulated an average 7-day period from a monitoring station in the Park. Treatments used in 1988 were: charcoal-filtered (CF), 1.0x ambient, 2.0x ambient, and ambient air-no chamber (AA). In 1989 a 1.5x ambient treatment was added, and in 1990, additional chambers were made available, allowing a 0.5x ambient treatment to be added. Height, diameter, and foliar injury were measured most years. Exposures were 3 years for Table Mountain pine (1988-90), 3 years for hemlock (1989-91), and 1 and 2 years for three different sets of Virginia pine (1990, 1990-91, and 1992). There were no significant (p<0.05) effects of ozone on any biomass fraction for any of the species, except for older needles in Table Mountain and Virginia pine, which decreased with ozone exposure. There were also no changes in biomass allocation patterns among species due to ozone exposure, except for Virginia pine in 1990, which showed an increase in the root:shoot ratio. There was foliar injury (chlorotic mottling) in the higher two treatments (1.0x and 2.0x for Table Mountain and 2.0x for Virginia pine), but high plant-to-plant variability obscured formal statistical significance in many cases. We conclude, at least for growth in the short-term, that seedlings of these three conifer species are insensitive to ambient and elevated levels of ozone, and that current levels of ozone in the Park are probably having minimal impacts on these particular species.

Journal Article↗

Contrasts between Antarctic and Arctic ozone depletion.

This work surveys the depth and character of ozone depletion in the Antarctic and Arctic using available long balloon-borne and ground-based records that cover multiple decades from ground-based sites. Such data reveal changes in the range of ozone values including the extremes observed as polar air passes over the stations. Antarctic ozone observations reveal widespread and massive local depletion in the heart of the ozone "hole" region near 18 km, frequently exceeding 90%. Although some ozone losses are apparent in the Arctic during particular years, the depth of the ozone losses in the Arctic are considerably smaller, and their occurrence is far less frequent. Many Antarctic total integrated column ozone observations in spring since approximately the 1980s show values considerably below those ever observed in earlier decades. For the Arctic, there is evidence of some spring season depletion of total ozone at particular stations, but the changes are much less pronounced compared with the range of past data. Thus, the observations demonstrate that the widespread and deep ozone depletion that characterizes the Antarctic ozone hole is a unique feature on the planet.

Journal Article↗

Light environment alters ozone uptake per net photosynthetic rate in black cherry trees.

Foliar ozone uptake rates of different-sized black cherry (Prunus serotina Ehrh.) trees were compared within a deciduous forest and adjacent openings in north-central Pennsylvania during one growing season. Study trees included open-grown seedlings and saplings, forest understory seedlings and saplings, and sunlit and shaded portions of mature canopy tree crowns. Instantaneous ozone uptake rates were highest in high-light environments primarily because of higher stomatal conductances. Low ozone uptake rates of seedlings and saplings in the forest understory could be attributed partially to lower average ambient ozone concentrations compared to the canopy and open environments. Among the tree size and light combinations tested, ozone uptake rates were highest in open-grown seedlings and lowest in forest-grown seedlings. Despite lower ozone uptake rates of foliage in shaded environments, ozone uptake per net photosynthesis of foliage in shaded environments was significantly higher than that of foliage in sunlit environments because of weaker coupling between net photosynthesis and stomatal conductance in shaded environments. The potential for greater ozone injury in shaded environments as a result of greater ozone uptake per net photosynthesis is consistent with previous reports of greater ozone injury in shaded foliage than in sunlit foliage.

Journal Article↗

Growth responses and related biochemical and ultrastructural changes of the photosynthetic apparatus in birch (Betula pendula) saplings exposed to low concentrations of ozone.

Saplings of ozone-sensitive and ozone-tolerant birch (Betula pendula Roth.), clones B and C, respectively, were exposed to ozone concentrations that were 1.7-fold higher than ambient for one growing season under open-field conditions. Ambient air was used as the control treatment. In the ozone-sensitive clone B, there was an initial stimulation of leaf area growth in response to the ozone treatment, but further ozone exposure caused reductions in leaf and stem biomass growth, Rubisco and chlorophyll a contents, net photosynthesis, water use efficiency and chloroplast size. It also caused an alteration in chloroplast shape and injury to thylakoid membranes. In the ozone-tolerant clone C, ozone fumigation did not affect growth rate, and there were no consistent changes in chlorophyll content, photosynthesis or water use efficiency. There were also fewer ultrastructural abnormalities in the chloroplasts of clone C than of clone B. Based on the observed biochemical, physiological and structural changes in chloroplasts of clone B in response to low concentrations of ozone, we conclude that the increasing concentration of tropospheric ozone represents a risk to natural birch populations.

Journal Article↗

Response of photosynthesis and cellular antioxidants to ozone in populus leaves.

Atmospheric ozone causes formation of various highly reactive intermediates (e.g. peroxyl and superoxide radicals, H(2)O(2), etc.) in plant tissues. A plant's productivity in environments with ozone may be related to its ability to scavenge the free radicals formed. The effects of ozone on photosynthesis and some free radical scavengers were measured in the fifth emergent leaf of poplars. Clonal poplars (Populus deltoides x Populus cv caudina) were fumigated with 180 parts per billion ozone for 3 hours. Photosynthesis was measured before, during, and after fumigation. During the first 90 minutes of ozone exposure, photosynthetic rates were unaffected but glutathione levels and superoxide dismutase activity increased. After 90 minutes of ozone exposure, photosynthetic rates began to decline while glutathione and superoxide dismutase continued to increase. Total glutathione (reduced plus oxidized) increased in fumigated leaves throughout the exposure period. The ratio of GSH/GSSG also decreased from 12.8 to 1.2 in ozone exposed trees. Superoxide dismutase levels increased twofold in fumigated plants. After 4 hours of ozone exposure, the photosynthetic rate was approximately half that of controls while glutathione levels and superoxide dismutase activity remained above that of the controls. The elevated antioxidant levels were maintained 21 hours after ozone exposure while photosynthetic rates recovered to about 75% of that of controls. Electron transport and NADPH levels remained unaffected by the treatment. Hence, elevated antioxidant metabolism may protect the photosynthetic apparatus during exposure to ozone.

Journal Article↗

Removal of pyrene and benzo(a)pyrene from contaminated water by sequential and simultaneous ozonation and biotreatment.

The removal of pyrene and benzo(a)pyrene from contaminated water by sequential and simultaneous ozonation-bioremediation techniques was investigated. During the sequential treatment, ozonation using 0.5 or 2.5 mg/L ozone was used as a pretreatment process, whereas, during the simultaneous treatment process, ozonation of hydrocarbon-contaminated water at a predetermined duration using 0.5 mg/L ozone was made in the presence of microbial biomass. Ozonation was not beneficial for the removal of pyrene. However, despite a decreased specific biodegradation rate, ozonation improved the overall elimination of benzo(a)pyrene during both treatment processes. The overall removal of benzo(a)pyrene increased from 23 to 91% after exposure of the water to 0.5 mg/L ozone for 30 minutes during the simultaneous treatment process and further to 100% following exposure to 2.5 mg/L ozone for 60 minutes during the sequential treatment mode, demonstrating the benefits of combined ozonation-biological treatment for the removal of polycyclic aromatic hydrocarbons.

Benzo(a)pyrene↗

Association of low-level ozone and fine particles with respiratory symptoms in children with asthma.

CONTEXT: Exposure to ozone and particulate matter of 2.5 microm or less (PM2.5) in air at levels above current US Environmental Protection Agency (EPA) standards is a risk factor for respiratory symptoms in children with asthma. OBJECTIVE: To examine simultaneous effects of ozone and PM2.5 at levels below EPA standards on daily respiratory symptoms and rescue medication use among children with asthma. DESIGN, SETTING, AND PARTICIPANTS: Daily respiratory symptoms and medication use were examined prospectively for 271 children younger than 12 years with physician-diagnosed, active asthma residing in southern New England. Exposure to ambient concentrations of ozone and PM2.5 from April 1 through September 30, 2001, was assessed using ozone (peak 1-hour and 8-hour) and 24-hour PM2.5. Logistic regression analyses using generalized estimating equations were performed separately for maintenance medication users (n = 130) and nonusers (n = 141). Associations between pollutants (adjusted for temperature, controlling for same- and previous-day levels) and respiratory symptoms and use of rescue medication were evaluated. MAIN OUTCOME MEASURES: Respiratory symptoms and rescue medication use recorded on calendars by subjects' mothers. RESULTS: Mean (SD) levels were 59 (19) ppb (1-hour average) and 51 (16) ppb (8-hour average) for ozone and 13 (8) microg/m3 for PM2.5. In copollutant models, ozone level but not PM2.5 was significantly associated with respiratory symptoms and rescue medication use among children using maintenance medication; a 50-ppb increase in 1-hour ozone was associated with increased likelihood of wheeze (by 35%) and chest tightness (by 47%). The highest levels of ozone (1-hour or 8-hour averages) were associated with increased shortness of breath and rescue medication use. No significant, exposure-dependent associations were observed for any outcome by any pollutant among children who did not use maintenance medication. CONCLUSION: Asthmatic children using maintenance medication are particularly vulnerable to ozone, controlling for exposure to fine particles, at levels below EPA standards.

Air Pollutants↗

Ozone therapy for the treatment of dental caries.

BACKGROUND: Dental caries is a bacterially mediated disease characterised by demineralisation of the tooth surface, which may lead to cavitation, discomfort, pain and eventual tooth loss. Ozone is toxic to certain bacteria in vitro and it has been suggested that delivering ozone into a carious lesion might reduce the number of cariogenic bacteria. This possibly could arrest the progress of the lesion and may, in the presence of fluoride, perhaps allow remineralisation to occur. This may in turn delay or prevent the need for traditional dental conservation by 'drilling and filling'. OBJECTIVES: To assess whether ozone is effective in arresting or reversing the progression of dental caries. SEARCH STRATEGY: We searched the Cochrane Oral Health Group's Trials Register (to 7 November 2003); Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 3, 2003); MEDLINE and PREMEDLINE (OVID, 1966 to November 2003); EMBASE (OVID, 1980 to November 2003); CINAHL (OVID, 1982 to November 2003); AMED (OVID, 1985 to November 2003). Quintessence was handsearched through 2002 and KaVo were contacted as manufacturers of the HealOzone apparatus for any additional published or unpublished trials. SELECTION CRITERIA: Inclusion was assessed independently by at least two reviewers. Trials were only included if they met the following criteria: randomisation in a controlled trial; single surface in vivo carious lesion accessible to ozone application; clear allocation concealment; ozone application to the lesions in the intervention group; no such application of ozone in the control group; outcomes measured after at least 6 months. DATA COLLECTION AND ANALYSIS: Reviewers independently extracted information in duplicate. A paucity of comparable data did not allow meta-analytic pooling of the included studies. MAIN RESULTS: Three trials were included, with a combined total of 432 randomised lesions (137 participants). Forty-two conference papers, abstracts and posters were excluded (from an unknown number of studies). The risk of bias in all studies appeared high. The analyses of all three studies were conducted at the level of the lesion, which is not independent of the person, for this reason pooling of data was not appropriate or attempted. Individual studies showed inconsistent effects of ozone on caries, across different measures of caries progression or regression. Few secondary outcomes were reported, but one trial reported an absence of adverse events. REVIEWERS' CONCLUSIONS: Given the high risk of bias in the available studies and lack of consistency between different outcome measures, there is no reliable evidence that application of ozone gas to the surface of decayed teeth stops or reverses the decay process. There is a fundamental need for more evidence of appropriate rigour and quality before the use of ozone can be accepted into mainstream primary dental care or can be considered a viable alternative to current methods for the management and treatment of dental caries.

Cariostatic Agents↗

What does ozone react with at the air/lung interface? Model studies using human red blood cell membranes.

We exposed human red blood cell (RBC) membranes to low levels of ozone and measured the oxidative damage that occurs to the proteins and the unsaturated lipids that are present. Oxidative damage to proteins causes significant decreases in the content of thiol groups, the fluorescence of protein-tryptophan residues, and the activity of membrane-bound acetylcholinesterase. Oxidative damage to lipids causes changes in some of the unsaturated fatty acids (UFA) in the lipid fraction of these RBC membranes. Significant amounts of hexanal, heptanal, and nonanal are formed from the ozonation of UFA. Although no decrease in the amount of oleate is detected, it does undergo ozonation to yield nonanal; thus, as would be expected, product appearance is a more sensitive measure of ozonation than is substrate disappearance. These results imply that both proteins and unsaturated lipids undergo simultaneous and competitive ozonation in human RBC membranes when ozone is the limiting reactant. The ratios of reaction of ozone with different targets can be predicted in reasonably good agreement with the observed values using calculations (W. A. Pryor and R. M. Uppu (1993) J. Biol. Chem. 268, 3120-3126; R. M. Uppu and W. A. Pryor (1994) Chem. Res. Toxicol. 7, 47-55) that take into account the reactivities and relative amounts of protein and lipid functionalities present in the RBC membranes. Similar calculations are used to predict the reaction of ozone with unsaturated lipids and proteins at the air/lung interface, and both UFA and proteins are predicted to react with ozone in the lung, as in RBC membranes.

Acetylcholinesterase↗

Memory effects in the action of ozone on conifers.

Conifers are known to possess relative ozone tolerance in short-term experiments. A scenario for ozone damage of conifers is now derived from the first exposure experiments in which both the initial biochemical response phase and delayed visible symptom development were studied. A number of early biochemical ozone responses could be detected in Norway spruce (Picea abies [L.] Karst.) and Scots pine (Pinus sylvestris L.). The stress metabolite catechin persisted over several months. In the year following ozone treatment of spruce, decreases in pigment content and photosynthetic capacity, as well as development of visible symptoms (chlorosis, banding), were determined in the needle age classes previously exposed to an accumulated hourly ozone dose above 40 ppb (AOT40) of >/=60-80 ppm small middle doth. The visible symptoms developed during spring emergence of the new flush. In the case of Scots pine, an ozone dose (AOT40) of >/=30 ppm small middle doth caused the premature shedding of needles 9 months after treatment. The delayed symptoms of both spruce and pine occurred during known phases of endogenous stress. The symptoms appeared to reflect an ozone "memory" imprinted by the induced early stress reactions. Ambient AOT40 ozone doses in Central Europe are in the range 4 and 50 ppm small middle doth per growing season. Ozone is proposed to potentially damage conifers through memory effects ("abiotic" pathway) or through predisposition for pathogen attack ("biotic" pathway).

Catechin↗

Effects of low ambient levels of ozone and sulfates on the frequency of respiratory admissions to Ontario hospitals.

To investigate the acute respiratory health effects of ambient air pollution, the number of emergency of urgent daily respiratory admissions to 168 acute care hospitals in Ontario were related to estimates of exposure to ozone and sulfates in the vicinity of each hospital. Ozone levels were obtained from 22 monitoring stations maintained by the Ontario Ministry of the Environment for the period January 1, 1983 to December 31, 1988. Daily levels of sulfates were recorded at nine monitoring stations representing three different networks operated by the Ontario Ministry of the Environment and Environment Canada. Positive and statistically significant associations were found between hospital admissions and both ozone and sulfates recorded on the day of admission and up to 3 days prior to the date of admission. Five percent of daily respiratory admissions in the months of May to August were associated with ozone, with sulfates accounting for an additional 1% of these admissions. Ozone was a stronger predictor of admissions than sulfates. Positive and statistically significant (P < 0.05) associations were observed between the ozone-sulfate pollution mix and admissions for asthma, chronic obstructive pulmonary disease, and infections. Positive associations were also found in all age groups, with the largest impact on infants (15% of admissions associated with the ozone-sulfate pollution mix) and the least effects on the elderly (4%). Temperature had no effect on the air pollution-admission relationship. Ozone (lagged 1 day) and sulfates (lagged 1 day) displayed a positive association with respiratory admissions for 91 and 100% of the 168 acute care hospitals, respectively. Air pollution was not related to a class of nonrespiratory admissions, which served as a negative control, nor was it related to admissions in the winter months of December to March, when ozone and sulfate levels are low and when people spend a considerable amount of time indoors.

Adolescent↗

Contractile responses and structure of small bronchi isolated from rats after 20 months' exposure to ozone.

Short-term exposure to high concentrations of ozone has been shown to increase airway responsiveness in normal humans and in all laboratory animal species studied to date. While our knowledge concerning the pulmonary effects of single exposures to ozone has increased rapidly over recent years, the effects of repeated exposures are less understood. The goal of the present study was to determine whether airway responsiveness is increased after near-lifetime exposure to ozone. Airway segments representing approximately eighth generation airways were isolated from Fischer 344 rats of both genders that had been exposed for 6 hr per day, 5 days per week for 20 months to 0, 0.12, 0.5, or 1.0 parts per million (ppm) ozone. Circumferential tension development was measured in isolated airways in response to bethanechol, acetylcholine, and electrical field stimulation. Responsiveness of the airways to the contractile stimuli was described by the effective dose or frequency that elicited half-maximum contraction (ED50) and the maximum response. Since ozone exposure is associated with remodeling of peripheral airways, smooth muscle area was determined and tension responses were normalized to the area measurements. Before normalization of tension data to smooth muscle area, neither the ED50 nor maximum response of small bronchi to the contractile stimuli was altered after chronic ozone exposure. Smooth muscle area was greater in airways isolated from animals that had been exposed to 0.5 ppm ozone. After accounting for smooth muscle area, maximum responses of the small bronchi isolated from male rats were significantly reduced after 0.12 and 0.5 ppm ozone. Although not significant statistically, a similar trend was observed in airways isolated from female rats. These results suggest that the increase in airway responsiveness associated with acute ozone exposure does not persist during near-lifetime exposure. Although the mechanism responsible for the adaptation to the effects of O3 on airway responsiveness is unknown, the results indicate that smooth muscle cell function was compromised by the chronic exposure. The mechanism(s) responsible for mediating this effect and the relevance of these results to humans remains to be determined.

Adaptation, Physiological↗

Ozone exposure may enhance airway smooth muscle contraction by increasing Ca(2+) refilling of sarcoplasmic reticulum in guinea pig.

Ozone induces airway hyperresponsiveness, but there is controversy about effects of ozone on smooth muscle per se. We therefore investigated effects of in vivo ozone exposure on intracellular calcium mobilization in relation to tracheal smooth muscle contractility in the guinea pig in vitro. Guinea pigs underwent ozone exposure or sham exposure (3 ppm, 2 h). Then, a tracheal smooth muscle strip was mounted in an organ bath to record isometric tension. Effects of ozone exposure on acetylcholine-induced contraction of smooth muscle were as follows. Contraction was not altered in normal Krebs solution, but was increased in Ca(2+)-free solution in ozone-exposed animals. Decline of tension on repetitive application of acetylcholine in Ca(2+)-free solution was reduced, while the tension decline rate while acetylcholine was washed out with Ca(2+)-free solution was facilitated in ozone-exposed animals. Tension decline during the continuous administration of acetylcholine in Ca(2+)-free solution was slowed. Contraction occurred more quickly in Ca(2+)-free solution in ozone-exposed animals. Results suggest that ozone has a direct action on airway smooth muscle by changing Ca(2+) mobilization; Ca(2+) refilling via a Ca(2+) pump and Ca(2+) release via Ca(2+) channels in the sarcoplasmic reticulum were increased, while Ca(2+) extrusion via the plasma membrane Ca(2+) pump was unchanged.

Acetylcholine↗

Effect of cumulative exposure on nasal response to ozone.

To assess the potential health risks associated with exposure to low levels of ozone, it is essential to know if the ozone-induced responses are dependent on cumulative exposures or on the peak concentrations. To answer this question female F344/N rats, 11-13 weeks of age, were exposed to a matrix of equal concentration x time values that included exposures to 0, 0.12, 0.24, and 0.48 ppm ozone for 3, 6, 12, or 24 hr. the response of the nasal epithelium was measured as induced DNA synthesis determined by the uptake of bromodeoxyuridine (a thymidine analog) into epithelial cells lining the nasal anterior maxilloturbinates. No increased DNA synthesis was observed in rats exposed to 0.12 ppm ozone for any of the time periods. For exposures higher than 0.12 ppm ozone, the response of the nasal epithelium was similar for equal cumulative exposures. The responses, however, were not linearly related to the cumulative (concentration x time) exposures. It appeared that some mitigating factor was present which decreased the responses at the higher cumulative exposures. No frank toxicity or cellular necrosis was observed, indicating that sublethal cell damage was sufficient to induce DNA synthesis. A simple mathematical model was developed to describe the relationship between ozone exposure and the induction of DNA synthesis in the nasal epithelium. The model predicted that the threshold concentration of ozone for inducing DNA synthesis in the nasal epithelium was 0.1 +/- 0.1 ppm. For one measure of ozone toxicity (induced DNA synthesis) at a sensitive site in the respiratory tract (maxilloturbinates), the effects of ozone were dependent on cumulative exposures at concentrations > 0.12 ppm and within the time and concentration ranges used in this study.

Administration, Inhalation↗