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PubMed1997

Differences in growth, leaf senescence and injury, and stomatal density in birch (Betula pendula Roth.) in relation to ambient levels of ozone in Finland.

The differences in growth, leaf senescence, visible ozone injuries and stomatal density between one coastal site (natural ozone) and two inland sites (natural and elevated ozone) in Finland were determined for saplings of Betula pendula clones grown under open-field conditions during two growing seasons. Responses in growth, leaf senescence, visible injuries, and stomatal density were determined in relation to cumulative ozone exposure accumulated over the thresholds of 30, 40 and 50 ppb (10(9)) during the exposure period. In addition, the effects of the different ozone exposures on ultrastructure of chloroplasts were studied. Increasing ozone exposure resulted in reduced shoot dry weight, stimulated (first year) or reduced (second year) height growth, accelerated autumn yellowing of leaves, increased stomatal density, visible symptoms and chloroplast injuries, and increased number and size of plastoglobuli. Newly expanded mature leaves in midsummer were more sensitive to ozone episodes than younger developing leaves in the early growing season. In most parameters, the best correlation was achieved with the exposure index AOT30. Ozone risk for birch is highest in the southern coastal area of Finland, where background ozone concentrations are higher than in inland sites.

Journal Article↗
PubMed2000

Quantifying simultaneous fluxes of ozone, carbon dioxide and water vapor above a subalpine forest ecosystem.

Assessing the long-term exchange of trace gases and energy between terrestrial ecosystems and the atmosphere is an important priority of the current climate change research. In this regard, it is particularly significant to provide valid data on simultaneous fluxes of carbon, water vapor and pollutants over representative ecosystems. Eddy covariance measurements and model analyses of such combined fluxes over a subalpine coniferous forest in southern Wyoming (USA) are presented. While the exchange of water vapor and ozone are successfully measured by the eddy covariance system, fluxes of carbon dioxide (CO(2)) are uncertain. This is established by comparing measured fluxes with simulations produced by a detailed biophysical model (FORFLUX). The bias in CO(2) flux measurements is partially attributed to below-canopy advection caused by a complex terrain. We emphasize the difficulty of obtaining continuous long-term flux data in mountainous areas by direct measurements. Instrumental records are combined with simulation models as a feasible approach to assess seasonal and annual ecosystem exchange of carbon, water and ozone in alpine environments. The viability of this approach is demonstrated by: (1) showing the ability of the FORFLUX model to predict observed fluxes over a 9-day period in the summer of 1996; and (2) applying the model to estimate seasonal dynamics and annual totals of ozone deposition and carbon, and water vapor exchange at our study site. Estimated fluxes above this subalpine ecosystem in 1996 are: 195 g C m(-2) year(-1) net ecosystem production, 277 g C m(-2) year(-1) net primary production, 535 mm year(-1) total evapo-transpiration, 174 mm year(-1) canopy transpiration, 2.9 g m(-2) year(-1) total ozone deposition, and 1.72 g O(3) m(-2) year(-1) plant ozone uptake via leaf stomata. Given the large portion of non-stomatal ozone uptake (i.e. 41% of the total annual flux) predicted for this site, we suggest that future research of pollution-vegetation interactions should relate plant response to actively assimilated ozone by foliage rather than to total deposition. In this regard, we propose the Physiological Ozone Uptake Per Unit of Leaf Area (POUPULA) as a practical index for quantifying vegetation vulnerability to ozone damage. We estimate POUPULA to be 0.614 g O(3) m(-2) leaf area year(-1) at our subalpine site in 1996.

Journal Article↗
PubMed2003

Regulation of phosphoenolpyruvate carboxylase in Pinus halepensis needles submitted to ozone and water stress.

Effects of ozone and/or drought stresses on phosphoenolpyruvate carboxylase (PEPc, EC 4.1.1.31) regulation in Pinus halepensis Mill. needles were assessed over 3 months in controlled conditions. Whereas moderated water stress applied to Aleppo pine had no effect on PEPc activity compared to the control, which was probably related to the high tolerance of this species to drought, ozone stress induced a dramatic increase of PEPc activity in pine needles. This stimulation of the anaplerotic pathway could provide substrates to repair processes, well known for being enhanced upon ozone exposure. The ozone-increased PEPc activity was related, to a certain extent, to an increase in protein and mRNA levels. The possible role of the stimulation of the phosphorylation status of the enzyme in the increased PEPc activity under ozone was also investigated. Following the demonstration of the existence of the phosphorylation site at the N terminal part of Aleppo pine PEPc, it was shown that, under ozone treatment, the light/dark PEPc activity ratio and the Ki (malate) for PEPc were increased. This strengthens the hypothesis of an ozone-related post-translational process, which could be part of an adaptation of the plants to prolonged stress. When ozone and water stress were applied in combination, the enhancement in PEPc activity was only related to changes in gene expression. This difference in PEPc regulation, compared to the effect of single stress, could be the consequence of the specific action of each stress on the enzyme. This study brings new insights into the regulation of PEPc in a C3 plant, Aleppo pine under these stresses. A different regulatory mechanism of PEPc is occurring according to the stress. The physiological implications of the increase in PEPc activity in response to ozone and/or water stress are discussed.

Journal Article↗
PubMed1996

Carbon partitioning and allocation in northern red oak seedlings and mature trees in response to ozone.

Northern red oak (Quercus rubra L.) seedlings and trees differ in their response to ozone. Previous work reported reductions in net photosynthesis, carboxylation efficiency and quantum yield of mature tree leaves, whereas seedling processes were unaffected by the same ozone exposure. To further characterize differences in ozone response between seedlings and mature trees, we examined carbon partitioning and allocation in 32-year-old trees and 4-year-old seedlings of northern red oak after exposure to subambient (seasonal SUM00 dose (sum of all hourly ozone exposures) = 31 ppm-h), ambient (SUM00 dose = 85 ppm-h) and twice ambient (SUM00 dose = 151 ppm-h) ozone concentrations for three growing seasons. For mature trees, ozone exposure decreased foliar starch partitioning, increased starch partitioning in branches and increased (14)C retention in leaves. In contrast, starch partitioning in leaves and branches, and foliar (14)C retention in seedlings were unaffected by ozone exposure, but soluble carbohydrate concentrations in coarse and fine roots of seedlings were reduced. Differences in carbohydrate demand between seedlings and mature trees may underlie the higher leaf ozone uptake rates and greater physiological response to ozone in mature northern red oak trees compared with seedlings.

Journal Article↗
PubMed1991

The effect of different atmospheric ozone partial pressures on photosynthesis and growth of nine fruit and nut tree species.

Nursery stock of peach (Prunus persica L. Batsch, cv. O'Henry), nectarine (P. persica L. Batsch, cv. Fantasia), plum (P. salicina Lindel., cv. Casselman), apricot (P. armeniaca L., cv. Tilton), almond (P. dulcis Mill., cv. Nonpareil), prune (P. domestica L., cv. Improved French), cherry (P. avium L., cv. Bing), oriental pear (Pyrus pyrifolia Rehd., cv. 20th Century), and apple (Malus pumula Mill., cv. Granny Smith) were planted in open-top chambers on April 1, 1988 at the University of California's Kearney Agricultural Center located in the San Joaquin Valley (30 degrees 40' N 119 degrees 40' W). Trees were exposed to three atmospheric ozone partial pressures (charcoal-filtered air (C), ambient air (A), or ambient air + ozone (T)) from August 1 to November 17, 1988. The mean 12-h (0800 to 2000 h) ozone partial pressures measured in open-top chambers during the experimental period were 0.030, 0.051, and 0.117 microPa Pa(-1) in the C, A and T treatments, respectively. Leaf net CO(2) assimilation rate decreased linearly with increasing 12-h mean ozone partial pressure for the almond, plum, apricot, prune, pear, and apple cultivars. Stomatal conductances of apricot, apple, almond, and plum decreased linearly with increasing ozone partial pressure. Cross-sectional area relative growth rates of almond, plum, apricot, and pear decreased linearly with increasing ozone partial pressure. Net CO(2) assimilation rate, stomatal conductance, and trunk growth of cherry, peach and nectarine were unaffected by the ozone treatments. Reduced leaf gas exchange probably contributed to ozone-induced growth reduction of the susceptible species and cultivars. Several of the commercial fruit tree species and cultivars studied were relatively tolerant to the ozone treatments.

Journal Article↗
PubMed1967

Inhibition of oxidative phosphorylation and respiration by ozone in tobacco mitochondria.

Ozone was found to inhibit oxidative phosphorylation and oxygen uptake in mitochondria of tobacco leaves (Nicotiana tabacum, L. var. White Gold). The inhibition appeared to occur at both substrate and electron-transport chain levels. The inhibition increased with the length of exposure to ozone, however, the phosphorylative system was more sensitive to ozone than the respiratory system. With mitochondria from detached leaves after being treated with ozone at 1 ppm for 1 hour, uncoupling of phosphorylation was demonstrated without any detectable change in the rate of respiration in the early stage of ozone effect. Inhibition of phosphorylation by ozone was also demonstrated in isolated mitochondria without apparent change in optical density of the mitochondrial suspension at 520 mmu. Therefore, mitochondrial swelling appears not to be a necessary first step for ozone-induced uncoupling of phosphorylation. The evidence suggests that inhibition of oxidative phosphorylation in mitochondria may be a primary effect of ozone in tobacco leaves.Sucrose and glucose, when fed to the detached tobacco leaves before ozone treatment, tended to raise the phosphorylative activity of mitochondria. Mannitol and lactose were less effective.

Journal Article↗
PubMed1980

Mechanism of Ozone Inactivation of Bacteriophage f2.

The inactivation kinetics of bacteriophage f2 were studied by using ozone under controlled laboratory conditions. The phage were rapidly inactivated during the first 5 s of the reaction by 5 and 7 logs at ozone concentrations of 0.09 and 0.8 mg/liter, respectively. During the next 10 min, the phage were further inactivated at a slower rate in both treatments. The [H]uridine-labeled f2 phage and its ribonucleic acid (RNA) were examined to elucidate the mechanism of ozone inactivation, utilizing adsorption to host bacteria, sucrose density gradient analysis, and electron microscopy. The specific adsorption of the phage was reduced by ozonation in the same pattern as plaque-forming unit reduction. RNA was released from the phage particles during ozonation, although it had reduced infectivity for spheroplasts. Electron microscopic examination showed that the phage coat was broken by ozonation into many protein subunit pieces and that the specific adsorption of the phage to host pili was inversely related to the extent of phage breakage. The RNA enclosed in the phage coat was inactivated less by ozonation than were whole phage, but inactivated more than naked RNA. These findings suggest that ozone breaks the protein capsid into subunits, liberating RNA and disrupting adsorption to the host pili, and that the RNA may be secondarily sheared by a reduction with and/or without the coat protein molecules, which have been modified by ozonation.

Journal Article↗
PubMed1998

Induction of interleukin-8 by ozone is mediated by tyrosine kinase and protein kinase A, but not by protein kinase C.

Ozone is one of the most common air pollutants humans routinely inhale. We have previously shown that in vitro ozone exposure induces the DNA-binding activities of NF-kappaB and NF-IL6 as well as the expression of interleukin 8 in respiratory epithelial cells. In this study, we investigated intracellular signaling steps mediating ozone-induced inflammatory mediator release. A549 cells, a type II like alveolar epithelial cell line, were exposed in vitro to air or 0.1 ppm of ozone in the presence of several kinase inhibitors. Exposure to ozone increased interleukin 8 expression and transcription factor activities in a protein tyrosine kinase (PTK)-dependent and protein kinase A (PKA)-dependent, yet protein kinase C (PKC)-independent, manner. Furthermore, ozone-induced PTK and PKA activities but failed to induce PKC activity. In addition, our results suggest that ozone-induced PTK and PKA activities were reactive oxygen intermediate dependent and occurred in parallel, because specific inhibitors for PTK and PKA failed to block the other kinase's activity. These results indicate that PTK and PKA activities are early events in the signal transduction cascade mediating the ozone-induced activation of NF-kappaB and NF-IL6 as well as the release of interleukin 8.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed1986

Mutagenicity studies in Salmonella: residues of ozonated and/or chlorinated water fulvic acids.

Aqueous residues of ozonated, chlorinated, and ozonated/chlorinated water fulvic acids (WFA) were tested for induction of His+ reversion in Salmonella typhimurium strain TA100 in fluctuation tests for mutagenicity. The data suggest that ozonation of natural organics present in sources of drinking water can prevent subsequent formation of by-products of chlorination that are mutagenic in bacteria. Ozonation of the WFA at different pH and at varying dose levels produced residues that were not or were only weakly mutagenic. Chlorination of WFA or of previously ozonated WFA led to residues that were highly mutagenic. However, mutagen formation in the ozonated/chlorinated residues could be prevented, depending upon the pH of the WFA solutions during ozonation-mutagenicity decreased as pH increased. This decrease in mutagenicity is associated with previous observations of enhanced ozone decomposition into its highly reactive oxidant species at higher pH. Since ozonation seems to be more effective at alkaline pH, alkaline raw water sources seem to be the best candidates for water treatment that involves ozonation.

Benzopyrans↗
PubMed2005

Application of quantitative structure activity relationship (QSAR) models to predict ozone toxicity in the lung.

The sequence of events leading to ozone-induced airway inflammation is not well known. To elucidate the molecular and cellular events underlying ozone toxicity in the lung, we hypothesized that lipid ozonation products (LOPs) generated by the reaction of ozone with unsaturated fatty acids in the epithelial lining fluid and cell membranes play a key role in mediating ozone-induced airway inflammation. To test our hypothesis, we ozonized 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylcholine (POPC) and generated LOPs. Confluent human bronchial epithelial cells were exposed to the derivatives of ozonized POPC-9-oxononanoyl, 9-hydroxy-9-hydroperoxynonanoyl, and 8-(5-octyl-1,2,4-trioxolan-3-yl-)octanoyl-at a concentration of 10 muM, and the activity of phospholipases A2 (PLA2), C (PLC), and D (PLD) was measured (1, 0.5, and 1 h, respectively). Quantitative structure-activity relationship (QSAR) models were utilized to predict the biological activity of LOPs in airway epithelial cells. The QSAR results showed a strong correlation between experimental and computed activity (r = 0.97, 0.98, 0.99, for PLA2, PLC, and PLD, respectively). The results indicate that QSAR models can be utilized to predict the biological activity of the various ozone-derived LOP species in the lung.

Cell Line↗
PubMed1998

Effects of ozone exposure in rats on memory and levels of brain and pulmonary superoxide dismutase.

Exposure to ozone results in increased production of free radicals, which causes oxidative stress. The objective of this study was to determine the effect of different doses of ozone exposure on memory and to correlate this with pulmonary and brain Cu/Zn superoxide dismutase (SOD) levels. Male Wistar rats were exposed for 4 h to one of the following ozone concentrations: 0, 0.1, 0.2, 0.5, or 1 ppm. Subsequently, they were tested in a passive avoidance conditioning protocol to measure short and long-term memory. Motor activity was determined 1 and 24 h after ozone exposure. Cu/Zn SOD levels in the brain and pulmonary tissue were also measured. Rats exposed for 4 h to 0.2, 0.5, and 1 ppm ozone showed long-term memory deterioration and decreased motor activity, which was reversed 24 h later. Brain and pulmonary Cu/Zn SOD levels were increased in animals exposed to 0.1, 0.2, and 0.5 ppm ozone doses, but decreased in animals exposed to 1 ppm ozone. The results suggest that ozone exposure affects long-term memory possibly in association oxidative stress.

Animals↗
PubMed1994

The relationship between delivered ozone dose and functional responses in humans.

The relationship between delivered ozone dose and variability of pulmonary function response to ozone was investigated in 20 young, healthy, nonsmoking male volunteers. The subjects were exposed to 0.4 ppm ozone for 1 hr during which time they walked on a treadmill at a speed and inclination sufficient to induce a minute ventilation (VE) of 20 liter/min/m2 body surface area. Prior to and immediately following exposure spirometric and plethysmographic measurements of lung function were made. In addition, 5 min after the beginning of exposure and 5 min before the end of exposure the uptake efficiency of ozone in the upper and lower respiratory tract, spontaneous tidal volume (Vt), and breathing frequency (f) were measured. During exposure subjects wore a noseclip in order to constrain breathing to the oral pathway. Uptake efficiencies in the upper (FURT) and lower (FLRT) respiratory tracts were determined by continuously drawing air from the posterior pharynx into a rapidly responding chemiluminescent ozone analyzer. Linear regression models were constructed to examine the relationships between pulmonary function and breathing pattern responses, and the instantaneous and average values of FLRT and VE. Initial VE and average VE (VE) were found to be significant predictors of FEV1 decrement (p = 0.011 and p = 0.006, respectively). In addition the cross-product term FLRT x VE was a significant predictor of Vt decrement (p = 0.02). These results suggest that delivered dose, as determined primarily by VE, is responsible for some of the intersubject variability of ozone response. The failure of FLRT to play a significant role may be due to the fact that it primarily reflects ozone uptake in the lung periphery distal to anatomical sites where the ozone response may be mediated.

Adult↗
PubMed1995

Cumulative labeling indices in epithelial cell populations of the respiratory tract after exposure to ozone at low concentrations.

Male Sprague-Dawley and F344 rats were exposed to concentrations of 0.12 ppm of ozone for 12 hr a night or for 24 hr a day, to 0.24 ppm for 24 hr a day, and to 0.36 ppm for 8 hr a night. Cumulative labeling indices were measured during the first and the third week of exposure in the terminal bronchioles, the large intrapulmonary airways, the trachea, and the anterior nasal passages. The most sensitive indicator for exposure to ozone after a 1-week exposure was an increased labeling index in the epithelium lining the terminal bronchioles. Sprague-Dawley and F-344 rats were equally sensitive to ozone. In the large intrapulmonary airways and in the maxillar turbinates, an increased cumulative labeling index was observed only at the highest dose (concentration x time). During the third week of exposure, no increases in labeling index were found in the large intrapulmonary airways and terminal bronchioles, whereas in the nasal passages the highest ozone concentration continued to elicit a proliferative response. Animals were also exposed for 1 week to ozone and then allowed to recover in air for another week. Renewed exposure to ozone produced a smaller, but still significant, increase in the labeling index compared to that in animals exposed to ozone for the first time. It was concluded that the determination of the cumulative labeling index in the terminal bronchioles may serve as a method to explore dose and time effects of such concentrations of ozone as may be encountered in heavily polluted urban environments.

Air Pollutants↗
PubMed1997

Ozone-induced stimulation of pulmonary sympathetic fibers: a protective mechanism against edema.

Tropospheric ozone exerts well-described toxic effects on the respiratory tract. Less documented, by contrast, is the ability of ozone to induce protective mechanisms against agents that are toxic to the lungs. In particular, interactions between ozone and the sympathetic nervous system have never been considered. Using a model of permeability edema in isolated perfused rabbit lungs, we report here that, immediately after exposure of rabbits to 0.4 ppm ozone for 4 hr, the pulmonary microvascular responses to acetylcholine and substance P are completely blocked. Several lines of evidence, including partial inhibition of the ozone-induced protective effect by several drugs (alpha2- and beta-adrenergic antagonists, neuropeptide Y antagonist, guanethidine), measured levels of released catecholamines in blood and urine and the in vitro response of isolated lungs exposed to 0.4 ppm ozone all seem to suggest that ozone can stimulate pulmonary adrenergic fibers and induce the local release of catecholamines and neuropeptide Y, this resulting in transient protection against pulmonary edema. We also showed that, 48 hr after the exposure, ozone increased the baseline microvascular permeability and the response to low concentrations of acetylcholine.

Acetylcholine↗
PubMed1998

Cytochrome P450 2E1 in rat tracheobronchial airways: response to ozone exposure.

The distal trachea and centriacinus of the lung are primary sites of acute injury during short-term ozone exposure; long-term exposure yields cells in these areas that are resistant to high doses of oxidant gases. Epithelial cells located in primary sites for ozone injury are also targets for chemicals that undergo cytochrome P450 (CYP)-dependent activation. These studies were designed to compare the effects of ozone exposure on pulmonary CYP2E1 in susceptible and nonsusceptible sites within the airway tree of lung. CYP2E1 activity was measured in well-defined regions of airways using p-nitrophenol, a CYP2E1-selective substrate, with HPLC/ electrochemical detection of the p-nitrocatechol. Alterations in distribution of CYP2E1 were evaluated by immunohistochemistry. CYP2E1 activities were highest in the distal bronchioles and minor daughter airways but were much lower in the lobar bronchi/ major daughter airways and trachea. Immediately after short-term ozone exposures (8 h, 1 ppm), CYP2E1 activities were elevated only in the lobar bronchi/major daughter airways. These activities remained above the filtered air control at 1 day but returned to control levels by 2 days. Immunohistochemical assessment of CYP2E1 protein in ozone and filtered air-exposed animals was consistent with the activity measurements. After long-term ozone exposures (90 days, 1 ppm), CYP2E1 activities were decreased in the major and minor daughter airways. These studies indicate that CYP2E1 activities vary substantially by airway level. However, ozone exposure only results in minimal alterations in activity with varying concentration of ozone, length of exposure, and time after exposure in any of the lung subcompartments examined.

Animals↗
PubMed2001

Nitric oxide and peroxynitrite in ozone-induced lung injury.

One of the hallmarks of the inflammatory response associated with tissue injury is the accumulation of macrophages at sites of damage. These cell types release proinflammatory cytokines and cytotoxic mediators to destroy invading pathogens and initiate wound repair. However, when produced in excessive amounts, these macrophage-derived mediators may actually contribute to tissue injury. This process involves both direct damage to target tissues and amplification of the inflammatory response. One group of macrophage-derived mediators of particular interest are reactive nitrogen intermediates including nitric oxide and peroxynitrite which have been implicated in tissue injury induced by a variety oftoxicants. Our laboratory has been investigating the role of reactive nitrogen intermediates in lung injury induced by oxidants such as ozone. Inhalation of ozone causes epithelial cell damage and Type II cell hyperplasia. This is associated with an accumulation of activated macrophages in the lower lungs which we have demonstrated contribute to toxicity. To analyze the role of macrophage-derived reactive nitrogen intermediates in ozone toxicity, we used transgenic mice lacking the gene for inducible nitric oxide synthase (NOSII). Treatment of wild type control animals with ozone (0.8 ppm) for 3 hr resulted in an increase in bronchoalveolar lavage (BAL) fluid protein reaching a maximum 24-48 hr after exposure. This was correlated with increased expression of NOSII protein and mRNA by alveolar macrophages and increased production of nitric oxide as well as peroxynitrite. Ozone inhalation also resulted in the appearance of nitrotyrosine residues in the lungs, an in vivo marker of peroxynitrite-induced damage. In contrast, in NOSII knockout mice, BAL protein was not increased demonstrating that these mice were protected from ozone-induced epithelial injury. Moreover, alveolar macrophages from the transgenic mice did not produce nitric oxide or peroxynitrite even after ozone inhalation. There was also no evidence for the formation of nitrotyrosine in lung tissue. These data indicate that ozone-induced lung injury is mediated by reactive nitrogen intermediates.

Animals↗
PubMed1988

Phosphatidylcholine synthesis in isolated type II pneumocytes from ozone-exposed rats.

Phosphatidylcholine (PC) synthesis by alveolar type II cells, as an indicator for the production of pulmonary surfactant, was studied after a 4-h exposure of rats to 4 mg ozone/m3 (2 ppm). Lung ravage fluid analysis after exposure revealed significant increases in proteins, which is indicative for pulmonary injury. When type II cells were isolated immediately and thereafter cultured for 20 h, the rate of PC synthesis in cells derived from ozone-exposed rats was not significantly different from that in cells from unexposed controls. Yet, a decreased rate of PC synthesis was observed when these cells were subsequently exposed to ozone in vitro. The activity of the enzyme glycerolphosphate acyltransferase (GPAT) was slightly enhanced in cultured type II cells isolated from ozone-exposed rats, while the lysophosphatidylcholine acyltransferase (LPCAT) activity was unchanged. However, ozone exposure of rats did result in a significant decrease of PC synthesis when measured in freshly prepared type II cell suspensions, although both GPAT and LPCAT activities were not affected. It is concluded that a decrease in pulmonary surfactant related PC synthesis after ozone exposure of rats can be demonstrated in freshly isolated type II pneumocytes. Cultured type II cells from exposed rats lack this effect and are therefore less useful to study changes in phospholipid biosynthesis after in vivo ozone exposure. The data on in vitro ozone exposure of cultured type II cells, however, support the view that ozone may impair pulmonary surfactant production.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMed1997

Rat lung phospholipid fatty acid composition in prepregnant, pregnant, and lactating rats: relationship to ozone-induced pulmonary toxicity.

Our laboratory has demonstrated recently that pulmonary inflammation induced by acute ozone exposure is much more severe in late stage pregnant and lactating rats than in postlactating rats or age-matched virgin females. It is currently widely believed that such pulmonary damage results, at least in part, from the reaction of ozone at sites of unsaturation in phospholipid fatty acid (PLFA) molecules located in the epithelial fluid layer lining the lung surfaces and/or the plasma membranes of epithelial cells underlying this fluid layer. The objective of this study was to compare the PLFA composition of lung tissue and surfactant from ozone-sensitive late stage pregnant and lactating rats with comparable tissue from relatively ozone-insensitive age-matched prepregnant (virgin female) rats to explore the possibility that changes in lung PLFA composition during pregnancy and/or lactation contribute to the enhanced sensitivity of these physiologic states to ozone. In addition, the correlation of changes in plasma PLFA composition with those in lung was investigated. There were minor differences in the composition of lung tissue and surfactant PLFAs between prepregnant rats and pregnant rats at day 17 of gestation and only slightly greater differences between prepregnant and lactating rats. Changes from the prepregnant state in the PLFA composition of lung tissue, but not surfactant, correlated with changes in the plasma only in lactating rats and not in pregnant rats. Overall, the double bond index of PLFAs in surfactant and lung tissue was decreased in pregnant and lactating rats compared with prepregnant rats. Thus, the increased sensitivity of pregnant and lactating rats to ozone-induced lung injury cannot be attributed to an increased availability of unsaturated fatty acids. In addition, the arachidonic acid composition of phospholipids did not appear to explain differences between prepregnant rats and pregnant or lactating rats in their inflammatory response to ozone. In conclusion, there is no evidence that the relatively minor changes in lung tissue PLFA composition which occur during pregnancy and lactation predispose rats in these physiologic states to ozone-induced pulmonary toxicity.

Animals↗