Chronic O3 Exposure Research Articles

Abstract P292: Possible Mechanism and Potential Markers for Ozone-Induced Cardiac Toxicity

A significant number of deaths each year in the US have been linked to environmental pollutants such as ozone (O 3 ). Earlier studies from our laboratory have shown that myocardial dysfunction, subsequent to chronic O 3 exposure, in normal adult rats may be associated with a decrease in antioxidant reserve and with an increased activity of inflammatory mediators. The present study tested the hypothesis that O 3 induced cardiac dysfunction in healthy normal adult rats may be due to changes in caveolin-1 and caveolin-3 levels. Sprague Dawley rats were exposed 8 hr/day for 28 and 56 days to filtered air or 0.8 ppm O 3 . In order to assess the chronic effects to O 3 , in-vivo cardiac function was assessed by measuring left ventricular developed pressure (LVDP), 24 hr after termination of O 3 exposure. Compared to rats exposed to filtered air, LVDP values significantly decreased in all O 3 exposed animals. This attenuation of cardiac function was associated with increased myocardial TNF-alpha (TNF-α) levels and decreased myocardial activities of superoxidase dismutase (SOD). Progressive increases in the expression of myocardial TNF-α in 4 and 8 week O 3 exposed animals were followed by decreases in cardiac caveolin-1 levels. However, differential changes in the expression of caveolin-3 in hearts from 4 and 8 week O 3 exposed animals were independent of intra-cardiac TNF-α levels. These novel findings suggest the interesting possibility that a balance between caveolin-1 and caveolin-3 may be involved in O 3 - mediated cardiac toxicity. Furthermore, differential changes in caveolin-3 content may serve as a marker that predicts moderate and chronic stages of cardiac injury specific to exposure to O 3 in human populations residing in urban areas with unhealthy levels of O 3 . The study is timely and has clinical significance related to environmental causes of cardiovascular disease. This novel study will form a basis for future studies to understand and define the various components of the mechanistic cascade responsible for generation of cell death signaling subsequent to O 3 exposure. The long-term goal of this study is in guiding regulatory policies to the USEPA regarding air quality standards pertaining to O 3 levels.

Effects of acidic fog and ozone on the growth and physiological functions of Fagus crenata saplings

The effects of simulated acid fog (SAF) and ozone (O3) stress on the growth and physiology of beech (Fagus crenata) saplings were investigated. Three-year-old beech saplings were exposed to SAFs of pH 3 and pH 5 (control) during May 2007 to July 2008. In each SAF treatment group, half of the saplings were exposed to 60 ppb of O3 during September 2007 to July 2008. In comparison to the control saplings, those from the pH 3 treatment had lower total plant biomasses, epicuticular wax amounts, Ca2+ concentrations in their leaves, and lower starch concentrations in their leaves and roots. The effect of O3 was significant only for the starch concentration in the roots, but the O3 exposure also negatively affected the growth and physiology of beech saplings. Results show that acid fog exerts various severe effects, and that both chronic acid fog and O3 exposure suppressed the physiological functions of beech saplings.

Erratum to: Do chronic aboveground O3 exposure and belowground pathogen stress affect growth and belowground biomass partitioning of juvenile beech trees (Fagus sylvatica L.)?

Erratum to: Do chronic aboveground O3 exposure and belowground pathogen stress affect growth and belowground biomass partitioning of juvenile beech trees (Fagus sylvatica L.)?

Do chronic aboveground O3 exposure and belowground pathogen stress affect growth and belowground biomass partitioning of juvenile beech trees (Fagus sylvatica L.)?

The impact of chronic free air ozone (O3) exposure and belowground pathogen stress on growth and total biomass development of young beech trees (Fagus sylvatica L.) was investigated in a lysimeter study. Plants were growing during four years under ambient or elevated atmospheric O3 concentrations. Additionally, in the last vegetation period the root rot pathogen Phytophthora citricola was introduced to study the interaction of ozone exposure and pathogen stress in the soil-plant system. A complete harvest at the end of the experiment enabled for the first time the assessment of fine and coarse root biomass of individual trees with a high vertical resolution down to two meter depth. Plant growth was significantly reduced by elevated ozone but not affected by P. citricola. Biomass partitioning between fine and coarse roots as well as vertical root distribution were significantly affected by both factors, whereas changes in root/shoot biomass ratio were not observed.

Chronicvs.Short-Term Acute O3Exposure Effects on Nocturnal Transpiration in Two Californian Oaks

We tested the effect of daytime chronic moderate ozone (O3) exposure, short-term acute exposure, and both chronic and acute O3 exposure combined on nocturnal transpiration in California black oak and blue oak seedlings. Chronic O3 exposure (70 ppb for 8 h/day) was implemented in open-top chambers for either 1 month (California black oak) or 2 months (blue oak). Acute O3 exposure (~1 h in duration during the day, 120–220 ppb) was implemented in a novel gas exchange system that supplied and maintained known O3 concentrations to a leaf cuvette. When exposed to chronic daytime O3 exposure, both oaks exhibited increased nocturnal transpiration (without concurrent O3 exposure) relative to unexposed control leaves (1.8× and 1.6×, black and blue oak, respectively). Short-term acute and chronic O3 exposure did not further increase nocturnal transpiration in either species. In blue oak previously unexposed to O3, short-term acute O3 exposure significantly enhanced nocturnal transpiration (2.0×) relative to leaves unexposed to O3. California black oak was unresponsive to (only) short-term acute O3 exposure. Daytime chronic and/or acute O3 exposures can increase foliar water loss at night in deciduous oak seedlings.

Differential effects of elevated ozone on two hybrid aspen genotypes predisposed to chronic ozone fumigation. Role of ethylene and salicylic acid.

The role of ethylene (ET) signaling in the responses of two hybrid aspen (Populus tremula L. x P. tremuloides Michx.) clones to chronic ozone (O(3); 75 nL L(-1)) was investigated. The hormonal responses differed between the clones; the O(3)-sensitive clone 51 had higher ET evolution than the tolerant clone 200 during the exposure, whereas the free salicylic acid concentration in clone 200 was higher than in clone 51. The cellular redox status, measured as glutathione redox balance, did not differ between the clones suggesting that the O(3) lesions were not a result of deficient antioxidative capacity. The buildup of salicylic acid during chronic O(3) exposure might have prevented the up-regulation of ET biosynthesis in clone 200. Blocking of ET perception with 1-methylcyclopropene protected both clones from the decrease in net photosynthesis during chronic exposure to O(3). After a pretreatment with low O(3) for 9 d, an acute 1.5-fold O(3) elevation caused necrosis in the O(3)-sensitive clone 51, which increased substantially when ET perception was blocked. The results suggest that in hybrid aspen, ET signaling had a dual role depending on the severity of the stress. ET accelerated leaf senescence under low O(3), but under acute O(3) elevation, ET signaling seemed to be required for protection from necrotic cell death.

Effect of Host Plant Ozone Stress on Colorado Potato Beetles

Effects of ozone (O3) stress of potato, Solanum tuberosum L., on fecundity, larval growth and survival of Colorado potato beetles, Leptinotarsa decemlineata (Say), were measured in greenhouse and field experiments. Chronic O3 exposure caused moderate to severe foliar injury on an O3-sensitive cultivar (‘Red Norland’) but caused only minor injury an O3-resistant cultivar (‘Superior’). Foliar injury caused by O3 was greater on old than on young leaves but feeding by adult beetles was greater on young leaves in all experiments. Foliar analyses of the five uppermost leaves (nodes 1–5) showed higher carbon (C) and higher nitrogen (N) concentration in Superior than in Norland. There were no significant O3 effects on C or N and no cultivar × O3 interactions. Egg production by newly emerged adult beetles feeding on plants exposed to high O3 levels was not significantly different from egg production on plants exposed to low O3 levels, regardless of cultivar O3 sensitivity. Feeding and energy conversion efficiency of neonates and survival of larvae to the adult stage were not significantly affected by the O3 treatment. Although present levels of tropospheric O3 are high enough to significantly affect yield of sensitive potato cultivars, our results indicate no significant effect of ambient O3 concentrations on Colorado potato beetle populations.

Nitrogen availability modifies the ozone responses of Scots pine seedlings exposed in an open-field system.

Three-year-old Scots pine (Pinus sylvestris L.) seedlings were exposed to either ambient or elevated (1.5-1.6 x ambient) ozone concentration ([O3]) for three growing seasons in an open-field fumigation facility where they were irrigated during the growing season with a nutrient solution providing nitrogen (N) at 70 (LN treatment), 100 (control) or 150% (HN treatment) of the optimum supply rate. Treatment effects were most evident during the third year of exposure, when the ambient [O3] + HN treatment enhanced whole-plant biomass, root/shoot dry weight ratio, needle pigment concentrations and the number of chloroplast plastoglobuli in the mesophyll cells in current-year (C) needles, whereas it reduced starch accumulation in C needles and abscission of 2-year-old (C+2) needles. In the control fertilization, 3 years of exposure to elevated [O3] decreased stem-base diameter and increased K concentration and electron density of chloroplast stroma in C needles. Plants in the HN treatment exposed for 3 years to elevated [O3] had significantly lower heights, current-year main shoot length and root/shoot dry mass ratio than control plants, and increased abscission of C+2 needles. In contrast, O3-induced changes in the ultrastructure of mesophyll cells were most evident in seedlings grown for 3 years in the LN treatment. We conclude that, in Scots pine, a relatively O3-tolerant species, chronic O3 exposure leads to cumulative growth reduction, increased needle abscission and changes in carbon allocation that are strongly influenced by plant N availability.

Hydroponically cultivated radish fed L-galactono-1,4-lactone exhibit increased tolerance to ozone.

Leaf L-ascorbate content of an ozone (O3)-sensitive radish genotype (Raphanus sativus L. cv. Cherry Belle) was increased 2-fold by feeding hydroponically cultivated plants L-galactono- 1,4-lactone (GalL). Plants were grown in controlled-environment chambers ventilated with charcoal/Purafil-filtered air, and administered one of two O3 fumigation regimes: chronic exposure (75 nmol O3 mol(-1) for 7 h day(-1) for 21 days) and acute exposure (180 nmol O3 mol(-1) for 9 h). Chronic O3 exposure decreased root growth by 11% in plants maintained in pure nutrient solution (-GalL), but resulted in no change in root growth in GalL-fed plants (+GalL). Similarly, GalL-feeding counteracted the negative effects of O3 on CO2 assimilation rate observed in control plants (-GalL). Under acute O3 exposure, GalL-fed plants showed none of the visible symptoms of injury, which were extensive in plants not fed GalL. Leaf CO2 assimilation rate was decreased by acute 03 exposure in both GalL treatments, but the extent of the decline was less marked in GalL-fed plants. No significant changes in stomatal conductance resulted from GalL treatment, so O3 Uptake into leaves was equivalent in + GalL and -GalL plants. Feeding GalL, on the other hand, enhanced the level of ascorbate, and resulted in the maintenance of the redox state of ascorbate under acute O3 fumigation, in both the leaf apoplast and symplast. The effect of GalL treatment on ascorbate pools was consistent with the reduction in O3 damage observed in GalL-fed plants. Attempts to model O3 interception by the ascorbate pool in the leaf apoplast suggested a greater capacity for O3 detoxification in GalL-fed plants, which corresponded with the increase in O3 tolerance observed. However, modelled data for GalL-fed plants suggested that additional constituents of the leaf apoplast may play an important role in the attenuation of environmentally-relevant O3 fluxes.

Airway responses to chronic ozone exposure are partially mediated through mast cells.

Airways inflammation and epithelial injury induced by chronic ozone (O(3)) in genetically mast cell-deficient mice (Kit(W)/Kit(W-v)) were compared with those in mast cell-sufficient mice (+/+) and Kit(W)/Kit(W-v) mice repleted of mast cells (Kit(W)/Kit(W-v)-BMT). Mice were exposed to 0.26 ppm O(3) 8 h/day, 5 days/wk, for 1-90 days. Background was 0.06 ppm O(3). Age-matched mice were exposed to filtered air for O(3) controls. Reversibility of lesions was evaluated 35 days after exposure. Compared with Kit(W)/Kit(W-v), O(3) caused greater increases in lavageable macrophages, epithelial cells, and polymorphonuclear leukocytes in +/+ and Kit(W)/Kit(W-v)-BMT mice. O(3) also caused lung hyperpermeability, but the genotypic groups were not different. Cells and permeability returned to air control levels after O(3). O(3) induced lung cell proliferation only in +/+ and Kit(W)/Kit(W-v)-BMT mice; proliferation remained elevated or increased in +/+ and Kit(W)/Kit(W-v)-BMT mice after O(3). Greater O(3)-induced cell proliferation was found in nasal epithelium of +/+ and Kit(W)/Kit(W-v)-BMT mice compared with Kit(W)/Kit(W-v) mice. Results are consistent with the hypothesis that mast cells affect airway responses induced by chronic O(3) exposure.

A decade of forest tree monitoring in Canada: evidence of air pollution effects

In Canada, the eastern tolerant hardwood forest is potentially at risk from air pollution. Surveys indicate that, overall, the condition of hardwood forests has either not changed or has marginally improved. However, stands growing on shallow, poorly buffered soils have a higher frequency and severity of decline symptoms, and some of these stands have continued to decline, in contrast to the general trend. In Ontario on the most sensitive sites (<6 mequiv. exchangeable bases/100 g), decline symptoms increased coinciding with a decrease in B horizon pH and base saturation and with an exchangeable Al increase. On these sites the chemical analysis of foliage, root, xylem, and soils indicate that nutrient deficiencies, nutrient imbalances, or metal/nutrient antagonism are related to stand decline. There is a consistent spatial relationship between white birch decline in the Bay of Fundy area and acidic sea fog. Acid fog injures and leaches foliage and hastens soil acidification, leaving the stands weakened and making them more sensitive to stress, particularly drought. Some recent studies suggest that forest growth rates are declining and that the relationship with climate has deteriorated, implying that the forests are responding to a regional, nonclimatic, nonpathogenic stress. This could be a response to altered forest nutrient cycling associated with acidic deposition and chronic O3exposure. A study of sugar maple in Ontario estimated that after the mid-1960s growth has declined between 0.66 and 0.96 m3·ha-1·year-1, and that the decline was greatest on poorly buffered soils. Without enhanced forest management and more stringent air pollution regulations, the sustainability of forest productivity in Eastern Canada is likely to be difficult because of air pollution and soil fertility losses.Key words: dendroecology, acid deposition, ozone, forest decline, sugar maple, climate change.

A decade of forest tree monitoring in Canada: evidence of air pollution effects

In Canada, the eastern tolerant hardwood forest is potentially at risk from air pollution. Surveys indicate that, overall, the condition of hardwood forests has either not changed or has marginally improved. However, stands growing on shallow, poorly buffered soils have a higher frequency and severity of decline symptoms, and some of these stands have continued to decline, in contrast to the general trend. In Ontario on the most sensitive sites (<6 mequiv. exchangeable bases/100 g), decline symptoms increased coinciding with a decrease in B horizon pH and base saturation and with an exchangeable Al increase. On these sites the chemical analysis of foliage, root, xylem, and soils indicate that nutrient deficiencies, nutrient imbalances, or metal/nutrient antagonism are related to stand decline. There is a consistent spatial relationship between white birch decline in the Bay of Fundy area and acidic sea fog. Acid fog injures and leaches foliage and hastens soil acidification, leaving the stands weakened and making them more sensitive to stress, particularly drought. Some recent studies suggest that forest growth rates are declining and that the relationship with climate has deteriorated, implying that the forests are responding to a regional, nonclimatic, nonpathogenic stress. This could be a response to altered forest nutrient cycling associated with acidic deposition and chronic O3 exposure. A study of sugar maple in Ontario estimated that after the mid-1960s growth has declined between 0.66 and 0.96 m3·ha-1·year-1, and that the decline was greatest on poorly buffered soils. Without enhanced forest management and more stringent air pollution regulations, the sustainability of forest productivity in Eastern Canada is likely to be difficult because of air pollution and soil fertility losses.Key words: dendroecology, acid deposition, ozone, forest decline, sugar maple, climate change.

Overproduction of Ascorbate Peroxidase in the Tobacco Chloroplast Does Not Provide Protection against Ozone.

Transgenic tobacco (Nicotiana tabacum cv Bel W3) plants were used to test the hypothesis that protection from O3 injury could be conferred by overproduction of ascorbate peroxidase (APX) in the chloroplast. The 10-fold increase in soluble APX activity in the chloroplast was expected to alleviate an implied increase in oxidative potential and prevent damage caused by O3. Three different O3 exposure experiments (one acute and two chronic) with two replicates each were conducted. APX activity in nontransgenic plants increased in response to chronic O3 exposure. However, most responses to O3 were similar between transgenic and nontransgenic plants. These included reductions in net photosynthesis and stomatal conductance, increases in ethylene emission and visible injury, and a decline in the level of the small subunit of ribulose-1,5-biphosphate carboxylase/oxygenase mRNA transcripts observed in response to the air pollutant in the acute and/or chronic experiments. No O3-induced effect on ribulose-1,5-biphosphate carboxylase/oxygenase quantity was observed in the chronic experiments. O3 did not induce acceleration of senescence, as expected from studies with most other species; rather, the tobacco plants rapidly developed necrotic lesions. Thus, overproduction of APX in the chloroplast did not protect this cultivar of tobacco from O3.

Ozone Adaptation in Rats after Chronic Exposure to a Simulated Urban Profile of Ozone

Ozone Adaptation in Rats after Chronic Exposure to a Simulated Urban Profile of Ozone. Wiester, M. J., Tepper, J. S., Doerfler, D. L., and Costa, D. L. (1995). Fundam. Appl. Toxicol.24, 42-51.Studies in both humans and rats have indicated that certain pulmonary responses induced by exposure to an acute provocative concentration of ozone (O3) will eventually attenuate if the exposure is repeated on a daily basis. This phenomenon is commonly referred to as O3 adaptation. Whether or not a "state" of adaptation develops due to long-term low level O3 exposure is unknown. Two human studies have reported adaptation in subjects living in Los Angeles during periods when ambient O3 concentrations have been relatively high. At present, however, we are not aware of comparable information from rats. This study assessed O3 adaptation in rats following chronic (12 or 18 months) exposure and after a 4-month recovery period. A chronic exposure pattern, similar to that found in an urban area during the summer (0.06 ppm O3 for 13 hr/day, 7 days/week; Monday-Friday, peak to 0.25 ppm O3, over 9 hr), was used. To assess whether adaptation had occurred and/or persisted, awake rats were challenged with high provocative concentrations of O3 for up to 2 hr. During a challenge, rats were monitored for typical O3-induced alterations in spontaneous breathing parameters (e.g., increase in breathing frequency and decrease in tidal volume). Adaptation was defined as attenuation of breathing response during the challenge in rats chronically exposed to O3 as compared to that in "control" rats (chronically exposed to air). Adaptation was found in the rats within 8 hr following the chronic O3 exposure but not after the 4-month recovery period. Spontaneous breathing parameters that were significantly attenuated in the chronically exposed rats were breathing frequency, tidal volume, inspiratory and expiratory times, and maximum expiratory flow. We conclude that rats demonstrated adaptation to O3 after long-term exposure to an urban-type O3 profile and that the adaptation was not seen 4 months postexposure. These results suggest that exposure to environmental O3 in Los Angeles air may have been responsible for the adaptation found in residential subjects.

Ozone Adaptation in Rats after Chronic Exposure to a Simulated Urban Profile of Ozone

Studies in both humans and rats have indicated that certain pulmonary responses induced by exposure to an acute provocative concentration of ozone (O3) will eventually attenuate if the exposure is repeated on a daily basis. This phenomenon is commonly referred to as O3 adaptation. Whether or not a “state” of adaptation develops due to long-term low level O3 exposure is unknown. Two human studies have reported adaptation in subjects living in Los Angeles during periods when ambient O3 concentrations have been relatively high. At present, however, we are not aware of comparable information from rats. This study assessed O3 adaptation in rats following chronic (12 or 18 months) exposure and after a 4-month recovery period. A chronic exposure pattern, similar to that found in an urban area during the summer (0.06 ppm O3 for 13 hr/day, 7 days/week; Monday–Friday, peak to 0.25 ppm O3, over 9 hr), was used. To assess whether adaptation had occurred and/or persisted, awake rats were challenged with high provocative concentrations of O3 for up to 2 hr. During a challenge, rats were monitored for typical O3-induced alterations in spontaneous breathing parameters (e.g., increase in breathing frequency and decrease in tidal volume). Adaptation was defined as attenuation of breathing response during the challenge in rats chronically exposed to O3 as compared to that in “control” rats (chronically exposed to air). Adaptation was found in the rats within 8 hr following the chronic O3 exposure but not after the 4-month recovery period. Spontaneous breathing parameters that were significantly attenuated in the chronically exposed rats were breathing frequency, tidal volume, inspiratory and expiratory times, and maximum expiratory flow. We conclude that rats demonstrated adaptation to O3 after long-term exposure to an urban-type O3 profile and that the adaptation was not seen 4 months postexpo-sure. These results suggest that exposure to environmental O3 in Los Angeles air may have been responsible for the adaptation found in residential subjects.

Use of human lung tissue for studies of structural changes associated with chronic ozone exposure: opportunities and critical issues.

Definitive information on the chronic effects of exposure to ozone (O3) in humans is not available. There is a strong concern that ozone could produce chronic lung damage in humans on the basis that exposures are ubiquitous at levels that produce transient symptoms, function deficits, and lung inflammation in humans and chronic lung damage in laboratory animals. Both prospective and national population surveys suggest an association between chronic O3 exposure and reduced lung function, and a pilot investigation of autopsied lungs of accident victims in Los Angeles reported an unexpectedly high incidence of disease in the centriacinar region, the lung region known to receive the highest dose of inhaled O3. This paper discusses the advantages and limitations of further studies of structural changes in human lung tissue in relation to chronic O3 exposure. The major advantages of such studies are that a) measurable effects may be related to realistic chronic exposures, b) the effects may be described quantitatively and compared directly to those obtained in chronic animal inhalation exposures, and c) evidence for chronic effects may be obtained much more rapidly than in prospective studies. The major limitations are the difficulties in obtaining sufficient reliable information on residential history, physical activity out-of-doors, and smoking and other confounding exposures to lung irritants from next of kin, and limited availability of adequate air quality data for determining ambient concentrations at places of residence and/or outdoor exercise. The paper also discusses approaches to minimizing these limitations in the design of specific studies.

Summary of papers and research recommendations of Working Group on Tropospheric Ozone, Health Effects Institute environmental epidemiology planning project.

This paper summarizes the themes and recommendations that emerge from the papers presented by the Working Group on Tropospheric Ozone. In terms of current knowledge, the following are considered of particular importance: a) lack of clear evidence for a human analogue of the terminal bronchiolar and proximal acinar changes observed in the lungs of ozone-exposed animals; b) lack of evidence for a connection between the acute respiratory effects of O3 and possible chronic respiratory effects; c) need to better define the characteristics of O3-susceptible individuals; d) the lack of adequate exposure assessment tools for reconstruction of lifetime O3 exposure; and e) incomplete information on the role of other ambient environmental pollutants in the facilitation of O3 effects or as a cause of effects attributed to O3 in human populations. Based on the above, several recommendations for epidemiologic research on health effects of O3 are offered. a) Studies to investigate the existence of chronic health effects of O3 are essential, particularly those that include autopsied human lung tissue and biologic and physiologic response markers. b) Studies are needed to link acute responses with chronic effects and should include joint epidemiologic and controlled-exposure assessments. c) Studies are needed to identify susceptible subgroups. Such studies should include newly emerging biologic markers of O3 exposure. d) Accurate and precise tools for chronic O3 exposure assessment need to be developed for use in retrospective and prospective studies. e) Collaborative studies between epidemiologists and laboratory investigators are needed to develop and evaluate markers of O3 exposure and to test O3 exposure models.

Growth and leaf senescence in spring wheat (Triticum aestivum) grown at different ozone concentrations in open‐top field chambers

Spring wheat (Triticum aestivum L. cv. Albis) was grown during two consecutive seasons (1987, 1988) in open‐top field fumigation chambers at a site in central Switzerland and exposed to different doses of ozone (O3) in order to study O3 effects on growth and leaf senescence. The O3 dose in nonfiltered air (NF) was 42.6 μl I‐1 h in 1987 and 49.2 μ I‐1 h in 1988. The other treatments used were: charcoal‐filtered air (CF) (0.5 × O3 dose in nonfiltered air) and nonfiltered air with one of two levels of O3 added daily (0900–1700 h) (O3‐1 with 1.5 × O3 dose in nonfiltered air and O3‐2 with 1.9 × O3) dose in nonfiltered air). From anthesis through senescence, dry weight of individual ears, and chlorophyll and protein content, glutamate dehydrogenase activity (GDH, EC 1.4.1.3), and the content of free and conjugated 1‐aminocyclopropane‐1‐carboxylic acid (ACC and MACC) in flag leaves were determined. With increasing O3 dose, the decline in chlorophyll and soluble protein contents started earlier, but the rate of decline decreased. Independent of the treatment used, GDH activity was highest during the period of maximal protein loss. With increasing O3 dose, the content of MACC increased, while that of free ACC remained unaffected. In 1988, temporal changes in MACC were related to other senescence processes. It is suggested that with increasing stress from chronic O3 exposure leaf duration is reduced, but that the pattern of senescence processes remains unchanged. Ozone‐induced acceleration of flag leaf senescence could contribute to the observed reduction in ear dry weight accumulation, which may account for yield reduction in spring wheat.

Effects of Low Concentrations of O3 on Net Photosynthesis, Dark Respiration, and Chlorophyll Contents in Aging Hybrid Poplar Leaves

Chronic exposure of hybrid poplar (Populus deltoides x trichocarpa) plants to low concentrations of ozone had negative impact upon net photosynthetic capacity, dark respiration, and leaf chlorophyll contents. Exposure to as much as 0.20 microliters per liter O(3) had no immediate effect on net photosynthesis (P(n)), but chronic exposure to 0.125 or 0.085 microliters per liter had a number of gradual effects on CO(2) exchange. These included increased dark respiration and consequently increased light compensation points in very young leaves (4-6 days old); and decreased P(n), leaf chlorophyll a and b contents, light saturation points, and apparent quantum yields in leaves 10 to 70 days old. Decreased P(n) was partially due to accelerated aging in leaves exposed to O(3), and lightsaturated P(n) was linearly related to chlorophyll a + b contents. Differences in light-saturated P(n) between control and O(3)-treated leaves of the same age were mostly due to photosaturation in O(3)-treated leaves and to a much lesser extent to lowered apparent quantum yields. Also, since P(n) and dark respiration were most affected by O(3) at different leaf ages, distinct modes of action are suggested. The effects of leaf aging on CO(2) exchange were considerable, but typical of other species. However, careful monitoring of the interacting effects of leaf age and pollutant exposure was needed in order to characterize the impact of chronic O(3) exposure upon CO(2) exchange.

Effects of ozone exposure in Canadians and Southern Californians. Evidence for adaptation?

Comparison of published reports on physiological effects of exposure to ozone (O3) suggests that Canadians are more reactive than southern Californians. Responses of subjects and experimental methods were compared in a cooperative investigation of this apparent difference in reactivity. Four Canadians and four Californians were exposed to 0.37 ppm O3 in purified air at 21 degrees C and 50% relative humidity for 2 hours with intermittent light exercise. Exposures to purified air alone served as controls. Responses of subjects were similar to those observed previously: Canadians on the average showed greater clinical and physiological reactivity to exposure than did Californians, who were no more than minimally reactive. Canadians also showed larger increases in erythrocyte fragility following exposure. No methodological differences sufficient to explain different results of previous studies were found. Although other possible explanations have not been ruled out entirely, adaptation of southern Californians to chronic ambient O3 exposure is a rational hypothesis to explain these results.