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PubMed2001

Passive ozone network of Dallas: a modeling opportunity with community involvement. 2.

Attaining the current lower tropospheric U.S. ozone standards continues to be a difficult task for many areas in the U.S. Concentrations of ozone above the standards negatively affects human health, agricultural crops, forests, and other ecosystem elements. This paper describes year two (1999) of a regional networking of passive and continuous ozone monitoring sites in the Dallas-Fort Worth (DFW) Metroplex region. The objectives of the second year of study were to (1) validate conclusions of the 1998 Passive Ozone Network of Dallas (POND) I study, (2) define the value of taking 12-h diurnal samples in addition to 24-h samples, and (3) add to the scientific knowledge base of rural/urban ozone comparison studies. Results of the POND II (1999) study demonstrated that ozone concentrations exceeding the new 8-h ozone standard could be recorded at least 130 km, or 80 miles, from the DFW Metroplex core in more rural areas. In addition, results of the POND II study indicated that ozone concentrations exceeding the 8-h standard probably occurred in areas recording a 12-h daytime ozone concentration above 60 parts per billion (ppb). The 12-h passive ozone data from POND II also suggests the relative magnitude of anthropogenic pollution influence could be assessed for rural passive ozone sites. The data from the POND II study provide modelers a rich database for future photochemical subgrid development for the DFW ozone nonattainment area. Indeed, the POND database provides a great amount of additional ozone ambient data covering 26 8-h and 13 1-h ozone standard exceedance days over an approximate 25000 km2 region. These data should help decrease uncertainties derived from future DFW ozone model exercises.

Air Pollutants↗

PubMed2005

Effects of an ozone-generating air purifier on indoor secondary particles in three residential dwellings.

UNLABELLED: The use of indoor ozone generators as air purifiers has steadily increased over the past decade. Many ozone generators are marketed to consumers for their ability to eliminate odors and microbial agents and to improve health. In addition to the harmful effects of ozone, recent studies have shown that heterogeneous and homogeneous reactions between ozone and some unsaturated hydrocarbons can be an important source of indoor secondary pollutants, including free radicals, carbonyls, carboxylic acids, and fine particles. Experiments were conducted in one apartment and two detached single-family dwellings in Austin, TX, to assess the effects of an ozone generator on indoor secondary organic aerosol concentrations in actual residential settings. Ozone was generated using a commercial ozone generator marketed as an air purifier, and particle measurements were recorded before, during, and after the release of terpenes from a pine oil-based cleaning product. Particle number concentration, ozone concentration, and air exchange rate were measured during each experiment. Particle number and mass concentrations increased when both terpenes and ozone were present at elevated levels. Experimental results indicate that ozone generators in the presence of terpene sources facilitate the growth of indoor fine particles in residential indoor atmospheres. Human exposure to secondary organic particles can be reduced by minimizing the intentional release of ozone, particularly in the presence of terpene sources. PRACTICAL IMPLICATIONS: Past studies have shown that ozone-initiated indoor chemistry can lead to elevated concentrations of fine particulate matter, but have generally been completed in controlled laboratory environments and office buildings. We explored the effects of an explicit ozone generator marketed as an air purifier on the formation of secondary organic aerosol mass in actual residential indoor settings. Results indicate significant increases in number and mass concentrations for particles <0.7 microns in diameter, particularly when an ozone generator is used in the presence of a terpene source such as a pine oil-based cleaner. These results add evidence to the potentially harmful effects of ozone generation in residential environments.

Aerosols↗

PubMedDate not supplied

Surface germicidal effects of ozone for microorganisms.

In this study the influences of microorganism species, relative humidity, and ozone dosage on ozone surface disinfection were evaluated. Bacterial and fungal cultures were spread on agar plates and exposed to ozone. The selected microorganisms included Escherichia coli, Bacillus subtilis, Candida famata, and Penicillium citrinum. Results showed that microorganism survival fraction and ozone dosage (ozone concentration times exposure time) have an exponential relationship. Results also indicated that E. coli was the most sensitive organism to ozone exposure. E. coli required only very low ozone doses of 2-2.5 and 3.5-4 mg to obtain 50 and 80% inactivation, respectively. In addition, P. citrinum was more resistant than E. coli and required ozone doses of 40-60 and 60-120 mg to obtain 50 and 80% inactivation. In addition, spores of B. subtilis were observed to be the most resistant organism, requiring ozone doses of 40-75 and 145-150 mg to obtain 50 and 80% inactivation. Yeast was less resistant than P. citrinum and B. subtilis, requiring ozone doses of 10 and 15-19 mg to obtain 50 and 80% inactivation. It was clearly indicated that the ozone dose differences for 80% microorganism inactivation could be as high as 40 times between B. subtilis and E. coli. Ozone surface germicidal efficiency increased as relative humidity increased, which could be related to more radicals generated from ozone reaction with more water vapor at higher relative humidity. It was concluded that ozone should be highly effective and provide a reliable safety factor in treating contaminated surface. In addition, workers might need to wear suitable respiratory protection at high ozone level operation.

Bacteria↗

PubMed2001

Inactivation of Escherichia coli O1 57:H7, Listeria monocytogenes, and Lactobacillus leichmannii by combinations of ozone and pulsed electric field.

Pulsed electric field (PEF) and ozone technologies are nonthermal processing methods with potential applications in the food industry. This research was performed to explore the potential synergy between ozone and PEF treatments against selected foodborne bacteria. Cells of Lactobacillus leichmannii ATCC 4797, Escherichia coli O157:H7 ATCC 35150, and Listeria monocytogenes Scott A were suspended in 0.1% NaCl and treated with ozone, PEF, and ozone plus PEE Cells were treated with 0.25 to 1.00 microg of ozone per ml of cell suspension, PEF at 10 to 30 kV/cm, and selected combinations of ozone and PEF. Synergy between ozone and PEF varied with the treatment level and the bacterium treated. L. leichmannii treated with PEF (20 kV/cm) after exposure to 0.75 and 1.00 microg/ml of ozone was inactivated by 7.1 and 7.2 log10 CFU/ml, respectively; however, ozone at 0.75 and 1.00 microg/ml and PEF at 20 kV/cm inactivated 2.2, 3.6, and 1.3 log10 CFU/ml, respectively. Similarly, ozone at 0.5 and 0.75 microg/ml inactivated 0.5 and 1.8 log10 CFU/ml of E. coli, PEF at 15 kV/cm inactivated 1.8 log10 CFU/ml, and ozone at 0.5 and 0.75 microg/ml followed by PEF (15 kV/cm) inactivated 2.9 and 3.6 log10 CFU/ml, respectively. Populations of L. monocytogenes decreased 0.1, 0.5, 3.0, 3.9, and 0.8 log10 CFU/ml when treated with 0.25, 0.5, 0.75, and 1.0 microg/ml of ozone and PEF (15 kV/cm), respectively; however, when the bacterium was treated with 15 kV/cm, after exposure to 0.25, 0.5, and 0.75 microg/ml of ozone, 1.7, 2.0, and 3.9 log10 CFU/ml were killed, respectively. In conclusion, exposure of L. leichmannii, E. coli, and L. monocytogenes to ozone followed by the PEF treatment showed a synergistic bactericidal effect. This synergy was most apparent with mild doses of ozone against L. leichmannii.

Colony Count, Microbial↗

PubMed1998

Effects of ozone on ovalbumin sensitization in guinea pigs.

The effects of ozone on allergen sensitization is still controversial. This study is aimed to clarify the effect of ozone on airway hypersensitivity to ovalbumin (OVA) in guinea pigs, by exposing them to ozone (3 ppm 2 hours daily) and OVA (1 gm/dL 10 min weekly) for two weeks. OVA specific IgG and airway hypersensitivity to methacholine were determined after the sensitization. The results demonstrated that there was a synergistic effect of ozone on OVA-induced IgG antibody production. OVA specific IgG was 0.51 +/- 0.1 U/mL and 0.46 +/- 0.1 U/mL using OVA and ozone alone respectively, which increased to 1.09 +/- 0.4 U/mL when both OVA and ozone were given simultaneously. Ozone exposure was able to cause airway hypersensitivity. The provocation dose of methacholine causing a 100% increase of airway resistance (PD 100 airway resistance) was 0.54 +/- 0.19 mg/mL and 1.17 +/- 0.30 mg/mL using OVA and ozone exposure alone, which had decreased to 0.49 +/- 0.18 mg/mL when both OVA and ozone were given simultaneously. There were macrophages around the peribronchial tissue in all guinea pigs except in the control. The macrophages in the group of OVA with ozone (24.2 +/- 7.2 cells/HPF) were significantly more than those in the OVA group (18.0 +/- 4.2 cells/HPF) and the ozone group (14.5 +/- 6.2 cells/HPF). When OVA-presensitized guinea pigs were exposed to ozone immediately or daily for two weeks, a restrictive type of lung function impairment with similar airway hypersensitivity post ozone exposure was observed. In conclusion, guinea pigs exposed to ozone in conjunction with aeroallergen may not only facilitate the damage of the airway but also enhance antibody production to the aeroallergen. The ozone-induced airway inflammation might have a contributing effect on OVA induced airway hypersensitivity in guinea pigs.

Allergens↗

PubMed1991

[The effect of a specific thromboxane A2 antagonist, AA-2414 on airway hyperresponsiveness induced by ozone exposure in dogs].

To determine whether thromboxane A2 (TxA2) is involved in airway hyperresponsiveness induced by ozone exposure, we studied the effect of a specific TxA2 antagonist, AA-2414 on ozone-induced airway hyperresponsiveness in seven dogs. Airway responsiveness to inhaled methacholine was determined by modified Astograph (7 Hz oscillation method), and numbers of neutrophils in the peripheral blood, neutrophil counts in bronchoalveolar lavage fluid (BALF), the levels of TxB2 and 6-keto-Prostaglandin F1 alpha (6-keto-PGF1 alpha) in BALF were measured before and after ozone exposure, and after ozone exposure with pretreated AA-2414. Ozone exposure was carried out for 2 hr at an ozone level of 3.06 +/- 0.06 ppm (mean +/- SE). Airway responsiveness to inhaled methacholine increased significantly after ozone exposure (p less than 0.01), and the hyperresponsiveness induced by ozone exposure was inhibited significantly by pretreated AA-2414 (p less than 0.01). Numbers of neutrophils in the peripheral blood and neutrophil counts in BALF increased after ozone exposure, and these increase were not inhibited by pretreated AA-2414. There was no apparent change in the levels of TxB2 in BALF after ozone exposure and after ozone exposure with pretreated AA-2414, however the levels of 6-keto-PGF1 alpha in BALF decreased after ozone exposure and after ozone exposure with pretreated AA-2414 (p less than 0.1). These results suggest that TxA2 plays an important role in the development of airway responsiveness after ozone exposure in dogs, and ozone-induced airway hyperresponsiveness may not be associated with the hyperproduction of TxA2 but with the relative increase of TxA2 due to the decrease of PGI2.

Animals↗

PubMed1991

Photosynthetic and stomatal conductance responses of Norway spruce and beech to ozone, acid mist and frost--a conceptual model.

Two-year-old beech and Norway spruce seedlings were exposed to a combination of ozone and acid mist treatments in open-top chambers in Scotland during the months of July through to September 1988. Replicate pairs of chambers received charcoal-filtered air (control), ozone-enriched air (140 nl ozone litre(-1)) or 140 nl ozone litre(-1) plus a synthetic acid mist (pH 2.5) composed of ammonium nitrate and sulphuric acid. Field measurements of assimilation and stomatal conductance were made during August. In addition, measurements of assimilation and conductance were made during September in the laboratory. Light response curves of assimilation and conductance were determined using a GENSTAT nonrectangular hyperbolic model. During February 1988/9 the Norway spruce were subject to a four day warming period at 12 degrees C and the light response of assimilation determined. The same plants were then subject to a 3-h night-time frost of -10 degrees C. The following day the time-course of the recovery of assimilation was determined. It was found that ozone fumigation did not influence the light response of assimilation of beech trees in the field, although stomatal conductance was reduced in the ozone-fumigated trees. The rate of light-saturated assimilation of Norway spruce was increased by ozone fumigation when measured in the field. Measurements of assimilation of Norway spruce made during the winter showed that prior to rewarming there was no difference in the rate of light-saturated assimilation for control and ozone-fumigated trees. However, the ozone plus acid mist-treated trees exhibited a significantly higher rate. The 4-day period of warming to 12 degrees C increased the rate of light-saturated assimilation in all treatments but only the ozone plus acid mist-treated trees showed a significant increase. Following a 3-h frost to -10 degrees C the control trees exhibited a reduction in the rate of light-saturated assimilation (Amax) to 80% of the pre-frost value. In comparison, following the frost, the ozone-fumigated trees showed an Amax of 74% of the pre-frost value. The ozone plus acid mist-treated trees showed an Amax of 64% of the pre-frost trees. The time taken for Amax to attain 50% of the pre-frost value increased from 30 min (control) to 85 min for ozone-fumigated trees to 190 min (ozone plus acid mist). These results are discussed in relation to the impact of mild, short-term frosts, which are known to occur with greater frequency than extreme, more catastrophic frost events. A simple conceptual framework is proposed to explain the variable results obtained in the literature with respect to the impact of ozone upon tree physiology.

Journal Article↗

PubMed1996

Response of giant sequoia canopy foliage to elevated concentrations of atmospheric ozone.

We examined the physiological response of foliage in the upper third of the canopy of 125-year-old giant sequoia (Sequoiadendron giganteum Buchholz.) trees to a 61-day exposure to 0.25x, 1x, 2x or 3x ambient ozone concentration. Four branch exposure chambers, one per ozone treatment, were installed on 1-m long secondary branches of each tree at a height of 34 m. No visible symptoms of foliar ozone damage were apparent throughout the 61-day exposure period and none of the ozone treatments affected branch growth. Despite the similarity in ozone concentrations in the branch chambers within a treatment, the trees exhibited different physiological responses to increasing ozone uptake. Differences in diurnal and seasonal patterns of g(s) among the trees led to a 2-fold greater ozone uptake in tree No. 2 compared with trees Nos. 1 and 3. Tree No. 3 had significantly higher CER and g(s) at 0.25x ambient ozone than trees Nos. 1 and 2, and g(s) and CER of tree No. 3 declined with increasing ozone uptake. The y-intercept of the regression for dark respiration versus ozone uptake was significantly lower for tree No. 2 than for trees Nos. 1 and 3. In the 0.25x and 1x ozone treatments, the chlorophyll concentration of current-year foliage of trees Nos. 1 and 2 was significantly higher than that of current-year foliage of tree No. 3. Chlorophyll concentration of current-year foliage on tree No. 1 did not decline with increasing ozone uptake. In all trees, total needle water potential decreased with increasing ozone uptake, but turgor was constant. Although tree No. 2 had the greatest ozone uptake, g(s) was highest and foliar chlorophyll concentration was lowest in tree No. 3 in the 0.25x and 1x ambient atmospheric ozone treatments.

Journal Article↗

PubMed1997

Carry-over effects of ozone on root growth and carbohydrate concentrations of ponderosa pine seedlings.

Ozone exposure decreases belowground carbon allocation and root growth of plants; however, the extent to which these effects persist and the cumulative impact of ozone stress on plant growth are poorly understood. To evaluate the potential for plant compensation, we followed the progression of ozone effects, with particular emphasis on the development of new roots. Ponderosa pine (Pinus ponderosa Dougl. ex Laws.) seedlings were exposed to ozone for 2 years. Following removal of the seedlings from ozone, root growth was assessed to characterize the carry-over effects on new root production, and carbohydrate concentrations were measured to determine if allocation strategies differed among ozone treatments. Four months after removal from ozone, dormant seedlings had significantly lower starch concentrations in stems, coarse roots and fine roots than control seedlings. Following root flushing, starch concentrations in all seedlings decreased, with ozone-treated seedlings containing significantly less starch, sucrose, fructose, glucose and total monosaccharides than control seedlings. There was some evidence that stem starch was mobilized to compensate partially for the lower concentrations of root starch in ozone-treated seedlings; however, there was significantly less new root production in seedlings previously exposed to ozone for 2 years than in control seedlings. Early senescence of older needle age classes, perhaps resulting in inadequate available photosynthate, may be responsible for the reduction in new root production during the year following exposure to ozone. Stored carbohydrate reserves, which were depleted in seedlings previously exposed to ozone, were insufficient to compensate for the ozone-induced reduction in canopy photosynthate. We conclude that there are carry-over effects of ozone exposure on ponderosa pine seedlings, including an enhanced potential for seedling susceptibility to other stresses even in respite years when ozone concentrations are low.

Journal Article↗

PubMed1996

Detection of aldehydes in bronchoalveolar lavage of rats exposed to ozone.

We report the detection of hexanal, heptanal, and nonanal in the bronchoalveolar lavage (BAL) of rats exposed to 0.5 to 10 ppm ozone with or without simultaneous 5% CO2. These three aldehydes primarily result from the Criegee ozonation of specific mono- or polyunsaturated fatty acids that are present in significant amounts in the rat lung; e.g., palmitoleic acid gives heptanal, oleic gives nonanal, and linoleic and arachidonic can give hexanal. Hexanal also is produced in the ozone-initiated autoxidation of any n-6 polyunsaturated fatty acid, and thus is a measure of generalized oxidative stress. (Monounsaturated fatty acids do not undergo appreciable autoxidation.) This detection and quantitation of aldehydes directly demonstrates for the first time that unsaturated fatty acids undergo Criegee ozonation in the lung when ozone is inhaled. Exposure to ozone alone produced smaller apparent yields of the three aldehydes than did exposure to ozone plus 5% CO2. Hexanal, heptanal, and nonanal can be detected in BAL of rats 5 hr after the end of the ozone exposure, but after more than 5 hr only hexanal can be found, probably from ozone-induced autoxidation of n-6 PUFA that continues after ozone exposure. The measured amounts of aldehydes are low, and that, coupled with inherent biovariability, suggests that aldehydes may not be useful as quantitative dosimeters. However, they can be useful biomarkers, since some of these aldehydes (e.g., nonanal) are produced in ozone-specific pathways and aldehydes are the most easily detected among the lipid ozonation products (LOP). Furthermore, our identification of these aldehydes by BAL, coupled with our recognition that ozone itself cannot penetrate far enough into the lung to cause many of the effects associated with the inhalation of ozone, suggests that these aldehydes, as well as other types of LOP (such as hydroxyhydroperoxides and Criegee ozonides), may act as signal transduction molecules, activating lipases and causing the release of inflammatory molecules by a variety of pathways not yet entirely elucidated.

Aldehydes↗

PubMed1991

The mixture of aldehydes and hydrogen peroxide produced in the ozonation of dioleoyl phosphatidylcholine causes hemolysis of human red blood cells.

Dioleoyl phosphatidylcholine (PC) liposomes were ozonized and the ozonized liposomes were tested for their lytic potency on human red blood cells (RBC). Ozonation of PC liposomes generated approximately 1 mole equivalent of hydrogen peroxide (H2O2) and 2 mole equivalents of aldehydes, based on the moles of ozone consumed. The time necessary for 50% hemolysis induced by ozonized liposomes (a convenient measure of hemolytic activity) was found to depend on the extent of ozonation of the PC liposomes, indicating the formation and accumulation of hemolytic agents during ozonation. Hemolysis was also observed when RBC were incubated with nonanal, the expected product of the ozonation of oleic acid, the principle unsaturated fatty acid in the liposomes. Hydrogen peroxide, another product of PC ozonation, did not induce hemolysis; however, a combination of H2O2 and nonanal was significantly more hemolytic than nonanal alone. A ratio of 1:2 H2O2/nonanal (the ratio observed in the ozonized liposomes) provided hemolytic activity comparable to that observed with ozonized dioleoyl PC. Among different antioxidants tested, ascorbate, catalase, and glutathione peroxidase partially inhibited hemolysis induced by ozonized liposomes and by H2O2/nonanal mixtures, but they were not protective against the nonanal-induced hemolysis. Identification of H2O2 and aldehydes as cytotoxic chemical species generated from the ozonation of unsaturated fatty acids may have an important bearing on the in vivo toxicity of ozone on the lung as well as on extrapulmonary tissues.

Aldehydes↗

PubMed1990

Age-dependent effect of ozone on pulmonary eicosanoid metabolism in rabbits and rats.

Acute exposures to ozone have previously been shown to cause quantitative changes in the spectrum of arachidonic acid (AA) metabolites in lung lavage fluid. Since age appears to be an important variable in the toxicity of inhaled ozone, we investigated its effect on ozone-induced changes in pulmonary eicosanoid metabolism. Rats and rabbits ranging in age from neonates to young adults were exposed either to air or to 1 ppm ozone for 2 hr. Lung lavage fluid was collected within 1 hr following exposure and analyzed for its content of selected eicosanoids. In both species, there was a pronounced effect of age on ozone-induced pulmonary eicosanoid metabolism. Ozone-exposed animals at the youngest ages examined had severalfold greater amounts of two products of the cyclooxygenase pathway, prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha), than did age-matched controls. This effect lessened and eventually disappeared as the animals grew toward adulthood. In rabbits, ozone also induced increases in 6-keto-prostaglandin F1 alpha and thromboxane B2, but these changes were of lesser magnitude and evident only in the youngest rabbits exposed. There was no observed effect of ozone on lung lavage content of leukothriene B4. Indices of nonspecific pulmonary damage, i.e., protein concentration in lung lavage fluid and total number and viability of lavaged lung cells, were affected by ozone exposure, but not in an age-dependent manner that correlated with changes in pulmonary eicosanoid metabolism. In vitro ozone exposure of lung macrophages from naive rabbits of the same age range as those exposed in vivo demonstrated that ozone is capable of stimulating the elaboration of PGF2 alpha and especially PGE2. However, the increase in lavage fluid PGE2 and PGF2 alpha caused by ozone inhalation could not be attributed to macrophage metabolism conclusively since elaboration of PGE2 and PGF2 alpha by cultured macrophages was not enhanced by prior in vivo ozone exposure. In an ancillary study it was shown that 15-hydroxyprostaglandin dehydrogenase (PGDH) activity in rabbit lung homogenates was not affected by prior exposure to ozone, indicating that the increase in lung lavage fluid eicosanoids that occurred in these animals could not be explained by inhibition of PGDH.

Aging↗

PubMed2005

FIA/MS analysis of temporally ozonated benzo[a]pyrene and pyrene and their reaction products: inhibition of gap junction-mediated intercellular communication.

In this study, the polycyclic aromatic hydrocarbons, benzo[a]pyrene (BaP) and pyrene, were subjected to temporal ozonation. The products from ozonation of 5 mg l(-1) BaP and 5 mg l(-1) pyrene, for varying time intervals (0, 1, 2, 3, 4, 5, 6, 8, 10, 20, and 30 min) were tested for their effects on gap junction-mediated intercellular communication (GJIC) in Clone 9 rat liver cells. Additionally, the ozonation products were also analyzed by flow injection analysis/mass spectrometry (FIA/MS) and the results were compared with the toxicity observed in the GJIC assay. Treatment of the Clone 9 cells with 5 mg l(-1) of ozonated BaP products resulted in a decrease in GJIC that was inversely proportional to the length of ozonation. The products from 1 min of ozonation resulted in a 92% decrease in the rate of GJIC, but with >5 min ozonation, the products did not suppress GJIC. In contrast, pyrene (0.5 mg l(-1)) required >10 min of ozonation to alleviate its effects on GJIC. FIA/MS, using atmospheric pressure chemical ionization (APCI), demonstrated products with higher molecular weights (MW) than their corresponding parent compounds, BaP (MW 252) and pyrene (MW 202). Ozonation of pyrene formed significantly fewer products than BaP. More importantly, pyrene ozonation products were constant from 1 to 10 min, while BaP ozonation products seemed to vary between time intervals. With the longer ozonation times (20 and 30 min), BaP and pyrene formed similar products (m/z peaks 157, 111, and 96). The suppression of GJIC by ozonated products seemed to correlate with oxidation of the aromatic ring framework. Further oxidation (longer ozonation times) to lower MW products correlated with restoration of normal GJIC.

Animals↗

PubMed2005

Efficiency of activated carbon to transform ozone into *OH radicals: influence of operational parameters.

Based on previous findings (Jans, U., Hoigné, J., 1998. Ozone Sci. Eng. 20, 67-87), the activity of activated carbon for the transformation of ozone into *OH radicals including the influence of operational parameters (carbon dose, ozone dose, carbon-type and carbon treatment time) was quantified. The ozone decomposition constant (k(D)) was increased by the presence of activated carbon in the system and depending on the type of activated carbon added, the ratio of the concentrations of *OH radicals and ozone, the R(ct) value ([*OH]/[O3]), was increased by a factor 3-5. The results obtained show that the surface chemical and textural characteristics of the activated carbon determines its activity for the transformation of ozone into *OH radicals. The most efficient carbons in this process are those with high basicity and large surface area. The obtained results show that the interaction between ozone and pyrrol groups present on the surface of activated carbon increase the concentration of O2*- radicals in the system, enhancing ozone transformation into *OH radicals. The activity of activated carbon decreases for extended ozone exposures. This may indicate that activated carbon does not really act as a catalyst but rather as a conventional initiator or promoter for the ozone transformation into *OH radicals. Ozonation of Lake Zurich water ([O3] = 1 mg/L) in presence of activated carbon (0.5 g/L) lead to an increase in the k(D) and R(ct) value by a factor of 10 and 39, respectively, thereby favouring the removal of ozone-resistant contaminants. Moreover, the presence of activated carbon during ozonation of Lake Zurich water led to a 40% reduction in the content of dissolved organic carbon during the first 60 min of treatment. The adsorption of low concentrations of dissolved organic matter (DOM) on activated carbon surfaces did not modify its capacity to initiate/promote ozone transformation into *OH radicals.

Charcoal↗

PubMed2005

Iron type catalysts for the ozonation of oxalic acid in water.

Two iron catalysts (Fe(III) and Fe2O3/Al2O3) have been used in the ozonation of oxalic acid in water at pH 2.5. Percentage removals of oxalic acid were 1.8%, 7% and 30% corresponding to the non-catalytic, homogeneous (Fe(III)) and heterogeneous (Fe2O3/Al2O3) catalytic ozonations, respectively. Catalytic oxalic acid ozonation leads in all cases to total mineralization. The mechanism of ozonation likely develops through formation of iron-oxalate complexes that further react with ozone without the participation of hydroxyl radicals. Because of the stringent acidic conditions, some metal leaching has been observed and quantified in the heterogeneous process. In the homogeneous catalysis, the kinetics was found to be first order with respect to ozone and oxalic acid while for the heterogeneous catalysis, the kinetic order depends on the concentration of ozone in the gas fed. Thus, at ozone concentrations lower than 30 mg L(-1), the heterogeneous ozonation is between first and zero order with respect to both ozone and oxalic acid while at higher ozone gas concentrations, the kinetics was found to be first and zero order with respect to oxalic acid and ozone, respectively. This kinetics is supported through an Eley-Rideal mechanism that involves a surface reaction between non-adsorbed ozone and adsorbed oxalic acid. Apparent activation energies of the homogeneous and heterogeneous catalytic ozonations were found to be 18.2 and 13.6 kcal mol(-1), respectively.

Adsorption↗

PubMedDate not supplied

Ozone emissions from a "personal air purifier".

Ozone emissions were measured above a "personal air purifier" (PAP) designed to be worn on a lapel, shirt pocket, or neck strap. The device is being marketed as a negative ion generator that purifies the air. However, it also produces ozone within the person's immediate breathing zone. In order to assess worst-case potential human exposure to ozone at the mouth and nose, we measured ozone concentrations in separate tests at 1, 3, 5, and 6 in. above each of two PAPs in a closed office. One PAP was new, and one had been used slightly for 3 months. Temperature, relative humidity, atmospheric pressure, room ozone concentration, and outdoor ozone concentration also were measured concurrently during the tests. Average ozone levels measured directly above the individual PAPs ranged from 65-71 ppb at 6 in. above the device to 268-389 ppb at 1 in. above the device. Ozone emission rates from the PAPs were estimated to be 1.7-1.9 microg/minute. When house dust was sprinkled on the top grid of the PAPs, one showed an initial peak of 522 ppb ozone at 1 in., and then returned to the 200-400 ppb range. Room ozone levels increased by only 0-5 ppb during the tests. Even when two PAPs were left operating over a weekend, room ozone levels did not noticeably increase beyond background room ozone levels. These results indicate that this "PAP," even without significant background ozone, can potentially elevate the user's exposures to ozone levels greater than the health-based air quality standards for outdoor air in California (0.09 ppm, 1-hour average) and the United States (0.08 ppm, 8-hour average).

Air Pollutants↗

PubMed1999

Ozone effects on airway responsiveness, lung injury, and inflammation. Comparative rat strain and in vivo/in vitro investigations.

Asthmatic individuals appear to be particularly sensitive to the effects of certain air pollutants-including ozone (O(3)), an oxidant ambient air pollutant-for reasons that are poorly understood. The general purpose of these studies, therefore, was to expand and improve upon toxicologic methods for assessing ozone-induced effects on the airways of the rat by (1) developing an in vivo testing procedure that allows detection of airway responsiveness changes in rats exposed to ozone; (2) identifying a strain of rat that may be inherently more sensitive to the effects of ozone; and (3) validation of an in vitro epithelial culture system to more directly assess airway cellular/subcellular effects of ozone. Using methacholine inhalation challenges, we detected increased airway responsiveness in senescent F344 rats acutely after ozone exposure (2 ppm x 2 h). We also determined that acutely after ozone exposure (0.5 ppm x 8 h), Wistar rats developed significantly greater lung injury, neutrophilic inflammation, and bronchoalveolar lavage (BAL) fluid concentrations of IL-6 than either Sprague-Dawley (SD) or F344 rats. SD rats had greater BAL fluid concentrations of prostaglandin E(2) (PGE(2)), while F344 rats consistently exhibited the least effect. Wistar rat-derived tracheal epithelial (RTE) cultures were exposed in vitro to air or ozone (0.1-1.0 ppm x 1 h), and examined for analogous effects. In a concentration-dependent manner, ozone exposure resulted in acute but minor cytotoxicity. RT polymerase chain reaction (PCR) analysis of RNA isolated from ozone-exposed cells demonstrated variable increases in steady-state gene expression of IL-6 at 4 h postexposure, while at 24 h cellular fibronectin expression (EIIIA domain) was decreased. Exposure was without effect on macrophage inflammatory protein 2 (MIP-2) or gamma-glutamyl cysteine synthetase expression. At 6 h postexposure, IL-6 synthesis and apical release appeared increased in ozone-exposed cells (1 ppm x 1 h). MIP-2 release was not significantly increased in ozone-exposed cells. At 2 h postexposure, ozone exposure resulted in minor increases in apical fibronectin, but exposure was without effect on basolateral accumulation of fibronectin. Exposure to 1.0, but not 0.1 ppm (x 1 h), increased production of cyclooxygenase (i.e., PGE(2)) and noncyclooxygenase products of arachidonic acid. Results demonstrate that multiple inflammatory mediator pathways are affected by ozone exposure. Such effects could exacerbate morbidity in individuals with preexisting airway inflammation such as asthmatics.

Animals↗

PubMed1990

Interactive effects of ozone and formaldehyde on the nasal respiratory lining epithelium in rats.

The combined effects on the nasal epithelium of mixtures of ozone and formaldehyde at cytotoxic and noncytotoxic concentrations were examined. Male Wistar rats were exposed by inhalation during 22 h/d for 3 consecutive days to 0.3, 1.0, or 3.0 ppm formaldehyde, or to 0.2, 0.4, or 0.8 ppm ozone, or to mixtures of 0.4 ppm ozone and 0.3, 1.0, or 3.0 ppm formaldehyde, or to 1.0 ppm formaldehyde and 0.2, 0.4, or 0.8 ppm ozone, or they were sham-exposed to clean air. The noses were examined for pathological changes at six standard cross levels by light microscopy and for epithelial cell proliferation by counting [3H-methyl]thymidine-labeled cells at cross levels II and III. Ozone at 0.4 ppm or 0.8 ppm or formaldehyde at 3 ppm enhanced cell proliferation at cross level II at all locations, except for the epithelium of the septum, which was not affected by ozone. At cross level III ozone alone did not induce cell proliferation, but formaldehyde at 0.3 and 1 ppm tended to reduce cell proliferation while at 3 ppm proliferation was slightly stimulated. The combined exposure to 0.4 ppm ozone and 0.3 ppm formaldehyde induced less cell proliferation at cross levels II and III when compared with that of 0.4 ppm ozone alone. Less cell proliferation was also seen at cross level II when animals were exposed to 0.4 or 0.8 ppm ozone in combination with 1 ppm formaldehyde than when exposed to these ozone concentrations alone. A more than additive increase in cell proliferation was found at cross level II after exposure to 0.4 ppm ozone in combination with 3 ppm formaldehyde, and at cross level III in animals exposed to 0.4 ppm ozone and 1 or 3 ppm formaldehyde. Treatment-related histopathological nasal changes, such as disarrangement, loss of cilia, and hyper/metaplasia of the epithelium were seen at 0.2, 0.4, and 0.8 ppm ozone and at 3 ppm formaldehyde. Simultaneous exposure to both materials did not noticeably affect type, degree, and size of the microscopic nasal lesions.

Animals↗