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PubMed1999

Long-term residence in areas of high ozone: associations with respiratory health in a nationwide sample of nonsmoking young adults [dsee comments].

Few studies have examined the respiratory effects of multiyear ozone exposures in human populations. We examined associations between current respiratory health status and long-term ozone exposure histories in 520 Yale College (New Haven, CT) students who never smoked. Questionnaires addressed current respiratory symptoms, respiratory disease history, residential history, and other factors. The symptoms of cough, phlegm, wheeze apart from colds, and a composite respiratory symptom index (RSI) were selected as outcome measures. Forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV(1)), forced expiratory flow rate between 25 and 75% of FVC (FEF(25-75)), and forced expiratory flow rate at 75% of FVC (FEF(75)) were obtained by forced expiration into spirometers. Ozone exposure was treated as a dichotomous variable, where subjects were assigned to the high-exposure group if they lived for 4 or more years in a U.S. county with 10-year average summer-season daily 1-hr maximum ozone levels [greater/equal to] 80 ppb. Lung function and respiratory symptoms were analyzed by multiple linear and logistic regression on ozone exposure, controlling for covariates. Lung function was lower in the group with high ozone exposures: differences were statistically significant for FEV(1) [-3.1%; 95% confidence interval (CI), -0.2 to -5.9%] and FEF(25-75) (-8.1%; CI, -2.3 to -13.9%), and nearly so for FEF(75) (-6.7%; CI, 1.4 to -14.8). Gender-specific analyses revealed stronger associations for males than for females. The symptoms of chronic phlegm, wheeze apart from colds, and RSI were increased in the ozone-exposed group, with odds ratios of 1.79 (CI, 0.83-3.82), 1.97 (CI, 1.06-3.66), and 2.00 (CI, 1.15-3.46), respectively. We conclude that living for 4 or more years in regions of the country with high levels of ozone and related copollutants is associated with diminished lung function and more frequent reports of respiratory symptoms.

Adolescent↗
PubMed2000

Intramammary application of ozone therapy to acute clinical mastitis in dairy cows.

The infusion of ozone into the inflamed quarter of cows with clinical mastitis was performed and the efficacy of ozone therapy was evaluated. Ozone was infused into the inflamed quarter via a teat canal using ozone gas generating equipment. Nineteen Holstein cows with acute clinical mastitis were divided into two groups: 15 cows treated with ozone therapy, and 4 cows treated with antibiotic therapy. Systemic and local clinical signs, California Mastitis Test scores, the mastitis causing pathogens, electronic conductivity of milk, and somatic cell counts in milk from ozone- and antibiotic-treated quarters, were compared between the groups. Sixty percent (9/15) of cows with acute clinical mastitis treated with ozone therapy, did not require any antibiotics for recovery. This newly developed ozone therapy method was proven to be effective, safe, and cost effective, and carries no risk of drug residues in milk.

Acute Disease↗
PubMed1994

Increase in atrial natriuretic factor in the lungs, heart, and circulatory system owing to ozone.

Ozone can cause pulmonary edema and simultaneously decrease blood pressure. Atrial natriuretic factor (ANF) may mediate both of these effects in that it increases pulmonary capillary permeability resulting in edema formation and vasodilates the vascular system. The present investigation was designed to test directly the effect of ozone on the content of ANF in the lungs, heart, and the circulatory system. Ozone (0.5 ppm) exposure for 8 h increased ANF content in the lungs fourfold (13.33 +/- 2.7 ng/g tissue) in six Fischer 344 rats compared with ANF content (3.03 +/- 0.2 ng/g tissue) in six Fischer 344 rats exposed only to room air. Ozone increased ANF content in the heart fivefold in the same animals from 288 +/- 39.6 ng/g tissue in the rats exposed to room air to 1,473 +/- 234.8 ng/g tissue in those exposed to ozone. Ozone also doubled the concentration of ANF in the circulatory system. This study demonstrates that ozone does increase ANF in the lungs, heart, and circulatory system, suggesting that ANF may mediate the decreased blood pressure and pulmonary edema observed with ozone exposure.

Animals↗
PubMed1994

Bronchoalveolar lavage neutrophilia in asthmatic and healthy volunteers after controlled exposure to ozone and filtered purified air.

STUDY OBJECTIVE: To characterize the pulmonary response of asthmatic and healthy nonsmoking adult men to 0.20 ppm ozone by controlled chamber exposure. DESIGN: A prospective, crossover study of five atopic asthmatic and five normal subjects randomly exposed to ozone and filtered purified air (FPA) for 6 h, consisting of 30-min alternating periods of rest and moderate exercise. The two exposures were separated by at least 30 days. SETTING: A controlled exposure in a stainless steel chamber. PATIENTS: Five atopic asthmatic and five normal subjects between 18 and 45 years of age. Treatment with medications was withheld from asthmatics prior to the exposures. All subjects were nonsmokers. INTERVENTIONS: Symptoms were assessed throughout the exposures. Pulmonary function was measured at baseline, hourly throughout an exposure, and after an exposure. Bronchoalveolar lavage (BAL) was performed 18 h after the completion of an exposure. The BAL fluid (BALF) was analyzed for cell count and differential; the cell-free supernatant was analyzed for albumin, tumor necrosis factor (TNF), interleukin 1 (IL-1), interleukin 6 (IL-6), and interleukin 8 (IL-8). RESULTS: There were statistically significant increases in IL-8 levels, as well as percent polymorphonuclear neutrophils (PMNs) and PMNs per milliliter of lavage in asthmatics exposed to ozone as compared with the same asthmatics exposed to FPA and the same normal subjects exposed to ozone and FPA. Interleukin 6 was also significantly increased in asthmatics exposed to ozone. The BALF albumin, TNF, and IL-1 levels were not significantly different among the four groups. There were no differences between asthmatics and healthy controls exposed to ozone or FPA in baseline to postexposure FEV1, FVC, FEV1/FVC, and sRaw. CONCLUSIONS: We conclude that asthmatics exposed to ozone develop a significant BALF neutrophilia and increased levels of the cytokines, IL-8 and IL-6. These BALF findings occur even though the level of ozone exposure was not significant enough to reduce pulmonary function.

Adolescent↗
PubMed2002

Ozone dynamics and deposition processes at a deforested site in the Amazon basin.

The goal of this study is to investigate the impact of deforestation on ozone dynamics and deposition in the Brazilian Amazon basin. This goal is accomplished through i) analyses of ozone levels and deposition rates at a deforested site during the rainy season; and ii) comparisons of these data with similar information derived at a forest. At the pasture site maximum ozone mixing ratios reach 20 parts per billion on a volume basis (ppbv) but about 6 ppbv prevail over the forest. Maximum ozone deposition velocities for pastures can reach 0.7 cm s-1, which is about threefold lower than values derived for forests. Combining ozone abundance and deposition velocities, pasture maximum ozone fluxes reach approximately 0.2 microgram (ozone) m-2 s-1. This flux represents approximately 70% of the deposition rates measured over the forest. Hence, this study suggests that conversion of rainforests to pastures could lead to a net reduction (30%) in the ozone sink in the Amazon.

Agriculture↗
PubMed2006

Toxicity of ozonated seawater to marine organisms.

Ballast water transport of nonindigenous species (NIS) is recognized as a significant contributor to biological invasions and a threat to coastal ecosystems. Recently, the use of ozone as an oxidant to eliminate NIS from ballast while ships are in transit has been considered. We determined the toxicity of ozone in artificial seawater (ASW) for five species of marine organisms in short-term (< or = 5 h) batch exposures. Larval topsmelt (Atherinops affinis) and juvenile sheepshead minnows (Cyprinodon variegatus) were the most sensitive to oxidant exposure, and the mysid shrimp (Americamysis bahia) was the most sensitive invertebrate. Conversely, benthic amphipods (Leptocheirus plumulosus and Rhepoxinius abronius) were the least sensitive of all species tested. Mortality from ozone exposure occurred quickly, with median lethal times ranging from 1 to 3 h for the most sensitive species, although additional mortality was observed 1 to 2 d following ozone exposure. Because ozone does not persist in seawater, toxicity likely resulted from bromide ion oxidation to bromine species (HOBr and OBr-), which persist as residual toxicants after at least 2 d of storage. Total residual oxidant (TRO; as Br2) formation resulting from ozone treatment was measured in ASW and four site-specific natural seawaters. The rate of TRO formation correlated with salinity, but dissolved organic carbon and total dissolved nitrogen did not affect TRO concentrations. Acute toxicity tests with each water over 48 h using mysid shrimp, topsmelt, and sheepshead minnows yielded results similar to those of batch exposure. Addition of sodium thiosulfate (Na2S2O3) to ozonated waters resulted in TRO elimination and survival of all organisms. Our results provide necessary information for the optimization of an efficacious ozone ballast water treatment system.

Animals↗
PubMed1984

A mechanism of synergistic lung damage by ozone and a respirable aerosol.

A hitherto unexpected synergism between the oxidant air pollutants ozone or nitrogen dioxide and a respirable-sized aerosol of ammonium sulfate was previously observed during controlled exposures of rats to these substances. In this paper we examine biochemical and morphometric changes in lungs of rats exposed for 3, 7, or 14 days to ozone (0.64-0.96 ppm), with or without an accompanying aerosol (approximately 1 micrometer mass median aerodynamic diameter) of ammonium sulfate (5 mg/m3). After 3 days of exposure to the mixture of pollutants, rat lung macrophage and macrophage precursors (monocytes) were increased 2- to 3-fold, fibroblasts were increased 2-fold, and apparent collagen synthesis rates were increased 2.5-fold, fibroblasts were increased 2-fold, and apparent collagen synthesis rates were increased 2.5-fold, as compared with values from animals exposed to ozone alone. Continued exposure to ozone alone for 7 or 14 days seemed to mimic changes seen at 3 days with the mixture of pollutants. Total number of lesions per lung was the same for ozone exposure with and without accompanying aerosol; lesions were larger in lungs of rats exposed to ozone plus ammonium sulfate. Based on these findings and a review of the literature, a mechanism for ozone-aerosol synergism is proposed. We suggest that the lifetime of free radicals arising from interaction of oxidants such as ozone or nitrogen dioxide with molecules within the lung is increased by either local pH changes or changes in the local sulfate concentration (or both) caused by inhalation of the respirable aerosol.

Aerosols↗
PubMed1985

Effects of ozone on phospholipid synthesis by alveolar type II cells isolated from adult rat lung.

Isolated alveolar type II cells were exposed to ozone by gas diffusion through the thin Teflon bottom of culture dishes. After exposure, type II cells were further incubated in the presence of labeled substrates to assess the capacity to synthesize surfactant lipids. The incorporation of [Me-14C]choline into both total and disaturated phosphatidylcholines in inhibited to 50% of the control values under conditions that result in a diffusion of 0.4 microgram O3/18 cm2-dish per 2.5 h. The incorporation rates of [1-14C]palmitate, [1-14C]acetate, D[U-14C]glucose, and [1,3-3H]glycerol into phosphatidylcholines are also lower after ozone exposure. Moreover, the synthesis of phosphatidylglycerols and phosphatidylethanolamines from these substrates is also inhibited by exposure of type II cells to ozone. These incorporation studies indicate that the effect of ozone is early in the biosynthetic pathway, probably at the step catalyzed by the enzyme glycerolphosphate acyltransferase. Determination of the activity of this enzyme after the ozone exposure shows that it is decreased, whereas the activity of lysophosphatidylcholine acyltransferase is increased. The activity of choline phosphotransferase also appears to be decreased after exposure of type II cells to ozone, although this enzyme was less susceptible than glycerolphosphate acyltransferase. Studies with the sulfhydryl reagent 5,5'-dithiobis (2-nitrobenzoic acid) indicate a positive correlation between the effect of this compound on enzyme activities in sonicated type II cells and the sensitivity of these enzymes in intact cells to ozone. This suggests that the effect of ozone on the synthesis of surfactant lipids is at least partially exerted via oxidation of the sulfhydryl groups of glycerolphosphate acyltransferase.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMed1988

Effect of 2 ppm ozone exposure on rat lung lipid fatty acids.

Based on in vitro studies, the initial damage to lung cells by ozone exposure is believed to result in part from the breakdown of lipid polyunsaturated fatty acids to aldehydes, ozonides, and peroxides. The present study measured lipid breakdown products in lungs isolated from rats pretreated with [1-14C]acetate 12 h before exposure for 4 h to either air or 2 ppm ozone. Lipid fatty acid breakdown was indicated by a 112% increase in thiobarbituric acid-reactive substances on ozone exposure and by changes in chemical and radioactive measurements of mono- and dicarboxylic acids formed by treatment of lipid fractions with hydrogen peroxide. Ozone exposure resulted in a 63% increase in recovery of short-chain fatty acids accounted for by increased recoveries of malonic acid by 37%, hexanoic acid by 47%, nonanoic acid by 118%, and azelaic acid by 107%. Recovery of glutaric acid was enhanced 15-fold by ozone exposure. Although decreases in tissue arachidonic acid could not be detected, oleic acid was significantly decreased by 36%. Recovery of radiolabel as short-chain fatty acids was increased by 65% on ozone exposure and was mainly accounted for by enhanced labeling of nonanoic and glutaric acid fractions. The failure to observe significant increases in 14C recovery in the other fractions suggested ozone-induced breakdown of unlabeled fatty acids. These results demonstrate the cleavage of unsaturated fatty acid double bonds following in vivo exposure of lungs to ozone. Breakdown of arachidonic and oleic acids was specifically identified by increased recoveries of glutaric and nonanoic acids, respectively.

Animals↗
PubMed1989

Bactericidal activity, eggshell conductance, and hatchability effects of ozone versus formaldehyde disinfection.

Ozone and formaldehyde were evaluated as disinfectants in a prototype laboratory setter against microorganisms that are naturally present on fertile, freshly laid, broiler hatching eggs. Significantly lower microbial counts of over 2.5 log10 (P less than .05) were observed for water-misted and ozonated (2.83% by weight) eggs or formaldehyde-fumigated (triple strength) eggs than for control and water-misted eggs. Eggshell conductance studies as measured by egg moisture losses in a desiccator showed no significant differences (P greater than .05) among untreated, water misted, ozonated (3.06% by weight) with water mist, or formaldehyde (triple strength)-fumigated eggs. Hatchability was significantly reduced (26.5 to 37.5%) following ozonation (3.03% ozone by weight, 2 h) in comparison with effects of no treatment or water misting. Misting with ozonation was equally as effective as formaldehyde fumigation in reducing microbial counts. However, ozone treatment at the concentrations tested significantly reduced hatchability when compared with results of either no treatment, water misting, or an average hatchability figure for formaldehyde fumigation. These findings indicate that ozone is a good disinfectant yet may adversely affect embryo development when given in the gaseous form.

Animals↗
PubMed1989

Comparison of ozone and formaldehyde as poultry hatchery disinfectants.

Ozone and formaldehyde were compared as poultry hatchery disinfectants in a poultry setter, and evaluated for effectiveness. Escherichia coli, Pseudomonas fluorescens, Salmonella typhimurium, and Proteus spp. were inoculated onto open petri plates and exposed to ozone or onto filter paper strips and exposed to ozone or formaldehyde in a poultry setter. Ozone (1.41 to 1.68% by weight) resulted in significant bacterial reductions of greater than 4 log10 on the open plates and greater than 3 log10 on filter paper strips, whereas formaldehyde (triple strength) resulted in greater than 7 log10 reduction on filter paper strips. Ozone was similarly lethal to organisms on filter paper strips at 90% relative humidity (RH) and 13.9 C, and at 50% RH and 37.7 C. Although under the conditions of this study formaldehyde (triple strength) was more lethal than ozone, ozone killed greater than 99.9% of the starting microbial populations. In the event that formaldehyde can no longer be used in the hatchery, an effective alternative may be ozone.

Animals↗
PubMed2003

Viability of Clostridium perfringens, Escherichia coli, and Listeria monocytogenes surviving mild heat or aqueous ozone treatment on beef followed by heat, alkali, or salt stress.

The threat of pathogen survival following ozone treatment of meat necessitates careful evaluation of the microorganisms surviving under such circumstances. The objective of this study was to determine whether sublethal aqueous ozone treatment (3 ppm of O3 for 5 min) of microorganisms on beef surfaces would result in increased or decreased survival with respect to subsequent heat, alkali, or NaCl stress. A mild heat treatment (55 degrees C for 30 min) was used for comparison. Reductions in three-strain cocktails of Clostridium perfringens, Escherichia coli O157:H7, and Listeria monocytogenes on beef following the heat treatment were 0.14, 0.77, and 1.47 log10 CFU/g, respectively, whereas reductions following ozone treatment were 1.28, 0.85, and 1.09 log10 CFU/g, respectively. C. perfringens cells exhibited elevated heat resistance at 60 degrees C (D60 [time at 60 degrees C required to reduce the viable cell population by 1 log10 units or 90%] = 17.76 min) following heat treatment of beef (55 degrees C for 30 min) but exhibited reduced viability at 60 degrees C following ozone treatment (D60 = 7.64 min) compared with the viability of untreated control cells (D60 = 13.84 min). The D60-values for L. monocytogenes and E. coli O157:H7 following heat and ozone exposures were not significantly different (P > 0.05). C. perfringens cells that survived ozone treatment did not exhibit increased resistance to pH (pH 6 to 12) relative to non-ozone-treated cells when grown at 37 degrees C for 24 h. The heat treatment also resulted in decreased numbers of surviving cells above and below neutral pH values for both E. coli O157:H7 and L. monocytogenes relative to those of non-heat-treated cells grown at 37 degrees C for 24 h. There were significant differences (P < 0.05) in C. perfringens reductions with increasing NaCl concentrations. The effects of NaCl were less apparent for E. coli and L. monocytogenes survivors. It is concluded that pathogens surviving ozone treatment of beef are less likely to endanger food safety than are those surviving sublethal heat treatments.

Animals↗
PubMed2003

Ozone treatment for reduction of Escherichia coli 0157:H7 and Salmonella serotype typhimurium on beef carcass surfaces.

The effectiveness of an aqueous ozone treatment in reducing Escherichia coli O157:H7 and Salmonella serotype Typhimurium on hot carcass surfaces was determined with the use of a model carcass spray cabinet. Carcass surface regions were removed from carcasses and inoculated with feces containing 10(6) to 10(7) CFU each of E. coli O157:H7 and Salmonella Typhimurium per g and were then exposed to a water wash or to a water wash followed by a sanitizing ozone treatment. Water washes were applied at 28 degrees C beginning at a pressure of 10 lb/in2 and gradually increasing to 400 lb/in2. Ozone treatment was carried out by spraying surfaces with an aqueous ozone solution (80 lb/in2 at 28 degrees C) containing 95 mg of ozone per liter. Pathogen reductions achieved with ozone treatment were not significantly different from those achieved with a water wash alone. In addition, ozone treatment did not reduce E. coli O157:H7 or Salmonella Typhimurium contamination that was spread over the carcass surface as a result of the water wash. Under the conditions of this study, the aqueous ozone treatment applied resulted in no significant improvement over a water wash in reducing pathogens on beef carcass surfaces.

Animals↗
PubMed1998

Susceptibilities of plasma antioxidants and erythrocyte constituents to low levels of ozone.

To evaluate the susceptibilities of human blood constituents to the low levels of ozone used in ozonated autohemotherapy (40 microgO3/ml), we quantified plasma antioxidants and erythrocyte constituents after rapid mixing of human whole blood with ozone at 20, 40, 60, and 100 microg/ml blood. Ascorbic acid, uric acid, and alpha-tocopherol in plasma decreased as ozone increased, but bilirubin was unaffected. The content of thiobarbituric acid-reactive substances in plasma was increased by ozone. However, the content of thiobarbituric acid-reactive substances and alpha-tocopherol in the erythrocyte membrane was not significantly affected. No significant changes occurred in the content of methemoglobin, cytoskeleton proteins or erythrocyte enzymes such as Na+/K+-ATPase, acetylcholinesterase, catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase at all the ozone levels tested. A decrease in reduced glutathione in erythrocytes was the only significant change caused by the ozone level used for autohemotherapy. It may be one of the chemical events responsible for the beneficial effects of ozonated autohemotherapy.

Adult↗
PubMed1998

[The acid-base status of preserved blood before and after processing with an oxygen-ozone mixture].

Effects were studied of oxygen and ozone mixture on the indices for the contained donor blood acid-base state. Ozonation of blood in 9 donors was carried out in different concentrations of ozone in the oxygen and ozone mixture. Revealed in blood after ozonation was increase in oxygen concentration and decrease in CO2 dissoluble fraction, with pH of blood, the content of bicarbonate being unchanged. There was no relatedness of the ozonized blood saturation with oxygen to the concentration of ozone in the oxygen and ozone mixture.

Acid-Base Equilibrium↗
PubMed1999

In vivo and in vitro effect of ozone and formaldehyde on human nasal mucociliary transport system.

The effect of ozone and formaldehyde on the nasal mucociliary transport system after short-term exposure was comparatively evaluated in human by using in vivo and in vitro test systems. Concentrations of ozone used were 10, 100, 500 and 1000 micrograms/m3 of ozone and of formaldehyde 100, 500 and 5000 micrograms/m3. The in vivo effect of ozone was monitored by measuring the saccharin transport time before and two hours after exposure to ozone. The in vitro effect of ozone and formaldehyde was evaluated by quantifying the ciliary beat frequency (CBF) of isolated respiratory epithelial cells before and after one, two, and three hours of exposure. Control experiments were performed using synthetic air. Ozone had no effect on the human nasal mucociliary transport system under the conditions tested here. Neither in vivo nor in vitro any significant changes of saccharin transport time nor CBF were measured. In contrast, formaldehyde significantly reduced (67.1%) CBF at the highest dosis (2 hours, 5000 micrograms/m3). These results will be discussed according to the environmental impact of ozone and formaldehyde in air pollutants and compared to sulphur dioxide and nitric oxide, which were tested under similar conditions, and to results revealed from animal experiments.

Adolescent↗
PubMed2001

Investigation of radical reactions for efficiency improvement in ozone-hydrogen peroxide treatment.

It was verified by laboratory-scale experiments that the two-port ozone injection method was more advantageous for reaction efficiency in the ozone-hydrogen peroxide treatment than the conventional one-port ozone injection method under the condition of same ozone dose. The reason for this effectiveness was also investigated in detail by computer simulations in the wide range of the rate constant of OH radical reacting with TOC (kTOC). The laboratory-scale experiments revealed that the amount of TOC decomposed (delta TOC) increased by up to 41% by the two-port injection method, indicating a 27% improvement in delta O3/delta TOC. A detailed investigation of these experimental results by computer simulations showed that by injecting ozone in two ports the amount of ozone consumed for the OH radical formation was increased more remarkably than that of ozone consumed for the radical chain reactions, and that the amount of OH radical reacting with TOC was increased more strikingly than that with ozone. Furthermore, it was found that the smaller the kTOC value with 10(5)-10(9) M-1s-1 was, the more advantageous for the reaction efficiency the two-port injection method was.

Environmental Pollution↗
PubMed2001

Oviductural carcinoma in B6C3F1 female mice exosed to 0.5 ppm ozone.

The toxicity and carcinogenecity of ozone was evaluated in B6C3F1 mice exposed to 0.5 ppm ozone via inhalation for 12 w, during which no ozone-related deaths occurred. Decreases in mean body weights of both genders exposed to ozone were sporadically seen, and mean absolute and relative weights of several organs from male and female groups receiving ozone were lower than those of respective air-control groups. No ozone-related increased neoplasm incidences were observed in most organs, including the lung; however, oviductural carcinomas were seen in the ozone-exposed females. Although ozone does not induce lung cancer under our experimental condition, it induces oviductural carcinomas in B6C3F1 mice.

Animals↗