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PubMed2004

Effect of alfalfa seed washing on the organic carbon concentration in chlorinated and ozonated water.

The bioassays assimilable organic carbon (AOC) and coliform growth response are better indexes than biological oxygen demand to determine water quality and water's ability to support the growth of bacteria. Ozonated (5 mg/liter) and chlorinated tap water were used to wash alfalfa seeds for 30 min. After washing in the ozonated tap water, the AOC concentration increased 25-fold, whereas the dissolved ozone decreased to undetectable levels. The AOC levels for the chlorinated water after washing the seeds also increased. These increases are due to ozone's strong oxidizing ability to break down refractory, large-molecular-weight compounds, forming smaller ones, which are readily used as nutrient sources for microorganisms. This same phenomenon was observed when using ozone in the treatment of drinking water. The AOC value increased from 1,176 to 1,758 micrograms C-eq/liter after the reconditioned wastewater was ozonated. When the ozonated wastewater was inoculated with Salmonella serotypes, the cells survived and increased generation times were observed. The increased nutrients would now become more readily available to any pathogenic microorganisms located on alfalfa seed surface as seen with the increase in the inoculated levels of Salmonella in the ozonated wastewater. If the washing process using ozonated water is not followed by the recommended hypochlorite treatment or continually purged with ozone, pathogen growth is still possible.

Area Under Curve↗
PubMedDate not supplied

Influence of ozone on oxidation of dental alloys.

PURPOSE: The purpose of this study was to examine the influence of ozone on the surface of removable partial denture (RPD) alloys to determine its usefulness as a cleaning method for RPDs, since ozone has powerful sterilizing and deodorizing properties. MATERIALS AND METHODS: Two types of ozone cleaning were used. The quantities of ozone generated by both methods were the same (20 mg/h). In method A, ozone was generated for 10 minutes every 12 hours and in method B, ozone was generated over 24 hours a day. Test specimens of 3 types of dental alloy (Co-Cr, Au-Ag-Pt, and Au-Cu-Ag-Pd) were subjected to different cleaning methods for 7 days and measured in terms of reflectance, surface roughness, and weight. Five different cleaning solutions (three commercial denture cleaners, acid-electrolyzed water with a pH of 2.4, and pure water) were used for comparison with the ozone treatments. RESULTS: No significant changes were detected after treatment of the Co-Cr and Au-Ag-Pt alloys with ozone. Ozone caused a slight change in the Au-Cu-Ag-Pd alloy in terms of reflectance, but the changes were significantly less than those caused by acid-electrolyzed water and one of the commercial denture cleaners. CONCLUSION: Ozone had little influence on the oxidation of dental alloys.

Chromium Alloys↗
PubMed2002

Ozonation application in activated sludge systems for a textile mill effluent.

The study investigates the effect of partial ozonation of textile wastewater, both at the inlet (pre-ozonation) and the outlet (post-ozonation) of biological treatment, for the optimization of COD and color removals, both typical polluting parameters associated with the textile industry. Pre-ozonation provides at optimum contact time of 15 minutes 85% color removal, but only 19% COD reduction. Removal of the soluble inert COD fraction remains at 7%, indicating selective preference of ozone for simpler compounds. Post-ozonation is much more effective on the breakdown of refractory organic compounds and on color removal efficiency. Ozonation after biological treatment results in almost complete color removal and a 14% soluble inert COD reduction. The polishing effect of post-ozonation also proves quite attractive from an economical standpoint, involving approximately 50% of the ozone utilization at the same ozone flux rate and contact time, yet providing a lower soluble residual COD level.

Bioreactors↗
PubMed2002

Catalytic ozonation of an organophosphorus pesticide using microporous silicate and its effect on total toxicity reduction.

Catalytic ozonation is promising as one of the advanced oxidation processes because of its effective use of ozone and its improved treatability of organic compounds through radical reactions. In this article, we investigated the feasibility of microporous silicates as a potential catalyst for a catalytic ozonation process. Organophosphorus insecticide, dichlorvos (DDVP), was employed as a model chemical for assessing conventional ozonation and catalytic ozonation, because its oxidative intermediate is toxic and is not degraded by direct ozonation. It was found that ozone was well adsorbed and simultaneously decomposed in microporous silicates, resulting in the production of possible radical species. In the presence of microporous silicates, radical reactions by decomposed ozone were evidenced by phosphate ion release that shows a degradation of a toxic intermediate of DDVP. Accordingly, cytotoxicity was successfully decreased. In a continuous treatment process combining a conventional ozonation vessel and a microporous silicate column for an effective use of residual ozone, enhanced degradation of DDVP was demonstrated by a decrease of DOC, an increase of the PO4(3-) concentration and reduction in the cytotoxicity. This new treatment mechanism is likely to be promising as an advanced water treatment process particularly when we think about better toxicity reduction of wastewaters.

Adsorption↗
PubMed2003

Minimally invasive oxygen-ozone therapy for lumbar disk herniation.

BACKGROUND AND PURPOSE: Oxygen-ozone therapy is a minimally invasive treatment for lumbar disk herniation that exploits the biochemical properties of a gas mixture of oxygen and ozone. We assessed the therapeutic outcome of oxygen-ozone therapy and compared the outcome of administering medical ozone alone with the outcome of medical ozone followed by injection of a corticosteroid and an anesthetic at the same session. METHODS: Six hundred patients were treated with a single session of oxygen-ozone therapy. All presented with clinical signs of lumbar disk nerve root compression, with CT and/or MR evidence of contained disk herniation. Three hundred patients (group A) received an intradiscal (4 mL) and periganglionic (8 mL) injection of an oxygen-ozone mixture at an ozone concentration of 27 micro g/mL. The other 300 patients (group B) received, in addition, a periganglionic injection of corticosteroid and anesthetic. Therapeutic outcome was assessed 6 months after treatment by using a modified MacNab method. Results were evaluated by two observers blinded to patient distribution within the two groups. RESULTS: A satisfactory therapeutic outcome was obtained in both groups. In group A, treatment was a success (excellent or good outcome) in 70.3% and deemed a failure (poor outcome or recourse to surgery) in the remaining 29.7%. In group B, treatment was a success in 78.3% and deemed a failure in the remaining 21.7%. The difference in outcome between the two groups was statistically significant (P <.05). CONCLUSION: Combined intradiscal and periganglionic injection of medical ozone and periganglionic injection of steroids has a cumulative effect that enhances the overall outcome of treatment for pain caused by disk herniation. Oxygen-ozone therapy is a useful treatment for lumbar disk herniation that has failed to respond to conservative management.

Adult↗
PubMed2004

[Ozone concentration distribution of urban].

The increase of ozone concentration in urban is one of the most important research topics on environmental science. With the increase of nitrogen oxides and hydrogen-carbon compounds which are exhausted from cars, the ozone concentration in urban is obviously increased on sunlight, and threat of photochemistry smog will be possible. Therefore, it is very important to monitor and study the ozone concentration distribution in urban. The frequency-distribution, diurnal variation and monthly variation of ozone concentration were studied on the campus of Shandong University during six months monitoring. The influence of solar radiation and weather conditions on ozone concentration were discussed. The frequency of ozone concentration less than 200 microg/m3 is 96.88%. The ozone concentration has an obvious diurnal variation. The ozone concentration in the afternoon is higher than in the morning and in the evening. The maximum appears in June, when it is the strong solar radiation and high air-temperature. The weather conditions also influence the ozone concentration. The ozone concentration in clear day is higher than in rainy and cloudy day.

Air↗
PubMed2006

[Degradation of endocrine disruptor bisphenol A in drinking water by ozone oxidation].

The ozone oxidation of endocrine disruptor (bisphenol A) in drinking water was investigated. With the initial concentration of 1.0 mg/L, the removal efficiency of BPA (bisphenol A) could be measure up to 70%, 82%, 90% when the dosage of ozone was 1 mg/L, 1.5 mg/L, 2 mg/L respectively within 30 minutes. The impacts of BPA degradation under the conditions of different ozone dosages, different water background value, different BPA initial concentration and different ozone adding time were analyzed. The results show that ozone dosage play a dominant role during the process of BPA degradation, while the impact of the contact time could be ignored. The UV wavelength scanning is used to conform that the by-products were produced, which can be absorbed at UV254, and the UV254 keeps changing with the ozonation process. From the change of UV254, it can be drawn that BPA can not be completely degraded with low ozone dosage, while less adding time of total ozone dosage, high ozone dosage, improvement of dissolved ozone concentration will do great contribution to the extent of BPA degradation.

Benzhydryl Compounds↗
PubMed1991

Effects of ozone on airway epithelial permeability and ion transport.

Ozone is a highly reactive form of oxygen produced in the atmosphere by photochemical reactions involving substrates emitted from automobile engines. Outdoor air concentrations as high as 0.4 parts per million (ppm) occur. The respiratory tract extracts about 90% of inhaled ozone. From the chemical reactivity of ozone, it is expected to attack organic molecules located on or near the respiratory surfaces. The airways are covered with a cohesive layer of epithelial cells that forms the boundary between the external environment and the respiratory tissues. One important role of this epithelial layer is its barrier function. Airborne particles that deposit (and dissolve) in the airway surface liquid are not readily absorbed, and soluble tissue components are excluded from the surface liquid. The epithelium also controls the volume and composition of the surface liquid. One important process in this regard is the absorption and secretion of ions and water. We have studied the effects of inhalation of ozone on the barrier function (permeability to dissolved molecules) and the ion transport activity of epithelium using both in vivo and in vitro techniques. All our experiments were performed with male Hartley strain guinea pigs. Conscious, unrestrained animals were exposed to a concentration of ozone of 1 ppm for three hours in controlled environmental chambers in the Health Effects Research Laboratory, U.S. Environmental Protection Agency (EPA), Research Triangle Park, NC. Such exposures caused a marked increase in the rate of appearance in blood of various water-soluble compounds instilled onto the surface of the trachea, indicating increased permeability of the airway epithelium. This interpretation was supported by electron microscopy, which showed that the tracer molecule horseradish peroxidase was present in the intercellular spaces of tracheal epithelium from ozone-exposed, but not air-exposed (control), animals. However, when the tracheas were excised after ozone exposure and mounted in a tissue bath before measurement of permeability, no increase was found. We suggest that the effect of ozone inhalation on airway permeability requires the action of mediators that are washed out in the in vitro situation. When we exposed animals to 1 ppm for 3 hours daily, we found that the increased permeability in vivo was no longer demonstrable after the fourth exposure. The mechanisms for this type of "adaptation" are not known. The phenomenon recalls the response of human subjects to repeated daily ozone exposures. Ozone exposure caused a sharp increase in active ion transport by tracheal epithelium.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

[The effect of AH 21-132 on airway hyperresponsiveness induced by ozone exposure].

We examined the effect of AH 21-132, which has been reported to relax airway smooth muscle and inhibit platelet activating factor (PAF)-induced airway hyperreactivity, on ozone-induced airway hyperresponsiveness (AHR) with airway inflammation in dogs. Airway responsiveness (AR) to methacholine was measured by modified Astograph (7 Hz oscillation method) before and after ozone exposure, and the numbers of neutrophils in the peripheral blood and total cell counts, differential cell counts and TXB2 in BALF were measured before and after ozone exposure. Ozone exposure was carried out for 2 hr at an ozone level of 3.46 +/- 0.10 ppm (mean +/- SE). There was a significant increase in AR to methacholine after ozone exposure (p less than 0.01), and the numbers of neutrophils in the peripheral blood and the total cell and neutrophil counts in BALF increased significantly (p less than 0.05). Pretreatment with AH 21-132 at an oral dose of 20 mg/kg significantly prevented the ozone-induced AHR to methacholine (p less than 0.01), and also inhibited the increase of neutrophil counts in the peripheral blood, and the total cell counts and the neutrophil counts in BALF after ozone exposure. There was no significant change in the levels of TXB2 in BALF before and after ozone exposure. In dogs not exposed to ozone, AR to methacholine and respiratory resistance to methacholine significantly decreased after administration of AH 21-132 at an oral dose of 20 mg/kg (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1991

[The ozone layer and its modification by N2O and inhalation anesthetics].

As a result of human activities the ozone layer in the stratosphere, which is necessary for life on earth, has changed. The main causes of ozone destruction are chlorofluorcarbons (CFCs) 11 and 12. Recently, caring anesthetists have wondered if and to what degree N2O and popular potent inhalation anesthetics may also contribute to ozone loss. Having consulted the literature, we attempt to answer that question. The ozone-destroying N2O is chiefly produced by burning fossil elements and nitrogenous fertilizing used in agriculture; the share of medically used N2O lies below 2%. Halothane, enflurane, and isoflurane are halogenated anesthetics that contain ozone-destroying halogens (bromine, chlorine, fluorine) to different extents. Complicated experimental calculations for these volatile anesthetics result in a potential for ozone destruction of 0.36 for halothane and 0.02 for enflurane and isoflurane if the potential for ozone destruction by CFCs is set at 1.0. The lifespan of the inhalation anesthetics in the troposphere is with less than 3 years, dramatically less than that of CFCs (70-140 years). The two most important CFCs, 11 and 12, are considered to be currently produced in a quantity of about 800,000 tons per year. On the other hand, the worldwide production of inhalation anesthetics is said to be only 2,000 tons. In view of the experimental calculations and the low worldwide production, the small greenhouse effect, the shorter lifespan in the troposphere, and the low potential for ozone destruction, the negative effects of medically used N2O and inhalation anesthetics on the ozone layer seem negligible. All in all, the inhalation anesthetics are considered to be responsible for only 0.0005% of the ozone destruction at present.

Air Pollutants↗
PubMed1984

Ozone: an overview of its toxicity in man and animals.

Ozone is one of the most toxic and ubiquitous air pollutants. This review focuses on the toxic effects of ozone in animals and on the similarities and disimilarities between the toxic effects in animals and humans. The molecular basis for the toxicity of ozone is discussed, based on the vigorous oxidizing properties of ozone. Despite the existence of anatomical differences between human, subhuman primate, and dog lungs versus common experimental rodent lungs, the anatomical lesion of ozone inhalation occurs at the functionally equivalent site of the junction between the conducting airway and the respiratory region. Ciliated cells of the upper airways and the type 1 cell of the centriacinar region are most affected. Type 2 cell proliferation is a hallmark of ozone toxicity. A wide variety of biochemical and physiological changes have been noted in several animal species and in humans. Considerable evidence for a free-radical-mediated or lipid peroxide-mediated toxicity is evident, especially in the induction of the glutathione peroxidase system and the protective effects of vitamins C and E. Ozone appears to be a weak mutagen and to produce chromosomal abnormalities. Defects in defense against airborne infection are present in animals, which are more susceptible to airborne infection after ozone exposure. Epidemiological studies, however, fail to detect increased respiratory infections in humans due to ozone. Despite the variety of toxic effects, few qualitative differences between species are apparent; rather, quantitative differences do occur. Ozone may thus be an ideal compound for quantitative extrapolation of toxicity from animals to humans.

Animals↗
PubMed1982

Ozone precursor monitor for investigating air pollution.

Ozone is designated by the Environmental Protection Agency as one of six principal air pollutants. Of the six, ozone alone is classified as a secondary pollutant since it is not emitted by a specific source. Ozone is formed in the lower atmosphere by photochemical reactions involving the precursors of ozone: gaseous organic compounds (mostly hydrocarbons), nitric oxide, and nitrogen dioxide. This paper describes a new automated method for quantifying the precursors of ozone. An ozone analyzer is coupled to a reaction vessel contained in an irradiation chamber. At timed intervals discrete samples of outside air are drawn into the reaction vessel and irradiated with ultraviolet light. The amount of ozone produced is a measure of the photochemical reactivity potential of the precursor blend. The ozone precursor monitor (OPM) is designed for urban air sampling stations where analyzers for the principal air pollutants are routinely operated. The monitor, however, has other uses. Among special applications of the method that are discussed are its use as an early warning device for forecasting elevated ozone concentrations, a screening system for assessing the photoreactivity of solvents, and a procedure for investigating the transport of ozone precursors from urban to rural areas.

Air Pollutants↗
PubMed1995

Consequences of prolonged inhalation of ozone on F344/N rats: collaborative studies. Part VIII: Morphometric analysis of structural alterations in alveolar regions.

Morphometric techniques were used to examine cellular and tissue changes occurring in male and female rat lungs exposed to ozone for a prolonged time. F344/N rats were exposed to 0.0, 0.12, 0.5, or 1.0 parts per million (ppm)* ozone for six hours per day, five days per week, for 20 months. Changes in cell volume, cell surface ratios, and cellular characteristics were studied in the terminal bronchioles and in the proximal alveolar regions of the lungs. Animals exposed for 20 months to 0.5 or 1.0 ppm ozone demonstrated dramatic increases in the volume of interstitium and epithelium along the alveolar ducts. The thickening of the epithelium was caused by an epithelial metaplasia in which the normal squamous epithelium was modified to a cuboidal epithelium similar, but not identical, to the type found in terminal bronchioles. This bronchiolar epithelial metaplasia was directly related to dose of ozone, and was characterized by differentiated ciliated cells and Clara cells similar to those found in terminal bronchioles; undifferentiated cuboidal cells also were found in the animals exposed to 0.5 and 1.0 ppm ozone. A mild fibrotic response was seen in the animals exposed to 1.0 ppm ozone, with increases in both the interstitial matrix and cellular interstitium. The individual components of the interstitial matrix, including collagen, elastin, basement membrane, and acellular spaces, all were increased. The increase in cellular interstitium was due to an increase in the volume of interstitial fibroblasts. A slight inflammatory response, identified by an increase in alveolar macrophages, was observed in the animals exposed to 1.0 ppm. The terminal bronchioles were less affected than the proximal alveolar region by the ozone exposures, which may indicate a resistance of this tissue to ozone damage. The changes in the terminal bronchioles mainly consisted of a shift in cell type from ciliated to Clara cells in the animals exposed to 1.0 ppm ozone. The bronchiolar epithelial metaplasia observed in the proximal alveolar ducts may indicate that a protective mechanism develops in response to prolonged exposure to high concentrations of ozone.

Analysis of Variance↗
PubMed1993

A kinetic model for the competitive reactions of ozone with amino acid residues in proteins in reverse micelles.

Lysozyme and 10 other proteins are solubilized in reverse micelles formed by 0.1 M sodium di-2-ethyl-hexylsulfosuccinate and 2.0-2.5 M water (pH 7.4) in isooctane solvent. Exposure of the protein-containing reverse micellar solutions to ozone causes oxidative damage to the proteins, as assessed by the oxidation of tryptophan residues. The oxidation product of the protein-bound tryptophan has a molar absorption coefficient of 3275 +/- 81 M-1 cm-1 (mean +/- S.D., n = 6) at 320 nm. The product is suggested to be a Criegee ozonide or a tautomer of the Criegee ozonide and not N-formylkynurenine. Ozonation of lysozyme in reverse micelles results in the formation of hydrogen peroxide in yields of only approximately 0.07 mol/mol of tryptophan residues oxidized. The recovery of hydrogen peroxide added as an internal standard to the lysozyme-containing reverse micellar solutions ranges from 84 to 88%, whether or not the samples are subjected to ozonation. This suggests that hydrogen peroxide is neither destroyed during the process of ozonation nor consumed by the protein to a significant extent in an adventitious reaction. A kinetic model for the overall reaction of ozone with the proteins is developed, taking into account the concentrations and the reactivities of individual amino acid residues toward ozone. The model predicts the fractional reaction of ozone with tryptophan residues in the proteins, despite differences in amino acid composition, molecular weight, and tertiary structures. The lack of influence of protein structure is confirmed further by the observation that the native lysozyme (with and without external S-carboxymethylcysteine) and S-carboxymethylated lysozyme give identical values of the fractional reaction of ozone with tryptophan residues. The kinetic equations for the competitive reactions of ozone with amino acid residues in proteins, with some minor modification, are applicable to ozonations on complex mixtures of lipids, proteins, and antioxidants.

Amino Acids↗
PubMed1994

Consequences of prolonged inhalation of ozone on F344/N rats: collaborative studies. Part IV: Effects on expression of extracellular matrix genes.

Increased deposition of lung extracellular matrix in terminal airways is associated with chronic ozone exposure. In situ hybridization was used to assess whether long-term ozone exposure causes elevated and continued expression of genes coding for connective tissue proteins. Accessory lobes were removed from the animals exposed to 0, 0.12, 0.5, or 1.0 parts per million (ppm)* ozone for 20 months as part of the National Toxicology Program (NTP)/HEI Collaborative Ozone Project. The lungs were perfused fixed under physiologic pressure and processed for in situ hybridization. Sections were hybridized with 35S-labeled probes for messenger RNA (mRNA) coding for various matrix proteins, including collagen types I and III, elastin, and fibronectin, and for interstitial collagenase, a matrix metalloproteinase. Fetal rat lung was used as a positive control for hybridization. No signal for any mRNA was detected in terminal airway stromal cells of lungs from animals exposed to ozone for 20 months or control animals breathing clean air. In all samples from animals exposed to ozone for 20 months and control animals, only a very weak signal was seen in occasional cells within the interstitial spaces around large airways and blood vessels. In contrast, a strong signal for matrix-related mRNA was detected in fetal lung tissue. These findings indicate that active or enhanced matrix production is turned off in the adult animals used in the ozone studies, suggesting that the increase in matrix deposition results from a transient and early fibrotic response. Indeed, signal for type I procollagen and tropoelastin mRNAs was seen in alveolar septal cells in lungs of rats exposed to ozone for two months. No signal was seen in alveolar cells of age-matched control animals. (These animals, exposed for two months, and age-matched controls were from earlier studies supported by the HEI.) These findings indicate that ozone mediates a transient fibrotic response that results in a sustained increase in lung extracellular matrix. Confirmation of this hypothesis would require additional studies using animals exposed to ozone for shorter times.

Administration, Inhalation↗
PubMed1994

A passive ozone sampler based on a reaction with iodide.

A new passive sampler for ozone and its simple analytical system have been developed. Because it is small and sensitive, the sampler can be used for determining personal exposures to ozone and oxidants and for multilocation measurements. The sampler consists of an electrode, a spacer, and several layers of membrane filters and Teflon meshes. The electrode is a carbon paper disk coated with nylon-6 polymer and potassium iodide. The membrane filters are used to remove interferences. A sampling rate of ozone is controlled by the spacer and Teflon meshes. Iodine is liberated by an oxidation reaction of potassium iodide with ozone. The iodine is stabilized by forming a charge transfer complex with nylon-6 and is accumulated in the nylon-6 layer. The amount of iodine, which is proportional to the level of ozone exposure, is quantified by constant current coulometry. The discharge time of a galvanic battery is measured using the electrode as a positive electrode and a zinc plate as a counter electrode. A time-weighted average concentration of ozone is derived from the discharge time after exposing the electrode to ozone. The effects of various environmental conditions on the sampler's performance were investigated. The results indicated that the sampler showed a linear response to ozone exposure up to 1,450 parts per billion for every hour of use (ppb.hour). The minimum detectable exposure was about 400 ppb.hour. The effects of surface wind velocity, temperature, and humidity were small. However, a relative humidity below 20% resulted in an underestimation of the ozone concentration. Because the electrode requires no pretreatment and the analytical method is very simple, this method is suitable for large-scale studies of personal exposures to ozone and oxidants using multilocation measurements.

Environmental Monitoring↗
PubMed1993

Response of macaque bronchiolar epithelium to ambient concentrations of ozone.

Recently, we reported that exposure to ambient concentrations of ozone, near the U.S. National Ambient Air Quality Standard (0.12 ppm), induced significant nasal epithelial lesions in a non-human primate, the bonnet monkey. The present study defines the effects of ambient concentrations of ozone on the surface epithelium lining respiratory bronchioles and on the underlying bronchiolar interstitium in these same monkeys. Bonnet monkeys were exposed to filtered air or to 0.15 or 0.30 ppm ozone 8 hours/day for 6 or 90 days. At the end of exposures, monkeys were anesthetized and killed by exsanguination. Microdissected bronchiolar airways of infusion-fixed lungs were evaluated morphometrically by light microscopy and quantitatively by scanning and transmission electron microscopy for ozone-induced epithelial changes. Hyperplasia of nonciliated, cuboidal epithelial cells and intraluminal accumulation of macrophages characterized ozone-induced lesions in respiratory bronchioles. There were no significant differences in epithelial thickness or cell numbers among ozone-exposed groups. Ozone-exposed epithelium was composed of 80% cuboidal and 20% squamous cells compared with 40% cuboidal and 60% squamous cells in filtered air controls. In addition, the arithmetic mean thickness of the surface epithelium, a measure of tissue mass per unit area of basal lamina, was significantly increased in all of the ozone-exposed groups. The number of cuboidal epithelial cells per surface area of basal lamina was increased above control values by 780% after 6 days exposure to 0.15 ppm, 777% after 90 days to 0.15 ppm, and 996% after 90 days exposure to 0.30 ppm. There was also a significant ozone-induced increase in the thickness of the bronchiolar interstitium that was due to an increase in both cellular and acellular components. These results demonstrate that exposure to low ambient concentrations of ozone, near the current. National Ambient Air Quality Standard, induces pulmonary lesions in primates. The alterations do not appear to be concentration- or time-dependent, suggesting that the current National Ambient Air Quality Standard may be at or above the threshold for deep lung injury in primates.

Analysis of Variance↗
PubMed1997

CFCS and the ozone layer.

Ozone is an important constituent of the atmosphere. Ozone forms a distinct layer in the lower stratosphere known as the ozone layer. The ozone layer acts as a fragile shield because it protects man and other life forms from exposure to harmful short-wavelength ultraviolet (UV) radiation. The agents, particularly chemical, which affect the amount of ozone present in the atmosphere have been a source of concern for more than 20 years. This has been reinforced by the dramatic decline of stratospheric ozone levels first measured in Antarctica and now apparent worldwide. The combination of routine measurements of ozone depletion, careful laboratory studies and mathematical modelling of ozone in the atmosphere, has demonstrated that the reactive fragments produced when chlorofluorocarbons (CFCs), halons and other halogenated compounds break down in the stratosphere are responsible for the ozone loss. As CFCs have widespread and sometimes apparently essential uses in modern society, there has been an intense effort to develop safe, effective replacements which have a negligible or much smaller impact on the environment. The Montreal Protocol, signed by over 140 nations, has been implemented to control and phase out the chemical compounds responsible for ozone loss.

Air Pollutants↗