Ppm Ozone Concentration Research Articles

Behaviour of alanine dosimeters in an ozone environment

Polymer-alanine dosimeters (PADs) have been irradiated, in air with a concentration of 5 ppm of ozone, with doses up to 10 kGy, by means of a 90Sr source. The electron spin resonance (ESR) signals were compared with the signals obtained after irradiations in normal air, and the amplitude reduction was found to be negligible. The evolution of the ESR signal of PADs irradiated in normal air and thereafter stored in air with 5 ppm ozone concentration was also investigated. No change was observed over a period of 2 months.

Water uptake by sunlight and ozone exposed diesel exhaust particles

Two types of experiments were conducted to investigate the effect of aerosol aging on water uptake by diesel soot particles. First, in three experiments diluted diesel soot was exposed to sunlight for up to 10 hours in a 190 m 3 Teflon film smog chamber and filter samples were collected at various time intervals. Second, diesel soot filter samples were exposed to 2 to 4 ppm ozone concentrations for 3 hours in a stainless steel chamber. Water uptake was measured by weighing the filter samples from each type of experiment by varying relative humidity in the weighing chamber of an electronic microbalance. When relative humidity was increased from 40% to 90% weights of fresh diesel soot samples from the smog chamber increased by less than 2% and sample weights of diesel soot aged in the chamber for 9 to 10 h increased by 7 to 8%. Sample weights for diesel soot filter samples aged in the stainless steel chamber in the presence of ozone in the dark increased by less than 2.5% over the same relative humidity range.

Morphologic injury and lipid peroxidation in monolayer cultures of rabbit tracheal epithelium exposed in vitro to ozone

Numerous reports have documented airway epithelial damage and lipid peroxidation in the lungs of animals exposed to ozone. However, the response of isolated tracheal epithelial (TE) cells to ozone has not been extensively studied. To assess ozone-induced injury in cultured TE cells, an in vitro exposure system was developed in which cells were maintained at gas-fluid interface analogous to in vivo conditions. Confluent monolayer cultures of rabbit TE cells were exposed for 30 min to atmospheres of 5% CO2/air containing 0.05, 0.1, 0.5, 1, 2, 4, 6, or 8 ppm ozone. Morphologic injury was assessed by phase-contrast microscopy and by determination of TE cell number and viability (trypan blue dye exclusion) pre- and postexposure, and the lipid peroxide content of TE cells was measured as thiobarbituric acid (TBA) reactive substances. Exposure to 5% CO2/air alone did not affect monolayer morphology, cell number of viability. Cultures exposed to 0.05 or 0.1 ppm ozone demonstrated no consistent light microscopic changes, whereas exposure to 0.5 ppm and higher ozone concentrations caused distortion of monolayer morphology, cytoplasmic vacuolization, and decreased viability. Exposure to 0.5 or 1 ppm resulted primarily in cytoplasmic vacuolization while exposure to 2, 4, 6, or 8 ppm induced more pronounced cellular injury associated with cell necrosis (viability post 8 ppm ozone 75.0 +/- 7.0%, vs. 95.9 +/- 2.6% for 5% CO2/air controls). Ozone exposure also caused changes in cell shape, which on occasion resulted in loss of cell-to-cell contact. Increased production of TBA-reactive substances was detected in TE cells following ozone exposure, including exposure to 0.05 and 0.1 ppm. The morphologic changes induced by in vitro ozone exposure in the cultured TE cells were similar to those described in the tracheal epithelium of ozone-exposed animals and occurred independent of recruited inflammatory cells or extravasated circulating mediators.

Preexposure to low ozone concentrations does not diminish the pulmonary function response on exposure to higher ozone concentrations.

To determine whether persons repeatedly exposed to low ozone concentrations would demonstrate a diminished responsivity, as a result of adaptation or desensitization, when subsequently exposed to a higher ozone concentration, we performed the following study. Respiratory sensitivity (pulmonary function response) to 2 h of exposure to 0.42 or 0.50 ppm ozone (acute exposure) was determined 3 months before or 6 to 8 wk after the study. Twenty-one subjects (8 men, 13 women) were exposed for 2 h or 5 consecutive days to filtered air, 0.20, 0.20, 0.20, and 0.42 to 0.50 ppm ozone, respectively. There were no significant differences between the responses of men and women to ozone. Subjects were divided into a sensitive group (greater than 20% drop in FEV1) and a nonsensitive group (less than 10% drop in FEV1) on the basis of their responses to the acute exposure. Neither the overall group nor the nonsensitive group showed a significant response to 0.20 ppm. Sensitive subjects (n = 9) showed small but significant decreases in FEV1 on exposure to 0.20 ppm. The predominant finding was that the 3 days of preexposure to 0.20 ppm ozone had no effect on the response to 0.42 or 0.50 ppm ozone on the fourth day (when compared with the previous acute exposure to 0.42 or 0.50 ppm). We conclude that subjects repeatedly (3 times) exposed to a low (0.20 ppm) concentration of ozone do not demonstrate a pulmonary function adaptation or desensitization on a subsequent exposure to a higher (0.42 or 0.50 ppm) ozone concentration.

Pulmonary functions observed by means of flow-volume curve in welders exposed to ozone (author's transl)

Pulmonary functions were observed by the flow-volume curve method on 68 healthy welders who had been exposed to comparatively high levels of ozone while engaged in arc welding process shielded by inert gas. The welders between 20 and 29 years of age were selected as subjects and classified into five groups according to ozone concentrations of the workshops. Results of pulmonary function tests were analyzed with reference to working experiences, dust concentrations of the workshops, smoking habits and air pollution levels of the location of factories. An attempt were made to evaluate the possible effects of prolonged exposure to ozone produced by welding upon the health or workers. The results obtained were as follows. 1. Values of both peak flow rate and maximum expiratory flow rate at 75% of vital capacity (V75) were decreased slightly in welder groups, but relationships between the observed values and ozone concentrations were not recognized. 2. Values of maximum expiratory flow rate at 25% of vital capacity (V25) of welders who had been exposed to ozone in concentration of 1.05 ppm or more were decreased significantly compared with groups exposed to ozone under 1.05 ppm. 3. In addition, values of both V25 and forced vital capacity (FVC) of the workers who had been engaged in welding for 4 years or more were significantly lower than those of the workers for less than 4 years of exposure. However, the relationship between the lung function values and smoking habits were not significant in both groups. 4. The decreases in V25 values were observed in several workers who had been exposed even to 0.46 ppm or higher (but under 1.05 ppm) ozone concentrations. 5. Relationships between the lung function values and either smoking habits or air pollutant levels of locations were not significant in all groups.

Ozone Effects on Radish (Raphanus sativus L. cv. Cherry Belle): Gradient of Ultrastructural Changes

Summary Ultrastructural changes produced by low (Z 0.5 ppm) levels of ozone may be attributed to water deficit resulting from injury to the sensitive paravenial cells. The drastic alterations, resulting from high (> 0.5 ppm) ozone concentrations, were apparently -due to, more direct effects. Although differential fixation images of membranes in control and ozone treated leaves were not obtained the significance of ozone attacking the olefinic groups of fatty acids in the membrane bilayer should not be completely ignored.