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Ozone exposure tests

This transitory behavior was observed to arise from all the weathering agents considered in this study except ozone. Instead, test coupons exposed to ozone exhibited an initial decline in the crosslink density of the silicone with the formation of surface cracks, which were difficult to distinguish with the naked eye. With continued exposure to ozone, however, the material would begin to crosslink. We proposed that ozone s greatest affinity... [Pg.30]

Since ozone attack on rubber is essentially a surface phenomenon, the test methods involve exposure of the rubber samples under static and/or dynamic strain, in a closed chamber at a constant temperature, to an atmosphere containing a given concentration of ozone. Cured test pieces are examined periodically for cracking. [Pg.476]

The length and amount of cracks is assessed according to the Bayer method [72,73]. The ISO standard ozone test conditions involve a test temperature of 40°C zE 1°C and an ozone level of 50 5 pphm, with a test duration of 72 h. Testing is done under static [72] and/or dynamic strain [73]. These are accelerated tests and should be used for the relative comparison of compounds, rather than for the prediction of long-term service life. The method is rather complicated and demands a long duration of ozone exposure. Therefore, in some cases the rate constants of the antiozonants reaction with ozone in solution are used instead to evaluate the efficiency of different antiozonants [74]. [Pg.476]

The effects of ozone appear to be cumulative for initial exposures followed by adaptation. Five of six subjects exposed to 0.5 ppm ozone 2 hours/day for 4 days showed cumulative effects of symptoms and lung function tests for the first 3 days, followed by a return to near control values on day 4." In animals exposure to 0.3-3 ppm for up to 1 hour permits the animals to withstand multilethal doses for months afterwards. However, repeated exposures impart protection from all forms of lung injury (e.g., susceptibility to infectious agents, enzyme activities, inflammation). Initial ozone exposure may act to reduce cell sensitivity and/or increase mucus thickness, factors which may modify the accessibility and action of the gas. It is not known how variations in the length, frequency, or magnitude of exposure modify the time course for tolerance. [Pg.549]

In an effort to determine the minimal time of ozone exposure required for the rats to develop significant tolerance, successively shorter periods of ozone pre-exposure were tested, from 18 hours to 1 hour. Tolerance to ozone is successively decreased in degree when pre-exposure is thus shortened, although some tolerance is demonstrated with as little as 1-hour pre-exposure to 1 p.pjn. of ozone (data lines 9 and 10). Tests for tolerance were made 24 hours after the start of the initial exposure, thus demonstrating the very rapid development of ozone tolerance. Because the 6-hour exposure to 1 p.p.m. of ozone developed a reproducible tolerance of significant degree, 6 hours was taken as a convenient pre-exposure time for subsequent studies to determine the duration of tolerance to ozone from a single exposure. [Pg.366]

It is interesting that the grave effects of pulmonary edema and hemorrhage from acute exposure of ozone may be prevented in animals by so simple a procedure as a combination of vitamins and reducing agents prior to ozone exposure (Table VI). The clues furnished by such substances on the mechanism of action of ozone, and related oxidative pulmonary irritants such as nitrogen dioxide, are considerable from such information a definitive hypothesis of action of these pulmonary irritants may be formulated and tested. [Pg.368]

The test matrix that will be carried out in the EUPHORE chamber is shown in Tables 1 and 2. These series of tests provide experiments that will examine the effects of aging, photolysis, HO, O3 and the NO3 radieal (in the dark) on the eomposition of diesel exhaust. The experiments are divided into dark (Table 1) and light (Table 2) exposures test matrixes. The dark experiments D-1, D-2, and D-5 provide baselines for other experiments. Experiment D-3 investigates the effeets of O3 on diesel exhaust in the dark and experiment D-4 allows the effect of the NO3 radical on diesel exhaust to be studied. Dinitrogen pentoxide is used as a source of NO3 radicals. N2O5 is prepared by reacting ozone with NO2 direetly in the chamber. [Pg.281]

Laboratory ozone resistance tests involve the exposure of stretched test pieces, usually strips or dumbbells, to a specified combination of ozone concentration and temperature. The standard concentrations permitted in ISO 1431/1 (BS903, Part A43) are 25, 50. 100. and 200 pphm ozone. For most purposes, SOpphm is considered suitable and is now found in a wide range of material and product specifications. The lowest concentration is intended for applications used under low-severity conditions, whereas 100 and 200 pphm are used to ensure that there is sufficient protection for badly polluted areas or to ensure the use of an inherently resistant rubber type. [Pg.303]

Table 3 [9] also gives the results of exposure tests in ozone-containing water for the 13 % chromium steel SAE 403 (1.4000, X6Crl3) and the 17 % chromium steel SAE 430 (1.4016, X6Crl7) (composition in Table 2). Both materials were resistant under the given test conditions. In contrast, the low-alloy chromium steel 34CrMo4 (UNS G41300,1.7220) is not resistant in ozone-containing water. Table 3 [9] also gives the results of exposure tests in ozone-containing water for the 13 % chromium steel SAE 403 (1.4000, X6Crl3) and the 17 % chromium steel SAE 430 (1.4016, X6Crl7) (composition in Table 2). Both materials were resistant under the given test conditions. In contrast, the low-alloy chromium steel 34CrMo4 (UNS G41300,1.7220) is not resistant in ozone-containing water.
Epithelial cels type I and squamous cells appear to be most sensitive to ozone [299]. An exposure to 0.5 ppm ozone increases the volume but reduces the area of epithelial cell types I [300]. These cells are regenerated to the normal condition after a week in fresh air and develop certain tolerance to ozone reexposure [301, 302]. The authors have studied tracheal cells (volume, density) by electron microscopy. They have found that all changes due to chronic ozone exposure were reversible, the normal values being regained if test animals are exposed to fresh air. [Pg.170]

Direct exposure to NO can cause respiratory problems. VOCs and NOjj are catalyzed by sunlight to form ground level ozone, often referred to as smog. NO can be generated from either stationary sources or mobile sources. In 1997, the EPA changed the ambient standard for ozone from 0.12 ppm to 0.08 ppm and the applicable test period was increased from I to 8 hours. [Pg.310]

Less than 1 pphm (parts per hundred million) of ozone in the atmosphere can severely attack non-resistant rubbers. However, there is far less, if any, problem with plastics and tests are rarely made. If required, the methods standardised for rubbers in ISO 1431 [24] could be used, which involve exposure in a special cabinet with controlled levels of ozone. [Pg.71]

We still lack an adequate dose-response relationship for humans exposed to ozone, particularly at concentrations less than about 0.2 ppm. The data base for the development of such a relationship for both short-and long-term exposures is inadequate. Although some data from controlled studies are available for concentrations above 0.3 ppm, methods for extrapolating to lower concentrations are needed. Moreover, it is not clear how to weight the results of pulmonary function tests on humans, animal studies, and epidemiologic studies in a general dose-response relationship. [Pg.2]

Exposures to ozone for a few hours result in a marked increase in the susceptibility of animals to controlled doses of infectious organisms introduced into the lung. This is the most sensitive test of any yet reported significantly increased susceptibility of mice to one microorganism occurred after exposure to ozone at a concentration as low as 0.08 ppm. [Pg.7]

With various tests of ventilatory function, it has been shown that healthy male college students experienced no effect of sulfur dioxide at 0.37 ppm, a 10% decline in function with ozone at 0.37 ppm, and a 20-40% decline in function with a combination of sulfur dioxide at 0.37 ppm and ozone at 0.37 ppm. Other experiments have suggested an adaptation of southern Californians to chronic exposure to ambient ozone. [Pg.8]

Dowell et al. reported an increase in the osmotic fragility of alveolar macrophage preparations obtained horn rabbits acutely exposed to ozone at 10 ppm for 3 h or intermittently exposed to ozone at 2 ppm for 8 h/day for 7 days. Similar intermittent exposure to ozone at 0.5 ppm was without effect. A test for malonaldehyde formation was negative, but this lipid peroxide breakdown product may have been lost during the preparatory procedure. [Pg.359]

In one study,human subjects were tested in a controlled-environ-ment chamber with a high (summer) temperature and with ozone, nitrogen dioxide, and carbon monoxide as pollutants. Performance on a divided-attention task given at the end of the exposure period and the subjects heartrate variability (a potential psychophysiologic measure of attention) were evaluated. The subjects displayed a significant decrement in peripheral attention associated with increased ambient temperature. Effects attributable to pollutant gases were variable. [Pg.397]

Differential susceptibility of individual clones of eastern white pine to ozone and sulfur dioxide was shown by Berry and Heggestad and Costonis. When Dochinger et a/. determined that chlorotic dwarf could be caused by an interaction of ozone and sulfur dioxide, th used a chlorotic dwarf-susceptible clone to eliminate the genotype variable. Houston tested the response of tolerant and susceptible clones of eastern white pine (on the basis of symptom expression under ambient conditions) to ozone or sulfur dioxide. Injury caused by sulfur dioxide or sulfur dioxide plus ozone correlated well with the earlier field responses, but ozone did not produce a consistent response. They also found that a 6-h exposure to a mixture of sulfur dioxide and ozone caused a difference in needle elongation between clones within tolerant and sensitive groups. This suggests that tolerance may function over a wide range of responses. [Pg.477]

HilF reported pollutant uptake values for a number of gaseous pollutants, including ozone and PAN, with alfalfa as his test organism (Table 11-26). These values were obtained with a dynamic, but closed, exposure facility. Uptake was determined by the amount of pollutant needed to maintain a constant chamber concentration over an alfalfa bed. Uptake values, expressed on the basis of leaf area, reflect the effect of the plant canopy on the exchange of gases within the canopy and do not... [Pg.534]

Yonkers et al, have tested the ozone susceptibility of 15 species of annuals common to the Mojave Desert just north and east of the Los Angeles basin (and San Bernardino Mountains). Compared with the susceptible pinto bean plants included in the experiment with ozone at 0.35 ppm, Plantago sp., Cercidium sp., and Prosopsis sp. were also sensitive. Further interpretation of these results is complicated by the influences of plant age and pre-exposure conditions. [Pg.625]

Studies have been conducted on creep compliance tests in which paint films were subjected to tensile loads of 4-7 psi (27.2-47.6 x 10 N/m ) and to 6% ozone for 505 h. A typical result for a high-quality emulsion-base paint is shown in Figure 13-1. Creep compliance is reduced by exposure to 6% ozone. If the effect is linearly related to ozone concentration, we might expect the same reduction in creep compliance at 0.1-ppm ozone in 3 x 10 h, or some 30,(XX) yr. Thus, reduction in creep compliance is not viewed as having a serious ozone contribution. [Pg.654]


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