Exposure to ozone

Beeause of the odour threshold of ea 0.015 ppm, exposure to ozone below the TLV ean usually be deteeted by smell. 

Oxidant Stipple small brown or black interveinal necrotic lesions on the adaxial surface of leaf tissue that can be attributed to exposure to ozone. 

The updtitcd stmidard recognizes the current scientific view that exposure to ozone levels at and below the current standard causes significant adverse health clTccts in cliildrcn and in healthy adults engaged in outdoor activities... 

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... 

Exposure to cigarette smoke Exposure to ozone Exposure to ionizing radiation... 

Figure 2. Kinetic curve of POOH groups formation in polypropylene film after 10 hours exposure to ozone.

Table 1. Change in the wettability of polypropylene film after exposure to ozone and ozone-UV irradiation...

T. Johnson and J. Capel, "Population Exposure to Ozone in the Northeast Corridor from May through October, 1979," PEDCo Environmental, Inc., Durham, North Carolina, 1980. 

Research dating back to the mid 1950 s has shown that volatile orgamc compounds (VOC s) photochemically react m the atmosphere and contribute to the formation of ground level ozone, a precursor to smog [1]. Medical studies have shown that human exposure to ozone can result in eye and smus tract irritation, and can lead to respiratory related illnesses [2]. Due to the unique and severe smog problems that affected many cities in the state of California, studies of the causes of ah pollution were initiated m the 1950 s [3]. Based on its findings, California formed the Motor Vehicle Pollution Control Board m 1960 to regulate pollution from automobiles. 

Burleson, G.R., Keyes, L.L., and Stutzman, J.D., Immunosuppression of pulmonary natural killer activity by exposure to ozone, Immunopharmacol. Immunotoxicol. 11, 4, 715, 1989. 

That night we went to a hotel, and the next day I started making calls from my bed. The first person I contacted, at the health department, said, Your symptoms are consistent with a high level exposure to ozone. I called the EPA and anybody else I was referred to in every conversation. 

Human exposure, to ethylene oxide, 10 660 Human exposure, to ozone, 17 815 Human factors, in process hazards control, 21 861-862... 

They can withstand exposure to ozone, ultraviolet light and weathering. They have excellent dielectric properties and are not affected by oils. They get more easily tom than mbber and dissolve in aromatic solvent. 

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. 

Convincing new information on the health effects of oxidant exposure has emerged from controlled studies on humans, from which tentative dose-response curves have been constructed. These data are reviewed in Chapter 9, with the types of experimental facilities now available for such measurements. The new data show reduced pulmonary function in healthy smokers and nonsmokers after exposure to ozone at 0.37 ppm and higher for 2 h. The federal standard is 0.08 ppm for a I-h exposure.) Other gases and aerosols found in an urban atmosphere were not present in these experiments. 

The major phytotoxic components of the photochemical oxidant system, discussed in Chapter 11, are ozone and peroxyacetylnitrate (PAN), but there is indirect evidence that other phytotoxicants are present. Con siderable effort has gone into controlled exposures to ozone and into field studies. Leaf stomata are the principal sites for ozone and PAN entry into plant tissue. Closed stomata will protect plants from these oxidants. Both ozone and PAN may interfere with various oxidative reactions within plant cells. Membrane sulfhydryl groups and unsaturated lipid components may be primary targets of oxidants. Young leaf tissue is more sensitive to PAN newly expanding and maturing tissue is most sensitive to ozone. Light is required before plant tissue will respond to PAN that is not the case with ozone. 

Oxidants reduce yields of many plants, especially sensitive cultivars. Chronic exposures to concentrations between 0.05 and 0.15 ppm will reduce soybean, com, and radish yields. The threshold appears to be between 0.05 and 0.1 ppm for some sensitive cultivars—well within values monitored in the eastern United States. Growth or flowering effects on carnation, geranium, radish, and pinto bean have been found at chronic exposures to ozone at 0.05-0.15 ppm. Estimated costs to consumers of agricultural losses from oxidant damage are several hundred million dollars a year. 

Bronchoconstriction caused by acute exposures to ozone or sulfur dioxide may be expected to change the ventilation distribution, local aerodynamics, and tissue dosage. Edema resulting from exposures to toxic gases may alter the gas-absorptive capacity of the airways, in addition to the aerodynamics. Reaction of irritant gases with surfactant material in the alveoli may alter the absorptive capacity and physical prop-... 

Boatman, E. S., and R. Frank. Morphologic and ultrastructural changes in the lungs of animals during acute exposure to ozone. Chest 65 (Suppl.) 9S-18S, 1974. 

Gross autopsy findings of pulmonary edema and hemorrhage after acute exposure to ozone have been known for some time. Several studies have shown that edema and an acute inflammatory response occur in several species after brief exposures to ozone. The minimal concentration of ozone... 

Stephens et al have shown that, in rats, the degenerative changes in Type I alveolar cells occur after exposure to ozone at concentrations as low as 0.2 ppm for 3 h and that cells are replaced by Type II alveolar cells beginning a day after the exposure. With electron microscopy, Bils noted that the swelling of the epithelial alveolar lining cells of mice occurred after exposure to ozone at 0.6-1.3 ppm for 4 h. These changes... 

Changes in pulmonary function have been observed in a variety of species after short-term exposure to ozone, including alterations in the elastic behavior of the lungs, increased resistance to flow, and decreased carbon monoxide diffusion capacity. 

According to Stokinger, at least three effects of long-term exposure to ozone have been recc ized effects on morphology and function of the lung, lung-tumor acceleration, and aging. An additional effect, the development of tolerance after exposure to low concentrations of ozone, may also be related to chronic toxicity. 

Acceleration of lung tumorigenesis (adenoma) in a strain of mice that was susceptible to lung tumors occurred after daily exposures to ozone at about 1 ppm. At 15 months, an incidence of 85% was seen in the ozone-exposed animals, compared with 38% in the controls the average number of tumors per mouse was 1.9, compared with 1.5 in the controls. ... 

There is some suggestive evidence that exposure to ozone accelerates the aging process(es). Bjorksten and Bjorksten and Andrews have presented evidence that aging is due to irreversible cross-linking between macromolecules, principally proteins and nucleic acids. Aldehydes were included in the list of cross-linking agents, and these can be produced in the lung as a result of ozone exposure. ... 

In a similar series of experiments conducted by Purvis et al., mice were exposed to ozone at 3.8-4.1 ppm for 3 h, 1-27 h before and 3-27 h after challenge with K. pneumoniae aerosol. Within 19 h after exposure to ozone, the resistance of mice to respiratory infection initiated by challenge with the aerosol was significantly reduced. The same effect was observed in infected animals exposed to ozone up to 27 h after challenge with the aerosol. 

These findings in rabbits are similar to those of E. Goldstein et who have related increased bacterial infectivity in mice to an ozone-induced impairment in the bactericidal capabilities of alveolar macrophages. They used radioactively labeled bacteria and observed a decrease in mouse lung bactericidal activity after a 4-h exposure to ozone at about 0.3-0.4 ppm. With this technique the effects of ozone and nitrogen dioxide are roughty addithre, and silicotic mice are no more susceptible to ozone than are control mice. ... 

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