0.1 ppm O 3 may increase the susceptibility to bacterial infections. Exposed
mice may have congenital abnormalities and neonatal deaths.
The development of hyper-reactivity following O 3 exposure has been shown
in humans and dogs. The most characteristic toxic effect of exposure to
relatively high-levels of O 3 is pulmonary edema,
46 a leakage of fluid into the
gas-exchange parts of the lung. This effect was seen at concentrations only
slightly above that observed in pollution in Los Angeles, California.
Humans and animals have been shown to develop tolerance to O 3 .
Tolerance refers to increased capacity of an organism that has been preexposed to a chemical agent, such as an oxidant, to resist the effects of later
exposures to ordinarily lethal, or otherwise injurious, doses of the same agent.
For example, rodents exposed to 0.3 ppm O 3 would become tolerant to
subsequent exposures of several ppm O 3 , a dose that would produce massive
pulmonary edema in animals exposed for the first time. Some human subjects
exposed to 0.3 ppm O 3 at intervals of approximately one day showed
diminished reactivity after later exposures. This response is termed adaptation.
47
8.4.5 BIOLOGICAL EFFECTS
A large volume of literature has been published describing the biochemical
effects of O 3 . Examples of the reported effects include:
reactions with proteins and amino acids
reactions with lipids
formation of free radicals
oxidation of sulfhydryl compounds and pyridine nucleotides
production of more or less nonspecific stress, with the release of histamine
As mentioned in the previous section, O 3 interacts with proteins and some
amino acids, altering their characteristics. In humans, the amount of lysozyme
in tears of individuals exposed to smog was shown to be 60% less than normal.
The concentrations of protein and nonprotein sulfhydryls in the lungs of rats
exposed to 2 ppm O 3 for 4 to 8 hours were shown to be decreased. A number of
investigators have shown that O 3 can cause the oxidation of the –SH group,
and that addition of SH compounds was protective.
The activities of several enzymes are either enhanced or depressed in
animals exposed to O 3 . Reports on decreases in enzyme activities include
glucose-6-phosphate dehydrogenase, glutathione reductase, and succinatecytochrome c reductase in the lungs of rats exposed to 2 ppm O 3 for 4 to 8
hours, whereas increased activities were shown with glucose-6-phosphate
dehyrogenase, 6-phosphogluconate dehydrogenase, and isocitrate dehydrogenase.
Balchum et al.
48 have provided evidence to support the concept that the
peroxidation or ozonization of unsaturated fatty acids in biological membranes
is a primary mechanism of the deleterious effects of O 3 . The hypothesis was
Air Pollution – Inorganic Gases
125
[16:53 26/8/04 P:/CRC PRESS/4365 MING-HO.751 (1670)/4365-008.3d]
Ref: 4365 MING-HO YU Chap-008 Page: 125 111-134
mice may have congenital abnormalities and neonatal deaths.
The development of hyper-reactivity following O 3 exposure has been shown
in humans and dogs. The most characteristic toxic effect of exposure to
relatively high-levels of O 3 is pulmonary edema,
46 a leakage of fluid into the
gas-exchange parts of the lung. This effect was seen at concentrations only
slightly above that observed in pollution in Los Angeles, California.
Humans and animals have been shown to develop tolerance to O 3 .
Tolerance refers to increased capacity of an organism that has been preexposed to a chemical agent, such as an oxidant, to resist the effects of later
exposures to ordinarily lethal, or otherwise injurious, doses of the same agent.
For example, rodents exposed to 0.3 ppm O 3 would become tolerant to
subsequent exposures of several ppm O 3 , a dose that would produce massive
pulmonary edema in animals exposed for the first time. Some human subjects
exposed to 0.3 ppm O 3 at intervals of approximately one day showed
diminished reactivity after later exposures. This response is termed adaptation.
47
8.4.5 BIOLOGICAL EFFECTS
A large volume of literature has been published describing the biochemical
effects of O 3 . Examples of the reported effects include:
reactions with proteins and amino acids
reactions with lipids
formation of free radicals
oxidation of sulfhydryl compounds and pyridine nucleotides
production of more or less nonspecific stress, with the release of histamine
As mentioned in the previous section, O 3 interacts with proteins and some
amino acids, altering their characteristics. In humans, the amount of lysozyme
in tears of individuals exposed to smog was shown to be 60% less than normal.
The concentrations of protein and nonprotein sulfhydryls in the lungs of rats
exposed to 2 ppm O 3 for 4 to 8 hours were shown to be decreased. A number of
investigators have shown that O 3 can cause the oxidation of the –SH group,
and that addition of SH compounds was protective.
The activities of several enzymes are either enhanced or depressed in
animals exposed to O 3 . Reports on decreases in enzyme activities include
glucose-6-phosphate dehydrogenase, glutathione reductase, and succinatecytochrome c reductase in the lungs of rats exposed to 2 ppm O 3 for 4 to 8
hours, whereas increased activities were shown with glucose-6-phosphate
dehyrogenase, 6-phosphogluconate dehydrogenase, and isocitrate dehydrogenase.
Balchum et al.
48 have provided evidence to support the concept that the
peroxidation or ozonization of unsaturated fatty acids in biological membranes
is a primary mechanism of the deleterious effects of O 3 . The hypothesis was
Air Pollution – Inorganic Gases
125
[16:53 26/8/04 P:/CRC PRESS/4365 MING-HO.751 (1670)/4365-008.3d]
Ref: 4365 MING-HO YU Chap-008 Page: 125 111-134