ozonization of fatty acids. When O 3 reacts with a polyenoic fatty acid, for
instance, the breakdown products include H 2 O 2 and malonaldyde.
43 The
structures of amino acids and proteins are also altered when these substances
are exposed to O 3 . Various amino acids, including methionine, tyrosine,
cysteine, and tryptophan, are oxidized when exposed to O 3 . For example, the
oxidation of methionine leads to methionine sulfoxide formation in a
concentration-dependent manner.
44
8.4.4 EFFECTS ON ANIMALS AND HUMANS
Ozone and other photochemical oxidants cause irritation of the respiratory
tract and the eye. The threshold limit value (TLV) for O 3 in industry is
0.1 ppm. Exposure to 0.6 to 0.8 ppm O 3 for 60 minutes resultes in headache,
nausea, anorexia, and increased airway resistance. Coughing, chest pain, and a
sensation of shortness of breath were shown in the exposed subjects who were
exercised.
45 Exposure of laboratory animals to 0.7 to 0.9 ppm O 3 may
predispose or aggravate a response to bacterial infection. Morphological and
functional changes occur in the lung in laboratory animals subjected to
prolonged O 3 exposure. Such changes as chronic bronchitis, bronchiolitis, and
emphysematous and septal fibrosis in lung tissues have been observed in mice,
rabbits, hamsters, and guinea pigs exposed daily to O 3 at concentrations
slightly above 1 ppm. Thickening of terminal and respiratory bronchioles was
the most noticeable change. For example, in the small pulmonary arteries of
rabbits exposed to O 3 , the walls were thicker and the lumens were narrower
than those of the controls. Mean ratios of wall thickness to lumen diameter
were 1:4.9 for the control, and 1:1.7 for the exposed animals.
46 This indicates
that the width of the lumen of exposed animals was only about one third that
of the controls.
As noted in Chapter 7, emphysema is a disease in which the alveoli in the
lungs become damaged. The disorder causes shortness of breath and, in severe
cases, can lead to respiratory or heart failure. Although emphysema is caused
mainly by cigarette smoking, atmospheric pollution due to O 3 and some other
pollutants are considered to be predisposing factors. Inhaled O 2 is passed
through the thin walls of alveoli, into the bloodstream, and CO 2 is removed
from the capillaries to be breathed out. Tobacco smoke and other air
pollutants are believed to cause emphysema by provoking the release of
chemicals within the alveoli that damage the alveolar walls. As the disease
progresses, the alveoli burst and form fewer, larger sacs with less surface area,
and so O 2 and CO 2 exchange is impaired (Figure 7.2b).
Other physiological effects include dryness of upper airway passages,
irritation of mucous membranes of nose and throat, bronchial irritation,
headache, fatigue, and alterations of visual response.
Evidence suggests that O 3 exposure accelerates the aging process. Some
investigators indicate that aging is due to irreversible crosslinking between
macromolecules, principally proteins and nucleic acids. Animals exposed to
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Ref: 4365 MING-HO YU Chap-008 Page: 124 111-134
instance, the breakdown products include H 2 O 2 and malonaldyde.
43 The
structures of amino acids and proteins are also altered when these substances
are exposed to O 3 . Various amino acids, including methionine, tyrosine,
cysteine, and tryptophan, are oxidized when exposed to O 3 . For example, the
oxidation of methionine leads to methionine sulfoxide formation in a
concentration-dependent manner.
44
8.4.4 EFFECTS ON ANIMALS AND HUMANS
Ozone and other photochemical oxidants cause irritation of the respiratory
tract and the eye. The threshold limit value (TLV) for O 3 in industry is
0.1 ppm. Exposure to 0.6 to 0.8 ppm O 3 for 60 minutes resultes in headache,
nausea, anorexia, and increased airway resistance. Coughing, chest pain, and a
sensation of shortness of breath were shown in the exposed subjects who were
exercised.
45 Exposure of laboratory animals to 0.7 to 0.9 ppm O 3 may
predispose or aggravate a response to bacterial infection. Morphological and
functional changes occur in the lung in laboratory animals subjected to
prolonged O 3 exposure. Such changes as chronic bronchitis, bronchiolitis, and
emphysematous and septal fibrosis in lung tissues have been observed in mice,
rabbits, hamsters, and guinea pigs exposed daily to O 3 at concentrations
slightly above 1 ppm. Thickening of terminal and respiratory bronchioles was
the most noticeable change. For example, in the small pulmonary arteries of
rabbits exposed to O 3 , the walls were thicker and the lumens were narrower
than those of the controls. Mean ratios of wall thickness to lumen diameter
were 1:4.9 for the control, and 1:1.7 for the exposed animals.
46 This indicates
that the width of the lumen of exposed animals was only about one third that
of the controls.
As noted in Chapter 7, emphysema is a disease in which the alveoli in the
lungs become damaged. The disorder causes shortness of breath and, in severe
cases, can lead to respiratory or heart failure. Although emphysema is caused
mainly by cigarette smoking, atmospheric pollution due to O 3 and some other
pollutants are considered to be predisposing factors. Inhaled O 2 is passed
through the thin walls of alveoli, into the bloodstream, and CO 2 is removed
from the capillaries to be breathed out. Tobacco smoke and other air
pollutants are believed to cause emphysema by provoking the release of
chemicals within the alveoli that damage the alveolar walls. As the disease
progresses, the alveoli burst and form fewer, larger sacs with less surface area,
and so O 2 and CO 2 exchange is impaired (Figure 7.2b).
Other physiological effects include dryness of upper airway passages,
irritation of mucous membranes of nose and throat, bronchial irritation,
headache, fatigue, and alterations of visual response.
Evidence suggests that O 3 exposure accelerates the aging process. Some
investigators indicate that aging is due to irreversible crosslinking between
macromolecules, principally proteins and nucleic acids. Animals exposed to
124
Environmental Toxicology
[16:53 26/8/04 P:/CRC PRESS/4365 MING-HO.751 (1670)/4365-008.3d]
Ref: 4365 MING-HO YU Chap-008 Page: 124 111-134