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5.3 TOXICITY AND RISKS INDUCED BY OCCUPATIONAL EXPOSURE TO CHEMICAL COMPOUNDS 295

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phatic system. Alternatively they may persist in the lungs. ' When macrophages
are phagocytizing the particles, they become activated and secrete large amounts
of oxygen radicals. While the radicals may have no effect whatsoever on the parti-
cles, they may well damage the surrounding cells and tissues. It has been suggested
that the mechanisms by which asbestos particles induce lung cancer and mesothe-
lioma (a fatal cancer type in the pleura) may be associated with excessive produc-
37
tion of reactive oxygen species by specialized phagocytes. An important
consequence of alveolar level damage is that it may sensitize the lungs to inflam-
mation. Serious air pollution episodes are associated with increased incidence of
lung inflammations, especially in the elderly.

Chronic Pulmonary Toxicity Chronic damage to the lungs may be due
to several subsequent exposures or due to one large dose that markedly ex-
ceeds the capacity of pulmonary defense, clearance, and repair mechanisms.
Chronic pulmonary toxicity includes emphysema, chronic bronchitis, asthma,
lung fibrosis, and lung cancer. The single most important reason for chronic
pulmonary toxicity is tobacco smoke, which induces all types of chronic pul-
monary toxicity, with the exception of fibrosis. 141
In developed countries, where the prevalence of chronic obstructive lung dis-
eases has increased rapidly, the finger of suspicion is often pointed at the air quality,
41
especially that in large cities. In emphysema, the walls separating alveoli from
each other disappear, and this reduces the surface area for gas exchange. Chronic
bronchitis is characterized by persistent cough and increased mucus secretion. In
asthma, the lungs become sensitive to bronchoconstriction induced by environ-
mental agents. In addition, asthma also involves inflammation of the airways. 58>59

Lung Cancer Lung cancer is one of the most common cancers. In many
countries, lung cancer is the most common cancer among the male population, and
its incidence among females has shown a dramatic and alarming increase. The inci-
dence of lung cancer has always carried a strong association with smoking in the
past, i.e., the latency period of lung cancer is about 20 years after the beginning of
the exposure to tobacco smoke. In addition to tobacco smoke, many chemicals can
increase the risk of lung cancer. These include asbestos, radon, nickel, chromium
and beryllium. Asbestos and radon are considered to be the next most important
factors after tobacco smoke causing lung cancer. Both also have a synergistic effect
with smoking. The number of asbestos-related diseases has remained high (these
include pleural diseases, asbestosis, and cancers), even though the use of asbestos
has dramatically decreased and is now totally banned in many countries. This is
41 58 59
due to the long latency period of asbestos-induced diseases. ' ' Figure 5.48 pro-
vides epidemiological data on the relationship between smoking and lung cancer.
64
See also Fig. 5.39 for the mechanism of asbestos toxicity.
Cardiovascular Toxicity
Several chemical compounds can have an adverse effect on the heart and
the vascular system. The effect may first appear as a transient change in the
cardiac function. However, prolonged exposure increases the risk of perma-
nent effects. Occasionally, functional effects such as cardiac arrhythmias
may even lead to death. Furthermore, in many cases the effects of chemicals