Chromosomal Aberrations in Lymphocytes Predict Human Cancer Independently of Exposure to Carcinogens
2000
An increased risk of cancer in healthy individuals with high levels of
chromosomal aberrations (CAs) in peripheral blood lymphocytes
has been described in recent epidemiological studies. This association
did not appear to be modified by sex, age, country, or time since CA
test, whereas the role played by exposure to carcinogens is still
uncertain because of the requisite information concerning occupation
and lifestyle was lacking. We evaluated in the present study whether
CAs predicted cancer because they were the result of past exposure to
carcinogens or because they were an intermediate end point in the
pathway leading to disease. A nested case-control study was performed
on 93 incident cancer cases and 62 deceased cancer cases coming from
two prospective cohort studies performed in Nordic countries (Denmark,
Finland, Norway, and Sweden) and Italy. For each case, four controls
matched by country, sex, year of birth, and year of CA test were
randomly selected. Occupational exposure and smoking habit were
assessed by a collaborative group of occupational hygienists. Logistic
regression models indicated a statistically significant increase in
risk for subjects with a high level of CAs compared to those with a low
level in the Nordic cohort (odds ratio, 2.35; 95% confidence
interval, 1.31–4.23) and in the Italian cohort (odds ratio,
2.66; 95% confidence interval, 1.26–5.62). These estimates were not
affected by the inclusion of occupational exposure level and smoking
habit in the regression model. The risk for high versus
low levels of CAs was similar in subjects heavily exposed to
carcinogens and in those who had never, to their knowledge, been
exposed to any major carcinogenic agent during their lifetime,
supporting the idea that chromosome damage itself is involved in the
pathway to cancer. The results have important ramifications for the
understanding of the role played by sporadic chromosome damage for the
origin of neoplasia-associated CAs.
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