Results provided by Bertazzi et al. on the 20-year mortality
of the Seveso population are of utmost importance,
because they bridge the gap between occupational and
environmental exposure levels. As a point of clarification,
people in the Seveso cohort had mean TCDD blood lipid
concentration of 136 ng TCDD/kg, which falls between
the typical occupational dioxin levels (> 1,000 ng TCDD/
kg) and background levels (2–3 ng TCDD/kg) [29].
Allowing for a latency time window of 15–20 years,
results for NHL clearly did stand out, according to Bertazzi
et al., with a relative risk of 2.8 (95% CI = 1.1–7.0)
[30,31]. These results have recently been confirmed in an
extended follow-up study (25 years) [32].
Recently, Baccarelli et al. proposed a biological mechanism
that could explain the dioxin-NHL association [33].
More than 80–90% of follicular and 20% of diffuse large
lymphomas carry the t(14;18) translocation, the most frequent
chromosomal translocation in human lymphoid
malignancies. They found that TCDD exposure was
related to increased numbers of t(14–18)-positive circulating
lymphocytes, but not to the proportion of t(14;18)-
positive subjects, in healthy individuals from Seveso, suggesting
that TCDD may promote clonal expansion of nonmalignant
cells carrying t(14;18).