The Scientific Committee of Medical Experts
for the Ministry of Work and Social Affairs
(Bundesministerium für Arbeit und Soziales)
documented a causal connection between
benzene and malignomas of the lymphohaematopoietic
system in September 2007.
The incidence of NHL has been steadily
increasing during the past 40 years. However,
changes in the NHL classification system
make it more difficult to compare data from
past studies with that from recent ones.
On the basis of biopersistence data and
exposure time, time-dependent risk-intervals
are reported in the literature for carcinogens
(smoking, radiation, chemotherapeutics, asbestos
etc.) and designated as latency or interim
periods after the end of exposure, that
is the time from the end of exposure to the
outbreak of disease. Extremely long latency
periods and steadily increasing tumour risks
are found only for biopersistent carcinogens
(asbestos, some persistent incorporated
sources of irradiation).
The epidemiological data for exposure
to benzene and NHL are inconsistent; in
particular, dose-response relationships cannot
be found. Reviews of the literature and
pooled data analyses do not yield consistent
results.
Studies of the long-term risk of developing
NHL demonstrate a critical time interval
of 15 years maximum after the end of benzene
exposure, after which there is no longer
a significant risk. The epidemiological data
indicate that this also applies for other lymphohaematopoietic
malignancies. The basic
mechanism for risk minimization is a time
dependent-process of elimination of the carcinogen
and its metabolites and the repair of
cellular damage.
Projection of carcinogenic risks for an
unlimited time is common in toxicology but
is not in agreement with the results of epidemiological
studies. It is not possible to
confirm the theory that latency periods after
exposure to carcinogens may be decadeslong
because of the „natural“ course of many
malignant diseases that generally become
more frequent with age.
Biopersistency, exposure time and repair
of cellular damage after exposure to a carcinogen
are of eminent importance for questions
of causality and compensation. These
considerations also have consequences in the
discussion of syncarcinogenesis which considers
the accumulated risks of often quite
separate exposures to carcinogens. There is
no reason to consider that an exposure which
took place decades ago involves a risk equal
to that associated with a recent exposure. The
proposal that the risk after exposure to a carcinogen
should remain constant life-long is
not in agreement with recent biological and
epidemiological data which take metabolic
and reparative processes into account.
