The cell-to-cell variance of an endpoint gives extra information, whic
h is highly model dependent and thus potentially useful for distinguis
hing between possible mechanisms. Some years ago, Virsik and Harder ca
lculated variances of dicentric chromosome aberrations using two assum
ptions: first, that dicentrics are produced independently by different
radiation tracks, and second, that the dicentric yield due to a singl
e track is Poisson distributed. It is shown that the formalism can be
generalised so that the Poisson assumption is dropped. This affects pr
edictions of neutron induced variances quite markedly. For lesions for
med directly, such as immediate, irremediable chromosomal breaks, the
formalism is general. For lesions formed by pairwise damage interactio
n, such as exchange-type chromosomal aberrations, the first assumption
(single track action) limits the applicability of the results to high
LET or low dose situations. In general, therefore, estimating varianc
es requires the use of spatially inhomogeneous models.