How Do We Smell? 89brain), these primordial neurons may not be sufficient in number so that once
they die, the brain may not have the capacity to regenerate that particular odor
recognition neuron(s). These are the germinal centers of those particular
odorant neurons.
We have shown recently by utilizing male and female neuroblastoma cell
lines (see details below) that these synthetic chemicals can also kill the neurons
that are particularly important in the development of a male brain (the oxy-
tocin‐ and arginine vasopressin‐receptor positive neurons) [24,25]. Oxytocin
promotes social interactions and recognition in many species and particularly
plays an important role in humans. Any disruption in the circuit mechanisms
through which oxytocin modifies olfactory processing can be detrimental for
normal social interaction [26]. Although anosmia (total loss of olfactory capac-
ity) may not occur, since the synthetic fragrances do not kill all ~450 different
kinds of odorant neurons found in man, the damage would be permanent.
We maintain that the same toxins that can cause olfactory damage, in the areas
behind the nose and those in the brain itself, can also lead to ASDs; hence the
importance of taking olfactory capacity loss seriously, as something far more
than loss of the normal ability to smell. Evidence of loss of selective odor
capacity in ASD is overwhelming and explains our notion that synthetic chem-
icals as well as other environmental agents may be killing off certain odorant
progenitor neurons during early fetal brain development.
It should be noted that if our hypothesis is correct that only selected progenitor
odorant neurons will be affected by the synthetic fragrant chemicals (as well as
other chemicals that can be toxic to these kinds of neurons), then one can
predict that there will be three groups of ASD children: one group would be
supersensitive to certain odors (since the dead neurons have been replaced
with surrounding neurons which have over grown to fill in the empty areas in
the fetal brain that were destroyed by the selective killing of other odorant
progenitor neurons); the second group would be deficient in certain odor sens-
ing ability; and the third group would be nearly normal [27–41]. By utilizing
the “sniff ” test, all three groups have been identified and have been reported by
numerous scientists. Just a reminder here that ASD is a “spectrum.” A keen
observer would notice a true spectrum in the symptomology of odor research
in ASD, with heightened odor sensitivity to the odor utilized in the ‘sniff ’ test
being reported, or abnormal response or no statistical differences, depending
on the odor and methods employed and the ASD population chosen to test the
assessments [4]. Heightened odor sense has been reported in ASD by some
investigators [27,28,30,31,37], with low odor responses in ASD children and
adults by other scientists [8,11–17,19,27,29–33], and no statistical differences
by yet other investigators [28,39,42].
It should be noted that the degree of loss of olfaction would depend on how
many kinds of synthetic odorant types and number of molecules actually
reached a fetal brain and at what stages of gestation. Furthermore, the fetal