Front Matter

182 Autism and Exposure to Environmental Chemicals

significant down‐regulation in oxytocin‐receptor positive neurons, reducing

the ability of the hormone oxytocin to bind effectively, when a child is born, to

certain parts of the brain that are essential for social interaction in humans.

It should be noted that, in fentomolar concentrations, when a pregnant woman

is exposed to a particular perfume, the perfume chemicals penetrate the blood

circulation via the lung (breathing) or through the woman’s skin (absorption).

These chemicals are diluted in about 6 liters of the woman’s blood/fluid vol­

ume and subsequently make their way to the tiny fetal brain. We believe that

only a few molecules make their way to the brain of the fetus and kill only a few

brain progenitor cells (hence the fentomolar concentrations used). However,

the impact of these few molecules could be enough to produce autism or ASD

(see below). One might wonder how only a few molecules can damage a fetal

brain. We all have encountered or know someone who has encountered an

allergic reaction to a bee, hornet, or certain perfumes. In each of these clinical

situations, only a few molecules trigger a cascade of events that can cause a

victim to break into hives or experience obstructive swelling of the lips, tongue,

and/or throat, trouble swallowing, shortness of breath or wheezing, turning

blue, a drop in blood pressure (feeling faint, confused, weak, passing out), loss

of consciousness, chest pain, or even death. All of these takes place due to very

few molecules of bee venom or perfume. We will take up the subject of allergic

reaction to fragrances later in this chapter.

As we covered in Chapter  4, oxytocin is involved in various social pro­

cesses that appear to be absent in ASD children, suggesting low binding

D3

control

D3

retinoic

acid

D6

control

D6

retinoic

acid

F11

control

F11

retinoic

acid

Synapto-

physin

CD56

Oxytocin

receptor

Chromo

-granin

A

Figure 7.2 An example of three clones developed by the single‐cell cloning method from a

female neuroblastoma cell line (i.e., CRL‐2266). Each of the clones was characterized by

using an array of antibody markers (four of which are shown here) that showed that each

single cell clone represents a unique progenitor neuron. In addition, each single‐cell clone

responded differently to retinoic acid.