170 Autism and Exposure to Environmental Chemicals
microdeletions and duplications (described in detail in Chapter 2), ASD has
been associated with a wide range of phenotypic features and severity. As we
have described in the previous chapter, wide variations observed in ASD chil
dren are most likely due to the timing during the prenatal period when the
fetus was exposed to a neurotoxic chemical and not the result of gene penetra
tion or degree of expression of ASD‐associated genes [1–7]. Support for the
possibility of an environmental contribution to the development of autism has
come from two major sources: first, the current understanding of the extreme
vulnerability of the developing human brain to toxic exposures in the environ
ment; and secondly, proof‐of‐concept studies that specifically link autism to
environmental exposure experienced prenatally [8]. There are numerous excel
lent review articles that have covered these subjects [8–20], so we will just
point out some of the types of agents involved: fragrances; lead; methylmer
cury; polychlorinated biphenyls (PCBs); arsenic; manganese; organophosphate
insecticides; DDT; and ethyl alcohol.
Are synthetic chemicals that humans are not evolutionarily exposed to
responsible for ASD? Over the last three decades, a substantial increase in the
prevalence of autism has been reported, from 4 to 5 children per 100,000 in the
1960s to around one in 45 children in 2015 [4,5]. Investigators have examined
many potential environmental factors including vaccination, maternal smok
ing, thimerosal exposure, and most likely assisted reproductive technologies,
but have decided that these factors are not related to risk for ASD. We maintain
that the alarming 20‐fold increase in autism in recent years is due to exposure
of the human population to an increasingly diverse set of synthetic chemicals
including herbicides, insecticides, food and drink flavors, drinking water, air
pollutants and fragrances, many of which have steroidogenic (male and female
hormone‐like chemicals) activity [1–5]. One can easily oppose the claims that
any of the chemicals in the food or liquid we consume are safe and that the US
government makes sure that all the chemicals in these common sources are
certified to be safe by independent Industrial Bio‐Test Laboratories (IBT). The
irony is that, according to published reports by Bioscience Resource (https://
bioscienceresource.org/) many of the safety documents cannot be trusted.
However, we do not want to get into the so called conspiracy realm and will
only present information from mainstream laboratory and epidemiological
studies, and show that undisclosed chemicals in fragrances, such as those that
produce different scents, increase shelf life, control time release of fragrances
and improve stability, have endocrine‐disrupting properties (reviewed in Ref.
[7]). This disruption has been linked to increased risks for cancer (reviewed in
Refs [4], [8], and [21]), adverse effects on developing fetuses [4,7], and meta
bolic diseases. For example, chemicals that have been shown to increase human
estrogen receptor (ER) expressions include octinoxate, oxybenzone, benzo
phenone‐1, benzophenone‐2, benzyl salicylate, benzyl benzoate, butylphenyl
methylpropional, and synthetic musks (galaxolide, tonalide, and musk ketone)