Teresa Binstock
Researcher in Developmental & Behavioral Neuroanatomy
April 13, 2009
EnvironmentalHealthNews.org (EHN) has
published a commentary (1) about a recently published study, "Ockman’s
Razor and Autism: The case for developmental neurotoxins contributing
to a disease of neurodevelopment" (2). The gist of the study is
summarized as, "Autism rates among school children living within a 10-
or 20-mile radius of toxic waste sites are nearly twice as likely to
have autism compared to children living farther away from such sites.
These data support the widely speculated but controversial idea that
exposure to chemical contaminants can increase the risk of developing
autism." (1)
The EHN commentary was allowed to be infused with politically charged
rhetoric offered by author Heather Patisaul, Ph.D., whose name
(Patisaul H) entered into PubMed generated no citations regarding
autism. Her phrase "widely speculated but controversial idea" in regard
to pollutants and autism is rank editorializing and implicitly suggests
few or no other findings support the association between autism rates
and pollution.
The most important omission in Dr. Patisaul's review is that she
doesn't mention a previous study with similar findings by Xue Ming,
M.D., Ph.D. (3; available free online). Nor does Dr. Patisaul mention
other peer-reviewed studies that have reported autism-rate associations
with pollutants, pesticides, and proximity to airborne pollutant
sources (eg, 4-8; see also 9)
Dr. Patisaul presents an absolute statement for which disagreement
abounds among autism researchers: She uttered declaratively, "Autism is
believed to result from improper brain organization during gestation."
(1) However, the fact that a substantial proportion of individuals with
autism or other autism-spectrum disorders have regressed (ie, have lost
previously acquired skills) is now widely recognized (eg, 10-12; see
also 13). As a result, the notion "improper brain organization during
gestation" may fits some and perhaps many individuals with autism, but
the notion no longer stands as the only model delineating an etiology
of autism.
Were Dr. Patisaul an undergraduate, her essay (1) would merit a grade
of 80% on a scale of 1 to 100, with 10% deducted for not mentioning
relevant studies already published, another 10% deducted for
reiterating an obsolete model that autism necessarily begins in utero
and thereby turning attention away from regressions into autism.
References:
1. Autism risk higher near toxic waste sites
Heather Patisaul, Ph.D.
http://www.environmentalhealthnews.org/ehs/newscience/autism-risk-higher-near-toxic-waste-sites
2. Ockman’s Razor and Autism: The case for developmental neurotoxins
contributing to a disease of neurodevelopment
M. Catherine DeSoto
Neurotoxicology Advance Publication in press, 2009
http://tinyurl.com/dxj7n7
3. Autism Spectrum Disorders and Identified Toxic Land Fills:
Co-Occurrence Across States
Xue Ming et al.
Departments of Neurosciences and Pediatrics
UMDNJ-New Jersey Medical School, Newark, NJ.
Environmental Health Insights 2008:2 55–59 [free online]
http://www.la-press.com/redirect_file.php?fileId=1420&filename=EHI-2-Ming-et-al&fileType=pdf
Abstract: It is believed that gene by environmental interactions
contribute to the pathogenesis of autism spectrum disorders (ASD). We
hypothesize that ASD are associated with early and repeated exposures
to any of a number of toxicants or mixtures of toxicants. It is the
cumulative effects of these repeated exposures acting upon genetically
susceptible individuals that lead to the phenotypes of ASD. We report
our initial observations of a considerable overlap of identified toxic
landfi lls in the State of New Jersey and the residence of an ASD
cohort, and a correlation between the identified toxic Superfund sites
on each U.S. state and the total number of diagnosed cases of ASD in
those states. The residence of 495 ASD patients in New Jersey by zip
code and the toxic landfill sites were plotted on a map of Northern New
Jersey. The area of highest ASD cases coincides with the highest
density of toxic landfill sites while the area with lowest ASD cases
has the lowest density of toxic landfi ll sites. Furthermore, the
number of toxic Superfund sites and autism rate across 49 of the 50
states shows a statistically signifi cant correlation (i.e. the number
of identified superfund sites correlates with the rate of autism per
1000 residents in 49 of the states (p = 0.015; excluding the state of
Oregon). These significant observations call for further organized
studies to elucidate possible role(s) of environmental toxicants
contributing to the pathogenesis of ASD.
4. Proximity to point sources of environmental mercury release as a
predictor of autism prevalence.
Palmer RF et al.
Health Place. 2009 Mar;15(1):18-24. Epub 2008 Feb 12.
http://images.huffingtonpost.com/2009-01-29-Palmer2008.pdf
"We found that for every
1000 pounds of industrial release, there was a corresponding 2.6%
increase in autism rates (p<.05) and a 3.7% increase associated with
power plant emissions(P<.05). Distances to these sources were
independent predictors after adjustment for relevant covariates. For
every 10 miles from industrial or power plant sources, there was an
associated decreased autism Incident Risk of 2.0% and 1.4%,
respectively (p<.05)."
5. Environmental mercury release, special education rates, and autism
disorder: an ecological study of Texas.
Palmer RF et al.
Health Place. 2006 Jun;12(2):203-9.
http://www.generationrescue.org/pdf/seed.pdf
"There was a significant
increase in the rates of special education students and autism rates
associated with increases in environmentally released mercury. On
average, for each 1,000 lb of environmentally released mercury, there
was a 43% increase in the rate of special education services and a 61%
increase in the rate of autism. The association between environmentally
released mercury and special education rates were fully mediated by
increased autism rates."
6. Autism spectrum disorders in relation to distribution of hazardous
air pollutants in the san francisco bay area.
Windham GC et al.
Environ Health Perspect. 2006 Sep;114(9):1438-44.
http://www.ehponline.org/members/2006/9120/9120.html
"The individual compounds that contributed most to these associations
included mercury, cadmium, nickel, trichloroethylene, and vinyl
chloride... Our results suggest a potential association between autism
and estimated metal concentrations, and possibly solvents, in ambient
air around the birth residence..."
7. Paraoxonase gene variants are associated with autism in North
America, but not in Italy: possible regional specificity in
gene-environment interactions.
D'Amelio M et al.
Mol Psychiatry. 2005 Nov;10(11):1006-16.
"These results are consistent with our model and provide further
support for the hypothesis that concurrent genetic vulnerability and
environmental OP [organochlorine pesticide] exposure may possibly
contribute to autism pathogenesis in a sizable subgroup of North
American individuals."
8. Maternal residence near agricultural pesticide applications and
autism spectrum disorders among children in the California Central
Valley.
Roberts EM et al.
Environ Health Perspect. 2007 Oct;115(10):1482-9.
"ASD risk increased with the poundage of organochlorine applied and
decreased with distance from field sites... The association between
residential proximity to organochlorine pesticide applications during
gestation and ASD among children should be further studied."
9. Cellular and mitochondrial glutathione redox imbalance in
lymphoblastoid cells derived from children with autism.
James SJ et al.
FASEB J. 2009 Mar 23. [Epub ahead of print]
"These results suggest that the autism LCLs exhibit a reduced
glutathione reserve capacity in both cytosol and mitochondria that may
compromise antioxidant defense and detoxification capacity under
prooxidant conditions."
"Exposure to oxidative stress via the sulfhydryl reagent thimerosal
resulted in a greater decrease in the GSH/GSSG ratio and increase in
free radical generation in autism compared to control cells."
10. Regression in autism: prevalence and associated factors in the
CHARGE Study.
Hansen RL et al.
Medical Investigation of Neurodevelopmental Disorders Institute
University of California, Davis, Sacramento 95817, USA
Ambul Pediatr. 2008 Jan-Feb;8(1):25-31.
"Subjects were aged 2 to 5 years, with autism (AU) or autism spectrum
disorder (ASD) confirmed by standardized measures. Children with
regression, defined as a) loss of both language and social skills or b)
loss of either language or social skills, were compared with each other
and to children with AU or ASD with no reported loss of skills on
developmental and adaptive functioning. Parents reported on seizure,
gastrointestinal, and sleep concerns. RESULTS: Fifteen percent (50/333)
of the combined AU-ASD group lost both language and social skills; 41%
(138/333) lost either language or social skills. No differences were
found between the 2 samples of children with regression. Few
developmental, demographic, or medical differences were found between
the combined regression group and children without loss of skills, in
both the larger AU-ASD sample and the more homogeneous AU-only sample.
Children with regression had significantly lower communication scores
than children without regression. CONCLUSIONS: The prevalence of
regression in a large sample of young children with AU and ASD varies
depending on the definition used; requiring loss of language
significantly underestimates the frequency of developmental regression.
Children with regression performed significantly less well than those
without regression on 2 measures of communication..."
11. Regression, developmental trajectory and associated problems in
disorders in the autism spectrum: the SNAP study.
Baird G et al.
Newcomen Centre, Guy's & St. Thomas' NHS Foundation Trust
London, SE1 9RT, UK.
J Autism Dev Disord. 2008 Nov;38(10):1827-36.
"We report rates of regression and associated findings in a population
derived group of 255 children aged 9-14 years, participating in a
prevalence study of autism spectrum disorders (ASD); 53 with narrowly
defined autism, 105 with broader ASD and 97 with non-ASD
neurodevelopmental problems, drawn from those with special educational
needs within a population of 56,946 children. Language regression was
reported in 30% with narrowly defined autism, 8% with broader ASD and
less than 3% with developmental problems without ASD. A smaller group
of children were identified who underwent a less clear setback.
Regression was associated with higher rates of autistic symptoms and a
deviation in developmental trajectory..."
12. Regression in autistic spectrum disorders.
Stefanatos GA.
Neuropsychol Rev. 2008 Dec;18(4):305-19.
"A significant proportion of children diagnosed with Autistic Spectrum
Disorder experience a developmental regression characterized by a loss
of previously-acquired skills. This may involve a loss of speech or
social responsitivity, but often entails both."
13. The autism myth of in-utero timing: a commentary on the
autism-timing speculations of Bauman and Kemper
by Teresa Binstock
http://members.jorsm.com/~binstock/bk.htm
Because the findings and speculations by Bauman and Kemper (B/K) are
often cited in autism articles and have shaped the way people think
about autism, a critique of those findings and speculations is
warranted, especially given that (i) the B/K findings are not in full
accord with findings from other researchers, (ii) the B/K speculations
about in-utero timings are based upon knife-lesions in an animal model
not necessarily applicable to humans, (iii) the B/K invocation of
non-gliosis as necessarily indicating in-utero timing is contrary to
recent findings about neuronal remodeling subsequent to excitotoxic
lesions, and (iv) the B/K inferior olive, cerebellum rationale (a)
derives primarily from a 1908 study in which cerebellar lesions were
the result of extreme pathologies not seen in autism, and (b) is
contrary to recent findings indicating lack of gliosis in
target-deprived neuronal alterations in adult animals. In this
critique, three conclusions are offered...
Contact Teresa Binstock by email
Return
to index of essays by Teresa Binstock
|