Teresa Binstock
Researcher in Developmental & Behavioral Neuroanatomy
November 24, 2009
The question, Does thimerosal cause autism, needs be tweaked by concern
for mixtures. For instance, given the numerous chemicals found in human
bodies, we might ask, What is the role of injected thimerosal amid
other intra-body pollutants? First link herein is a synopsis of one of
the rare studies about mixtures (1). Other links, cites, and abstracts
herein typify mixture components relevant to ASDs including autism. The
citations speak for themselves and correspond to numbers in the
following list.
1. Synopsis of mixtures study: exposure may be “safe” only with one
chemical at a time
2. Association of environmental toxicants and conduct disorder in U.S.
children: NHANES 2001-2004
3. Traffic fumes can increase miscarriage risk - Telegraph
4. Risk factors for uteroplacental vascular compromise and
inflammation
5. Impact of gasoline inhalation on some neurobehavioural
characteristics of male rats
6. Autism spectrum disorders in relation to distribution of hazardous
air pollutants in the san francisco bay area.
7. Phthalates exposure and attention-deficit/hyperactivity disorder in
school-age children
8. Proximity to point sources of environmental mercury release as a
predictor of autism prevalence
9. Environmental mercury release, special education rates, and autism
disorder: an ecological study of Texas
10. Hepatitis B triple series vaccine and developmental disability in
US children aged 1-9 years
11. Hepatitis B vaccination of male neonates and autism
12. Mercury (Hg) and Lead (Pb) etc in AD and ADHD
13. A review of Thimerosal (Merthiolate) and its ethylmercury breakdown
product: specific historical considerations regarding safety and
effectiveness
The citations presented herein are not a thorough listing but instead
are symbolic of the complex interactions of exposures and intra-body
mixtures that are altering development of the central nervous system of
human embryos, fetuses, and infants.
When reporters declare that "autism is a mystery", they perpetuate a
cruel fiction.
References:
1. Synopsis of mixtures study: exposure may
be “safe” only with one chemical at a time
http://www.environmentalhealthnews.org/ehs/newscience/bad-mix-exposures-safe-only-one-chemical-at-a-time/
2. Association of environmental toxicants
and conduct disorder in U.S. children: NHANES
2001-2004
Braun JM, Froehlich TE, Daniels JL, Dietrich KN, Hornung R, Auinger P,
Lanphear BP.
Environ Health Perspect. 2008 Jul;116(7):956-62.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2453167/?tool=pubmed
OBJECTIVE: The purpose of this study was to examine the association of
tobacco smoke and environmental lead exposure with conduct disorder
(CD). METHODS: The National Health and Nutrition Examination Survey
(NHANES) 2001-2004 is a nationally representative cross-sectional
sample of the noninstitutionalized U.S. population. We examined the
association of prenatal tobacco, postnatal tobacco, and environmental
lead exposure with CD in children 8-15 years of age (n = 3,081). We
measured prenatal tobacco exposure by parent report of cigarette use
during pregnancy, and postnatal tobacco using serum cotinine levels. We
assessed lead exposure using current blood lead concentration. Parents
completed the Diagnostic Interview Schedule for Children to determine
whether their children met criteria of the Diagnostic and Statistical
Manual of Mental Disorders, 4th edition (DSM-IV ) for CD. RESULTS:
Overall, 2.06% of children met DSM-IV criteria for CD in the past year,
equivalent to 560,000 U.S. children 8-15 years of age. After
adjustment, prenatal tobacco exposure was associated with increased
odds for CD [odds ratio (OR) = 3.00; 95% confidence interval (CI),
1.36-6.63]. Increased blood lead levels (fourth vs. first quartile) and
serum cotinine levels (fifth vs. first quintile) were associated with
an 8.64-fold (95% CI, 1.87-40.04) and 9.15-fold (95% CI, 1.47-6.90)
increased odds of meeting DSM-IV CD criteria. Increasing serum cotinine
levels and blood lead levels were also associated with increased
prevalence of CD symptoms (symptom count ratio, lead: 1.73; 95% CI,
1.23-2.43; symptom count ratio, cotinine: 1.97; 95% CI, 1.15-3.40).
CONCLUSIONS: These results suggest that prenatal tobacco exposure and
environmental lead exposure contribute substantially to CD in U.S.
children.
3. Traffic fumes can increase miscarriage
risk - Telegraph
Oct 23, 2009 ...
http://www.telegraph.co.uk/health/healthnews/6408168/Traffic-fumes-can-increase-miscarriage-risk.html
4. Risk factors for uteroplacental vascular
compromise and inflammation
Baker AM, Braun JM, Salafia CM, Herring AH, Daniels J, Rankins N, Thorp
JM.
Am J Obstet Gynecol. 2008 Sep;199(3):256.e1-9.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680821/?tool=pubmed
OBJECTIVE: The purpose of this study was to identify potentially
modifiable risk factors of placental injury that reflect maternal
uteroplacental vascular compromise (UPVC) and acute and chronic
placental inflammation. STUDY DESIGN: A prospective epidemiologic study
was conducted. A total of 1270 placentas were characterized by gross
and microscopic examination. Placental pathologic condition was coded
for features of amniotic fluid infection syndrome (AFIS), chronic
villitis, UPVC, and fetal vascular obstructive lesions. Odds ratios
between UPVC, the acute and the chronic inflammatory lesions, and risk
factors of interest were calculated. RESULTS: After adjustment for
confounders, we found that women with a history of preterm birth had
1.60 times the odds of chronic inflammation (95% CI, 1.10, 2.55). Women
with a previous elective termination had 3.28 times the odds of acute
inflammation (95% CI, 1.89, 5.70). The odds of chronic villitis
increased with parity; the odds of AFIS decreased with parity.
CONCLUSION: We have identified several predictors of UPVC, AFIS, and
chronic villitis. Further studies are needed to examine whether
interventions to alter UPVC, AFIS, and chronic villitis will lead to
improved pregnancy outcomes.
5. Impact of gasoline inhalation on some
neurobehavioural characteristics of male rats
Amal A Kinawy
BMC Physiology 2009, 9:21 (24 November 2009)
Abstract
Provisional
PDF
6. Autism spectrum disorders in relation to
distribution of hazardous air pollutants in the san francisco bay
area.
Windham GC, Zhang L, Gunier R, Croen LA, Grether JK.
Environ Health Perspect. 2006 Sep;114(9):1438-44.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570060/?tool=pubmed
OBJECTIVE: To explore possible associations between autism spectrum
disorders (ASD) and environmental exposures, we linked the California
autism surveillance system to estimated hazardous air pollutant (HAP)
concentrations compiled by the U.S. Environmental
Protection Agency. METHODS: Subjects included 284 children with ASD and
657 controls, born in 1994 in the San Francisco Bay area. We assigned
exposure level by census tract of birth residence for 19 chemicals we
identified as potential neurotoxicants, developmental toxicants, and/or
endocrine disruptors from the 1996 HAPs database. Because
concentrations of many of these were highly correlated, we combined the
chemicals into mechanistic and structural groups, calculating summary
index scores. We calculated ASD risk in the upper quartiles of these
group scores or individual chemical concentrations compared with below
the median, adjusting for demographic factors. RESULTS: The adjusted
odds ratios (AORs) were elevated by 50% in the top quartile of
chlorinated solvents and heavy metals [95% confidence intervals (CIs) ,
1.1-2.1], but not for aromatic solvents. Adjusting for these three
groups simultaneously led to decreased risks for the solvents and
increased risk for metals (AORs for metals: fourth quartile = 1.7 ; 95%
CI, 1.0-3.0 ; third quartile = 1.95 ; 95% CI, 1.2-3.1) . The individual compounds that contributed most to
these associations included mercury, cadmium, nickel,
trichloroethylene, and vinyl chloride. CONCLUSIONS: Our
results suggest a potential association between autism and estimated
metal concentrations, and possibly solvents, in ambient air around the
birth residence, requiring confirmation and more refined exposure
assessment in future studies.
7. Phthalates exposure and
attention-deficit/hyperactivity disorder in school-age
children
Kim BN, Cho SC, Kim Y, Shin MS, Yoo HJ, Kim JW, Yang YH, Kim HW, Bhang
SY, Hong YC.
Biol Psychiatry. 2009 Nov 15;66(10):958-63.
BACKGROUND: Very few studies have examined the association between
attention-deficit/hyperactivity disorder (ADHD) and phthalate exposure
in humans. The aim of this study was to investigate the impact of
phthalates on symptoms of ADHD in school-age children. METHODS: A
cross-sectional examination of urine phthalate concentrations was
performed, and scores on measures of ADHD symptoms and
neuropsychological dysfunction with regard to attention and impulsivity
were obtained from 261 Korean children, age 8-11 years. RESULTS:
Mono-2-ethylheyl phthalate (MEHP) and mono-2-ethyl-5-oxohexylphthalate
(MEOP) for metabolites of Di-2-ethylhexylphthalate (DEHP) and
mono-n-butyl phthalate (MNBP) for metabolites of dibutyl phthalate
(DBP) were measured in urine samples. The mean concentrations of MEHP,
MEOP, and MNBP were 34.0 microg/dL (SD = 36.3; range: 2.1-386.7), 23.4
microg/dL (SD = 23.0; range: .75-244.8), and 46.7 microg/L (SD = 21.4;
range: 13.2-159.3), respectively. After adjustment for covariates,
teacher-rated ADHD scores were significantly associated with DEHP
metabolites but not with DBP metabolites. We also found significant
relationships between the urine concentrations of metabolites for DBP
and the number of omission and commission errors in continuous
performance tests (CPT) after adjustment for covariates. CONCLUSION:
The present study showed a strong positive
association between phthalate metabolites in urine and symptoms of ADHD
among school-age children.
8. Proximity to point sources of
environmental mercury release as a predictor of autism
prevalence
Palmer RF, Blanchard S, Wood R.
Health Place. 2009 Mar;15(1):18-24. Epub 2008 Feb 12.
http://images.huffingtonpost.com/2009-01-29-Palmer2008.pdf
The objective of this study was to determine if proximity to sources of
mercury pollution in 1998 were related to autism prevalence in 2002.
Autism count data from the Texas Educational Agency and environmental
mercury release data from the Environmental Protection Agency were
used. 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). While design limitations preclude
interpretation of individual risk, further investigations of
environmental risks to child development issues are warranted.
9. 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.
{free online}
http://www.generationrescue.org/pdf/seed.pdf
The association between environmentally released mercury, special
education and autism rates in Texas was investigated using data from
the Texas Education Department and the United States Environmental
Protection Agency. A Poisson regression analysis adjusted for school
district population size, economic and demographic factors was used.
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. This
ecological study suggests the need for further research regarding the
association between environmentally released mercury and developmental
disorders such as autism. These results have implications for policy
planning and cost analysis.
10. Hepatitis B triple series vaccine and
developmental disability in US children aged 1-9
years
Gallagher C, Goodman M. Toxicol Environ Chem 2008 90(5):997-1008.
{free online}
http://fourteenstudies.org/pdf/hep_b.pdf
This study investigated the association between vaccination with the
Hepatitis B triple series vaccine prior to 2000 and developmental
disability in children aged 1-9 years (n = 1824), proxied by parental
report that their child receives early intervention or special
education services (EIS). National Health and Nutrition Examination
Survey 1999-2000 data were analyzed and adjusted for survey design by
Taylor Linearization using SAS version 9.1 software, with SAS callable
SUDAAN version 9.0.1. The odds of receiving
EIS were approximately nine times as great for vaccinated boys (n = 46)
as for unvaccinated boys(n = 7), after adjustment for
confounders. This study found statistically significant evidence to
suggest that boys in United States who were vaccinated with the triple
series Hepatitis B vaccine, during the time period in which vaccines
were manufactured with thimerosal, were more susceptible to
developmental disability than were unvaccinated boys.
11. Hepatitis B vaccination of male
neonates and autism
CM Gallagher, MS Goodman
Annals of Epidemiology
Vol. 19, No. 9 ABSTRACTS (ACE)
September 2009: p. 659
Stony Brook University Medical Center, NY
PURPOSE: Universal newborn immunization with hepatitis B vaccine was
recommended in 1991; however, safety findings are mixed. The Vaccine
Safety Datalink Workgroup reported no association between hepatitis B
vaccination at birth and febrile episodes or neurological adverse
events. Other studies found positive associations between hepatitis B
vaccination and ear infection, pharyngitis, and chronic arthritis; as
well as receipt of early intervention/special education services (EIS);
in probability samples of
U.S. children. Children with autistic spectrum disorder (ASD) comprise
a growing caseload for EIS. We evaluated the association between
hepatitis B vaccination of male neonates and parental report of ASD.
METHODS: This cross-sectional study used U.S. probability samples
obtained from National Health Interview Survey 1997–2002 datasets.
Logistic regression modeling was used to estimate the effect of
neonatal hepatitis B vaccination on ASDrisk amongboys age 3–17 years
with shot records, adjusted for race, maternal education, and
two-parent household.
RESULTS: Boys who received the hepatitis B vaccine during the first
month of life had 2.94 greater odds for ASD (nZ31 of 7,486; OR Z 2.94;
p Z 0.03; 95% CI Z 1.10, 7.90) compared to later- or unvaccinated boys.
Non-Hispanicwhite boys were 61% less likely to have ASD(ORZ0.39;
pZ0.04; 95% CIZ0.16, 0.94) relative to non-white boys.
CONCLUSION: Findings suggest that U.S. male neonates vaccinated with
hepatitis B vaccine had a 3-fold greater risk of ASD; risk was greatest
for non-white boys.
12. Mercury (Hg) and Lead (Pb) etc in AD
and ADHD
Citations compiled by Teresa Binstock, June 2008
http://www.generationrescue.org/adhd/adhd-HgPbEtc.htm
13. A review of Thimerosal (Merthiolate)
and its ethylmercury breakdown product: specific historical
considerations regarding safety and effectiveness
Geier DA, Sykes LK, Geier MR.
J Toxicol Environ Health B Crit Rev. 2007 Dec;10(8):575-96.
{free online}
http://www.informaworld.com/smpp/content~db=all?content=10.1080/10937400701389875
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Binstock by email
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